title: Human and Murine Kidneys Contain Transcriptionally and Spatially Orthologous Resident Macrophage Subpopulations in Acute Kidney Injury

city: Birmingham

last: George

address: 1720 2nd Ave South

institute: University of Alabama at Birmingham

summary: Acute kidney injury (AKI) is a major health burden in the United States. Macrophages have been shown to mediate AKI in murine models. Murine kidneys contain multiple subpopulations of kidney resident macrophages (KRM) that are transcriptionally and spatially distinct. We hypothesized the human kidney contains orthologous KRM subpopulations, both transcriptionally and spatially. We utilized kidney sections from donors diagnosed with mild to moderate AKI in order to increase the translatability of murine research to clinical settings. We used spatial transcriptomics and single cell RNA sequencing to identify five distinct human KRM subpopulations. Using the AddModuleScore function in Seurat, we were able to compare the murine KRM transcriptional profiles from pre and post-AKI to the human KRM subpopulations. As a result, we identified four  orthologous to known murine KRM subpopulations. The remaining population was identified in the kidney cortex and expresses a profile similar to activate microglia, the resident macrophage population in the brain. Again, we used AddModuleScore to determine a set of marker genes that will allow for the identification of KRM subsets across species and injury.

overall_design: CD45+ immune cells were isolated from human kidney samples by Fluorescence-activated cell sorting (FACS) and a FITC tagged CD45 antibody. Visium samples include 10 micron sections of human kidneys.

first: Elise

last: Erman

first: Kyle

last: Moore

first: Rehman

last: Soliman

first: Matthew

last: Cheung

first: Anupam

last: Agarwal


title: The nucleoskeleton protein NuMA maintains local chromatin architecture partially through promoting linker histone H1’ binding to chromatin and nucleosome stacking [ATAC-Seq]

status: Public on Mar 01 2024

city: Beijing

first: Wenxue

last: Zhao

address: Yiheyuan Road

country: China

institute: Peking University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Nucleoskeleton is generally considered to be the grid structure involved in regulation of genome expression and maintenance in the eukaryotic nucleus. However, its actual biological functions and mechanisms remain controversial. Here, we show the nuclear mitotic apparatus protein (NuMA), an essential regulator of the spindle, serve as one of the components of nucleoskeleton to regulates genome high-order architecture. In the interphase, fast depletion of NuMA leads to changes in chromatin organization, including increased accessibility of the genome, remodeling of nucleosome fibers and changes of transcription levels in certain heterochromatin regions. These effects are probably due to NuMA and linker histone H1’s interplay. We prove that NuMA interacts with linker histone H1 and linker DNA through its C-terminal domain. Such interaction facilitates H1’s binding to DNA and promotes nucleosome stacking, and might be part of the reason that NuMA maintains the local condensed state of heterochromatin. Collectively, our results reveal new biological functions of NuMA in the interphase, and also associates nucleoskeleton with genome organization at the mono-nucleosome level for the first time. This in-depth study on the mechanism of NuMA’s regulation on H1 and nucleosomes shed new light on how nucleoskeleton regulates genome architecture and gene expression.

overall_design: ATAC-seq (Assay for Transposase-Accessible Chromatin with high throughput sequencing) analysis of wildtype and NuMA-depleted HCT116 cells.

first: Yao

last: Wang


title: Role of folic acid in regulating intestinal flora and short-chain fatty acids based on in vitro fermentation model

city: Hangzhou

first: xiaogu

last: zheng

state: Zhejiang

address: Xiasha University Town

institute: Zhejiang Gongshang university

summary: Folic acid deficiency is common worldwide and is linked to intestinal flora imbalance. The intestinal microbial utilization of folic acid based on model animals faces the challenges of repeatability and individual variability. In this study, we built an in vitro fecal slurry culture model deficient in folic acid. We examined the effects of supplementation with different forms of folic acid (5-methyltetrahydrofolate and non-reduced folic acid) on the modulation of intestinal flora. 16S rDNA gene sequencing showed alpha diversity increased after folic acid supplementation compared to fermentation samples with folic acid deficiency. In the non-reduced folic acid (FA) group, the relative abundance of the Firmicutes phylum dropped to 56.7%, whereas in the 5-methyltetrahydrofolate (MTHF) supplementation group, it grew to 64.9%. Lactobacillus genera became more prevalent, reaching 22.8% and 30.8%, respectively. Additionally, Bifidobacterium and Pedioccus, two common probiotic bacteria, were in higher abundance. Short-chain fatty acids (SCFAs) analysis showed that supplementation with folic acid (non-reduced folic acid, 5-methyltetrahydrofolate) decreased acetic acid and increased the fermentation yield of isobutyric acid. The in vitro fecal slurry culture model developed in this study can be utilized as a human folic acid deficiency model for studying intestinal microbiota and demonstrated that both 5-methyltetrahydrofolate and non-reduced folic acid have effects on the regulation of intestinal microecology.

overall_design: Comparison of intestinal microecology between non-reducing folic acid and 5-methyltetrahydrofolic acid by 16s rRNA amplicon analysis.

first: Ping

last: Li

first: Xiaogu

last: Zheng

first: Chenlan

last: Xia

first: Manman

last: Liu

first: Hongchen

last: Wu

first: Jiaqian

last: Yan

first: Zihao

last: Zhang

first: Jieying

last: Huang

first: Qing

last: Gu


title: Transcriptome analysis of wild type and transgenic plants with excessive stomatal lineage cells

city: Shenyang

first: Wang

middle: Ming

last: Lin

address: 120 Dongling Road

institute: shenyang agricultural university

type: Expression profiling by high throughput sequencing

summary: To identify new regulators of stomatal development, we assay the transcriptomes of plants bearing enriched stomatal lineage cells undergoing active divisions.

overall_design: Overexpression of a truncated SPCH variant, SPCH∆49 that is insensitive to MAPK-triggered protein phosphorylation for degradation, produces excessive stomatal lineage cells in wild type and basl mutant background. Then comparative transcriptome analysis was conducted to identify noval stomata formation regulators

first: Xueyi

last: Xue

first: Zehao

first: Yuying

last: Sang

first: Huiling

first: Juan

last: Dong


title: Identifying gene expression changes in fibroblasts treated with an inhibitor targeting MLL1-MENIN complex and depleted for MEN1 gene during reprogramming using RNA-seqeuncing

city: İstanbul

first: Tamer

last: Önder

state: ANKARA

address: Rumelifeneri Yolu 34450, Sarıyer, İstanbul

country: Turkey

institute: Koc University

summary: Here we investigated the effects of MLL1-MENIN inhibition and MENIN depletion on somatic cell reprogramming.

overall_design: For samples 1-6, dH1f human fibroblasts were infected with lentiviral vectors expressing OCT4, SOX2, KLF4 and c-MYC and one day later treated with VTP50469 (1 uM) for 6 days. Control cells for the VTP50469 treatment were treated with DMSO. For samples 7-12, dH1f cells were not infected with the reprogramming vectors but were treated with the chemicals at the same concentrations for 6 days. For samples 13-18, dH1f human fibroblasts expressing Cas9 and non-targeting (NT1) and gRNA targeting MEN1 gene were infected with lentiviral vectors expressing OCT4, SOX2, KLF4 and c-MYC. For samples 19-24, dH1f cells were not infected with the reprogramming vectors. Total RNA was collected after 6 days of growth from all of the samples.

middle: T

last: Onder


title: Pancreatic juice-derived microRNA-4516 and microRNA-4674 as novel biomarkers for pancreatic ductal adenocarcinoma

city: Kurume

first: Takahiko

last: Sakaue

state: Fukuoka

address: 67 Asahi-machi

country: Japan

institute: Kurume University School of Medicine

summary:
<Background & Aims> Precise diagnostic biomarkers are urgently required for pancreatic ductal adenocarcinoma (PDAC). Therefore, the aim of this study was to identify PDAC-specific exosomal microRNAs (Ex-miRs) from pancreatic juice (PJ) and evaluate their diagnostic potential. <Methods> Exosomes in PJ and serum were extracted using ultracentrifugation and confirmed morphologically and biochemically. PDAC-specific Ex-miRs were identified using our original miR arrays, in which Ex-miRs derived from the PJ of patients with chronic pancreatitis (CP) were subtracted from Ex-miRs commonly expressed in both human PDAC cell lines and the PJ of PDAC patients. We verified the expression of these miRs using qRT-PCR. Changes in serum Ex-miR levels were assessed in two PDAC patients who underwent curative resection. In situ hybridization (ISH) was performed to directly visualize PDAC-specific miR expression in cancer cells.
<Results> We identified novel Ex-miR-4516 and Ex-miR-4674 from the PJ of PDAC patients, and they showed 80.0% and 81.8% sensitivity, 80.8% and 73.3% specificity, and 90.9% and 80.8% accuracy, respectively. The sensitivity, specificity, and accuracy of a triple assay of Ex-miR-4516/4674/PJ cytology increased to 93.3%, 81.8%, and 88.5%, respectively. In serum samples (n = 88), the sensitivity, specificity, and accuracy of Ex-miR-4516 were 97.5%, 34.3%, and 68%, respectively. Presurgical levels of Ex-miR-4516 in two patients with relatively early disease stages clearly declined after curative resection. ISH demonstrated that Ex-miR-4516 expression exclusively occurred in cancer cells. <Conclusions> Liquid assays using the in situ-proven Ex-miR-4516 may have a high potential for detecting relatively early stage PDAC and monitor its clinical course.

first: Hironori

last: Koga

first: Hideki

last: Iwamoto

first: Takuji

last: Torimura

first: Takumi

last: Kawaguchi


title: Effect of hypoxia on canine glioma stem-like cells metabolism

city: Davis

first: Ryan

last: Toedebusch

state: CA

address: 1 Shields Avenue

country: USA

institute: University of California

type: Methylation profiling by high throughput sequencing

summary:
To investigate the role of hypoxia treatment on the metabolic profiles of canine glioma cells
We then performed reduce representation bisulfite sequencing on 3 unique canine cell lines and correlated with functional assays

overall_design: Following hypoxia treatment, migration, viability, gene expression, and RRBS profiling was carried out to understand the role of metabolism-related changes in canine glioma cells

first: Christine


title: Mutation in mitochondrial chaperone TRAP1 is responsible for male-specific autism

city: Warsaw

first: Anna

middle: Maria

last: Hojka-Osińska

address: 4 Ks. Trojdena Street

country: Poland

institute: International Institute of Molecular and Cell Biology

summary: There is growing evidence of mitochondrial disturbance in autism spectrum disorders (ASD) but causative relations remain to be established. We identified postzygotic mozaicp.Q639* mutation in the TRAP1 gene encoding mitochondrial chaperone of the HSP90 family in ASD patient whose monozygotic twin brother was healthy. An additional survey of 176 unrelated ASD probands showed identical TRAP1 variant in a single male patient. We generated a knock-in Trap1 p.Q641*mouse which displayed behavioral abnormalities relevant for ASD, that were more pronounced in males. This effect was corroborated by gender-specific differences in synaptic plasticity and the density of synaptic mitochondria. Next we performed transcriptome profiling by sequencing of RNA isolated from hippocampi of WT, HET and MUT male and female mice

overall_design: Comparative transcriptome profiling analysis of RNA-seq data of the hippocampii of Trap1WT, Trap1WT/Q641*  and Trap1Q641* mice .

first: Bożena

last: Kuźniewska

first: Magdalena

last: Dziembowska


title: Concomitant inhibition of the thioredoxin system and non-homologous DNA repair potently sensitizes Philadelphia-positive lymphoid leukemia to tyrosine kinase inhibitors

first: Łukasz

middle: Wit

last: Komorowski

state: Mazovian

address: Jana Nielubowicza 5

department: Department of Immunology

institute: Medical University of Warsaw

summary: BCR-ABL1 gene fusion is an essential driver lesion in both chronic myeloid leukemia (CML) and Philadelphia-positive (Ph+) B-cell acute lymphoblastic leukemia (B-ALL). While tyrosine kinase inhibitors (TKIs) cure up to 95% of CML patients, 50 % of Ph+ B-ALL cases do not respond to treatment or relapse. This calls for new therapeutic approaches for Ph+ B-ALL. Dysregulated redox homeostasis manifested by the increased reactive oxygen species (ROS) levels and the upregulation of the thioredoxin (TXN) antioxidant system has been previously shown in B-ALL. Pharmacological inhibition of the TXN system with auranofin (AUR) efficiently kills B-ALL cells, indicating that the TXN system plays a major role in maintaining redox homeostasis in B-ALL cells. Here we show that peroxiredoxin-1 (PRDX1), one of the enzymes of the TXN system responsible for scavenging H2O2, is upregulated in Ph+ lymphoid as compared to Ph+ myeloid cells. The genomic knockout of PRDX1 negatively affects the viability of Ph+ B-ALL cells and sensitizes them to TKIs, while no such effects occur in myeloid cells. By analyzing global changes in gene expression in PRDX1-deficient cells treated with imatinib we discover non-homologous end-joining (NHEJ) DNA repair pathways as a novel vulnerability of Ph+ B-ALL cells. Accordingly, pharmacologic inhibition of the TXN system diminishes the viability of Ph+ B-ALL cells and enhances their sensitivity to TKIs and NHEJ inhibitors. Finally, we propose a novel combination of TKIs, TXN inhibitors, and NHEJ inhibitors as a potential therapeutic approach for the treatment of Ph+ B-ALL.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for BV173 cells and its KD derivatives (sgPRDX1). Cells were either untreated or treated with 250nM imatinib for 12 or 24h

first: Lukasz

first: Joanna

last: Madzio

first: Agata

last: Pastorczak

first: Kacper

last: Szczygieł

first: Martyna

last: Poprzeczko

first: Klaudyna

last: Fidyt

first: Maksymilian

last: Bielecki

first: Jaromir

last: Hunia

first: Agnieszka

last: Dabkowska

first: Tomasz

last: Stoklosa

last: Winiarska

first: Elzbieta

last: Patkowska

first: Jakub

last: Golab

first: Malgorzata

last: Firczuk


title: Hepatocyte E4BP4 promotes liver fibrosis via enhancing hepatic stellate cells activation

city: Ann Arbor

first: Sujuan

last: Wang

state: MI

address: 2800 Plymouth Road

department: Molecular & Integrative Physiology

institute: University of Michigan

summary: To investigate the role of E4bp4 during non-alcholic liver diseases, we subjected the WT mice and E4bp4 liver specific knockout (E4bp4-LKO) mice to NASH diet for 20 weeks.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for liver from NASH diet feeding WT mice and E4bp4 liver specific knockout mice.

first: Meichan

last: Yang

first: Deqiang

last: Zhang


title: The nucleoskeleton protein NuMA maintains local chromatin architecture partially through promoting linker histone H1’ binding to chromatin and nucleosome stacking [Hi-C]

first: Wenxue

last: Zhao

overall_design: Hi-C analysis of 3D genome architecture in wildtype and NuMA depleted HCT116 cell lines.

first: Yao


title: Transcriptomic and lipidomic analyses unravel the responses of Faecalibacterium prausnitzii to calcium palmitate

city: Groningen

first: Hermie

last: Harmsen

state: Groningen

address: Hanzeplein 1

country: Netherlands

institute: University Medical Center Groningen

summary: We investigate the underlying mechanism of the CP inhibition on F. prausnitzii by analysing its effects at the transcriptomic and lipidomic levels.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for the effect of 0.01 mg/mL calcium palmitate on F. prausnitzii.

first: Lu

first: Lei

last: Liu


title: Enhancing the direct reprogramming towards human naïve and expanded pluripotency

city: Hong Kong

first: Mingxi

last: WENG

state: Not Applicable

address: L408A, Laboratory Block, 21 Sassoon Road, Pokfulam, Hong Kong

country: Hong Kong

institute: School of Biomedical Sciences, The University of Hong Kong

summary: Naïve pluripotent and expanded potential stem cells (EPSCs) represent the pre-implantation epiblast which are molecularly, epigenetically and developmentally distinct from conventional primed pluripotent stem cells representing the epiblast of post-implantation embryo. These stem cell types offer expanded developmental potential towards extraembryonic tissues, clonality at the single cell level, high homogeneity and are more amenable for genome engineering. Here we use a polycistronic cassette to directly reprogram fibroblasts into induced EPSCs without a detour to primed pluripotency. When we replace SOX2 with engineered SOX17 factor (eSOX17),  we obtain 7 to 10 -fold more iEPSC colonies within shorter time periods. We next tested our reprogramming regimen in four media supporting naïve pluripotency reprogramming and could reproducibly obtain large numbers of clonally expandable colonies with eSOX17 whilst SOX2 occasionally fails. The resultant naïve pluripotent and expanded potential stem cells molecularly and functionally resemble their counterparts derived from embryonic stem cells. In sum, the use of engineered SOX17 factor enables a direct, fast, efficient and reproducible reprogramming of somatic cells into cells representative of the pre-implantation epiblast from somatic cells.

overall_design: We analyzed the gene expression profiles of induced expanded potential stem cells (iEPSCs) reprogrammed from human dermal firoblasts with OCT4/KLF4/C-MYC/SOX17FNV or OCT4/KLF4/C-MYC/SOX2.

last: Weng

first: Derek

last: Ho

first: Ralf

last: Jauch


title: Transcriptional regulation by FOXO1 in Human endothelial cells

city: Kumamoto

first: Shunsuke

last: Kamei

address: 2-2-1 Honjo

institute: Kumamoto University

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Trasncripional regulation by overexpression of constitutively active FOXO1 (CA-FOXO1) in human endothelial cells

summary: To identify genes regulated by FOXO1, we performed RNA-seq analysis of human unbilical vein endothelial cells (HUVECs) overexpressing CA-FOXO1 by adenovirus. CA-FOXO1 is constructed by mutating three amino-acids phosphorylated by Akt, T24, S256, and S319, and is constitutively localized in the nucleus compared to wild-type FOXO1.

overall_design: HUVEC cells were treated with adenovirus of either CA-FOXO1 or IRES-EGFP (Control). A total RNA sample was used for RNA-seq analysis.

first: Yuri

last: Miyamura

first: Takashi

last: Minami


title: ChIP-seq analysis for endogenous FOXO1 in human endothelial cells

summary: FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes.  Therefore, to identify genes regulated by FOXO1-binding in long-term VEGF stimulation, we performed ChIP-seq analysis of human unbilical vein endothelial cells (HUVECs) stimulated by VEGF for 18h.

overall_design: HUVEC cells were treated with human recombinant VEGF-A165 for 18h. The chrometin sample was used for ChIP-seq analysis with FOXO1 antibody and inputs.


title: The effect of Gelsevirine on ischemia penumbra

city: Nanjing

first: chen

last: xiang

address: chunhua street

institute: nanjing medical university

summary: Gelsevirine plays an important role in  modulating of  the neuroinflammation in ischemia penumbra

overall_design: Examination of different genes expression in ischemia penumbra of C57/BL6J mice

first: Chunlei

last: Xing

first: Li

last: Su

first: Yu


title: Trasncripional regulation by Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

summary: HUVEC cells were treated with human recombinant VEGF-A165 for either 0h or 18h. A total RNA sample was used for RNA-seq analysis.


title: Patient derived tumoroids of high grade neuroendocrine neoplasms for more personalized therapies

city: Bern

first: Philipp

last: Kirchner

address: Murtenstrasse 31

department: Pathology

country: Switzerland

institute: University of Bern

summary: Purpose: Advanced high-grade gastroenteropancreatic neuroendocrine neoplasm (GEP-NEN) are highly aggressive and heterogeneous epithelial malignancies with poor clinical outcomes. No therapeutic predictive biomarkers exist and representative preclinical models to study their biology are missing. Patient-derived (PD) tumoroids may enable fast ex vivo pharmacotyping and provide subsidiary biological information for more personalized therapy strategies in individual patients.  Experimental Design: PD tumoroids were established from rare biobanked surgical resections of advanced high-grade GEP-NEN patients. Using targeted in vitro pharmacotyping and next-generation sequencing of patient samples and matching PD tumoroids, we profiled individual patients and compared treatment-induced molecular stress response and in vitro drug sensitivity to the clinical therapy response.  Results: We demonstrate high success rates in culturing PD tumoroids of high-grade GEP-NENs within clinically meaningful timespans. PD tumoroids recapitulate biological key features of high-grade GEP-NEN and mimic clinical response to cisplatin and temozolomide in vitro. Moreover, investigating treatment-induced molecular stress responses in PD tumoroids in silico, we discovered and functionally validated Lysine demethylase 5A (KDM5A) and interferon-beta (IFNB1) as two vulnerabilities that act synergistically in combination with cisplatin and may present novel therapeutic options in high-grade GEP-NENs.  Conclusion: Patient-derived tumoroids from high-grade GEP-NENs represent a relevant model to screen drug sensitivities of individual patients within clinically relevant timespans and provide novel functional insights into drug-induced stress responses. Clinical patient response to standard-of-care chemotherapeutics matches with drug sensitivities of PD tumoroids. Together, our findings provide a functional precision oncology approach for gathering patient-centered subsidiary treatment information that will potentially increase therapeutic opportunities in the framework of personalized medicine.

overall_design: Differential expression from RNA-Seq of Original tumor tissue (fresh frozen tumor specimen) and patient-derived tumoroids (DMSO control; Temozolomide; Cisplatin)

first: Simon

middle: L

last: April-Monn

first: Aurel

last: Perren

first: Bertram

last: Wiedenmann


title: The transcriptional factor ONECUT3 is a driver and therapeutic target for complex karyotype MDS

first: Hongyan

last: Tong

address: No. 79 Qingchun Rd., Shangcheng District, Hangzhou, Zhejiang, China

department: Department of Hematology

institute: The First Affiliated Hospital, Zhejiang University School of Medicine


title: Role of Tubular Cpt1a in Aging Murine Kidneys

city: St. Louis

first: Leslie

middle: Stuart

last: Gewin

state: MO

address: 660 S Euclid Ave, McDonnell Science Building, Rm 718

department: Medicine (Nephrology)

institute: Washington University in St. Louis

summary: To compare the transcriptional profile in aged kidneys lacking tubular Cpt1a with floxed littermate controls.

overall_design:
All mice were males and on a mixed background.
Kidneys were either from mice that had Cpt1a deleted specifically in renal tubules (crossing Cpt1a floxed mice with Pax8-rTTA;tetO-Cre, which will be called Cpt1aCKO) or floxed controls. They had been treated for 3 weeks with doxycycline to activate Cre at age5-8 weeks.


title: MicroRNA-9 on the tumorigenesis of breast cancer in MMTV-PyMT mice model

first: Lufeng

last: Zheng

state: Jiangsu

address: Tongjia Xiang 24

department: School of Life Science and Technology, Jiangsu Key Laboratory of Carcinogenesis and Intervention

institute: China Pharmaceutical University


title: Genome-wide maps in tumors of MMTV-PyMT mice with or without miR-9 knockout

summary: Analysis of the transcriptome change of tumours of MMTV-PyMT mice with or without miR-9 knockout. MiR-9 regulates various transcripts and signaling pathways. Results provide insight into the role of miR-9-involved mechanisms underlying miR-9-mediated effects on breast cancer progression.

overall_design: MRNA profiles of tumours of MMTV-PyMT mice with or without miR-9 knockout were generated by deep sequencing, in two repeats, using Illumina NovaSeq 6000.

first: Tao

last: Xi


title: Specific serum methylome of the serrated pathway of colorectal carcinogenesis

city: Vigo

first: María

last: Gallardo-Gómez

address: Campus As Lagoas Marcosende

country: Spain

institute: Universidad de Vigo

summary: This study was conducted to explore the serum methylome of precancerous lesions belonging to the serrated pathway of colorectal carcinogenesis in a prospective multicentre cohort. Individuals were grouped into five main categories: (i) serrated adenocarcinoma (SAC), (ii) high-risk serrated polyps (HR-SP) comprising traditional serrated adenomas (TSA), sessile serrated lesions (SSL), and serrated polyps (SP) with dysplasia or ≥ 10 mm; (iii) high-risk hyperplastic polyps (HR-HP), defined as HP ≥ 10 mm; (iv) low-risk serrated lesions (LR-SL) including SP without dysplasia < 10 mm and HP < 10 mm; and (v) healthy individuals with no colorectal findings (NCF). First, epigenome-wide methylation levels were quantified in pooled cfDNA samples to characterize the differential methylation profile between no serrated neoplasia (NSN: NCF and LR-SL) and high-risk serrated lesions (HR-SL: HR-HP and HR-SP); concordance with tissue methylation levels was assessed using external datasets. Then, the pathway-specific cfDNA methylation signature was evaluated together with cfDNA pools from the conventional CRC pathway. cfDNA was extracted from serum samples and methylation measurements were assessed with the Infinium MethylationEPIC BeadChip. Data was mainly preprocessed and analyzed with R/Bioconductor packages.

overall_design: cfDNA was extracted from 106 serum sample with a modifyed phenol-chlorophorm protocol. A total of 11 cfDNA pooled samples were constructed using equal amounts of cfDNA from 5 men and 5 women with the same colorectal pathology as described in Gallardo-Gómez et al., Clinical Epigenetics 2018;10:53 (PMID: 29686738). Due to limited sample availability, hyperplastic polyps pooled samples contained 8 individuals (4 male, 4 female) each. cfDNA was bisulfite treated and was analyzed with the Infinium MethylationEPIC BeadChip microarray, covering over 850,000 CpG sites across the genome.

first: Maria

first: Loretta

last: De Chiara


title: Trasncripional regulation by FOXO1 in Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

first: Shunsuke

summary: FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes.  Therefore, to identify genes regulated by FOXO1 in long-term VEGF stimulation, we performed RNA-seq analysis of FOXO1-knockdowned human unbilical vein endothelial cells (HUVECs) by siRNA and 18h VEGF treatment.

overall_design: HUVEC cells were treated with either siFOXO1 or siControl for 24h, and human recombinant VEGF-A165 for 18h. A total RNA sample was used for RNA-seq analysis.

first: Yuri


title: Comparative cofactor screens reveal the influence of transactivation domains and core promoters on the mechanisms of transcription [RNA-seq]

city: Melbourne

first: Charles

middle: C

last: Bell

state: VICTORIA

address: VCCC, Gate 1, 14 Flemington Road

department: Cancer Research

country: Australia

institute: Peter MacCallum Cancer Centre

summary: Eukaryotic transcription factors (TFs) activate gene expression by recruiting cofactors to promoters. However, the relationships between TFs, promoters and their associated cofactors remain poorly understood. Here, we combine GAL4-transactivation assays with comparative CRISPR-Cas9 screens to identify the cofactors required by nine different TFs in human cells. Using this dataset, we associate key TFs with their cofactors, classify cofactors as ubiquitous or specific, discover novel transcriptional co-dependencies and demonstrate that certain TFs use the tail 2 and kinase submodules of Mediator to potentiate transcriptional elongation. By employing a reductionistic and comparative approach, we demonstrate that TFs do not display discrete mechanisms of activation. Instead, each TF is dependent on a unique combination of cofactors, which influences distinct steps in the transcriptional process. We also extend our screens to nine different core promoters to explore how core promoter elements influence cofactor dependence. Our data suggest that different classes of promoter are constrained by either initiation or pause release, which influences their dynamic range of gene expression and compatibility with specific cofactors. Overall, our comparative cofactor screens uncover the interplay between TFs, cofactors and core promoters and reveal general principles by which they influence transcription.

overall_design: RNAseq that includes 3 replicates for each sample. RNA-seq libraries were prepared using an in-house library preperation method similar to DRUG-seq. The method results in 3' RNA-seq libraries.

first: Mark

middle: A

last: Dawson

first: Laure

last: Talarmain

first: Andrea

last: Gillespie


title: Genome-wide maps in  mammary glands of MMTV-PyMT mice with or without miR-9 knockout.

summary: Analysis of the transcriptome change of mammary glands of MMTV-PyMT mice with or without miR-9 knockout. MiR-9 regulates various transcripts and signaling pathways.Results provide insight into the role of miR-9-involved mechanisms underlying miR-9-mediated effects on breast cancer progression.

overall_design: MRNA profiles of mammary glands of MMTV-PyMT mice with or without miR-9 knockout were generated by deep sequencing, in two repeats, using Illumina NovaSeq 6000.


title: Identifying transcriptional targets of ONECUT3 by ChIP-seq

summary: We report the direct target genes of the aberrant expression of ONECUT3 through next generation sequencing. We combine RNA-seq and ChIP-seq to identify target genes of ONECUT3 overexpression. RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) assays were performed on TP53-KO mouse embryonic fibroblast MEF with or without Doxycycline (100 ng/ml) to identify target genes both bound and regulated by ONECUT3. We found that genes related with sister chromosome exchange separation, mitotic nuclear division, and chromosome segregation were significantly upregulated by high level of ONECUT3. The top 10 directly activated target genes predicted by Binding and Expression Target Analysis (BETA) include Incenp and Cdca8, which are the critical components of Chromosomal Passenger Complex (CPC). Through this observation, we conclude that main role of ONECUT3 as transcription factors is to upregulate mRNA transcription of mitotic process. This sutdy provide new insight of genetic network of how dysfunctional ONECUT3 underlies mitotic defects and Chromosomal instability.

overall_design: Chromatin immunoprecipitation sequencing (ChIP-seq) assays were performed on p53 KO MEF without (Ctrl) or with (OE) Doxycycline (100 ng/ml) to identify target genes.

first: Yingwan

last: Luo

first: Gang

last: Huang


title: Comparative cofactor screens reveal the influence of transactivation domains and core promoters on the mechanisms of transcription [ChIP-seq]

overall_design: ChIP-seq to assess the effect of loss of various Mediator subunits and to assess the effect of loss of various cofactors on response to TNF treatment. Cells were harvested on D4 after infection with relevant sgRNAs. TNF treatment was performed for 6hrs prior to harvest at 25ng/ml. For all ChIP experiments, at least 20 million cells were crosslinked for 15 mins with 1% formaldehyde. Crosslinked material was sonicated to approximately 200-1000bp using the Covaris Ultrasonicator e220. Sonicated material was incubated overnight with each antibody, then incubated for 3hrs with Protein A magnetic beads. Beads were washed with low and high salt wash buffers, LiCl buffer and TE, before being eluted and de-crosslinked overnight. DNA was purified using Qiagen Minelute columns. All ChIP antibodies were used at ~10ug per IP and are listed under the antibodies section. Sequencing libraries were prepared from eluted DNA using Rubicon ThruPLEX DNA-seq kit. Libraries were size selected between 200-500bps and sequenced on the NextSeq500 using the 75bp single-end chemistry.


title: Overcoming dysfunctional innate sensing in myeloid cells circumvents cancer vaccine resistance

city: Dallas

first: Jiahui

last: Chen

state: TEXAS

address: 5323 Harry Hines Blvd

department: SCCC

institute: UTSW

summary: Chronic pathologic conditions like cancer exploit checkpoints to suppress T cell cytotoxicity and immune activity. Vaccines aiming to induce and amplify tumor-specific T cell responses have received promising anti-tumor effect in early clinical trials. However, the underlying mechanism driving resistance are poorly understand. Here, we sought to elucidate the myeloid cell populations which act as cellular checkpoints after perturbing the immune equilibrium in tumors using a T cell nanovaccine. We performed single cell RNA-sequencing of over 60,000 tumor infiltrating leukocytes isolated from a temporal profile of response and resistance following sub-optimal therapy. Though antigen specific T cells were highly boosted by the nanovaccine (70% of CD8+ cells), these cells became terminally exhausted over time with restricted T cell receptor diversity. Within the myeloid compartment, a MHChi-M2 macrophage population became dominant among late-stage resistance timepoint, which also exhibited progressively decreased STING activation (especially type I interferon expression). Terminally exhausted T cells and MHChi-M2 macrophages co-occurred in late-stage resistance and expressed ligand-receptor pairs that suggest their direct interaction to mediate T cell dysfunction, corroborated by immunohistochemistry. We combined the nanovaccine with another nanoparticle therapy targeting the STING pathway, which shifted the myeloid compartment towards a less suppressive state and increased progenitor and effector antigen-specific T cells while limiting terminal exhaustion. This study comprehensively profiled the highly dimensional, temporal dynamics of acquired vaccine resistance and associated immune dysfunction and identified cell populations which could serve as therapeutic targets to improve T cell immunotherapy.

overall_design: Different time points of tumor infitrated CD45+ immune cells in resistance induced by HPV+ E7 vaccine

first: Jinming

last: Gao

first: Longchao

last: Liu

first: Jonathan

last: Wilhelm


title: Genome-wide maps in MCF-7 cells with or without MiR-9 overexpression.

first: Lufeng

summary: Analysis of MCF-7 cells following miR-9 stable overexpression or not. MiR-9 regulates various mRNA expression in MCF-7 cells.Results provide insight into the role of miR-9-involved mechanisms underlying miR-9-mediated effects on breast cancer stemness.

overall_design: MRNA profiles of MCF-7 cells treated with or without miR-9 overexpression were generated by deep sequencing, in two repeats, using Illumina NovaSeq 6000.


title: TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

city: Bonn

first: Dirk

last: Baumjohann

state: NRW

address: Venusberg-Campus 1

department: Medical Clinic III

country: Germany

institute: University Hospital Bonn

summary: Naive murine CD4+ T cells from GREAT/SMART-17A mice were cultured under Th1 or Tfh(1 ng/ml TGF-β)-polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days; sorted by flow cytometry on IFNg+ (Th1), or CXCR5-IL17A+ (Th17) and CXCR5+IL17A- (Tfh); and subjected to bulk RNA-seq.

overall_design: Seq02: bulk RNA-seq: Th1IFNg+, Tfh(1)CXCR5+IL-17A–, Tfh(1)CXCR5+IL-17A–

first: Yinshui

last: Chang


title: Identifying transcriptional targets of ONECUT3 by RNAseq

city: Hangzhou

first: Hongyan

last: Tong

overall_design: RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) assays were performed on p53 KO MEF without (Ctrl) or with (OE) Doxycycline (100 ng/ml) to identify target genes both bound and regulated by ONECUT3.


title: High coverage single cell RNA-Seq of pooled MCF7 and HEK293-ZRT cells to discover expression patterns of the LINE1 retrotransposon

city: New Orleans

first: Victoria

last: Belancio

state: LA

address: 1430 Tulane Avenue

department: Structural and Cellular Biology

institute: Tulane University School of Medicine

summary:
We performed high coverage scRNA-Seq on a pool of MCF7 and HEK293-ZRT cells in a 9:1 ratio, respectively, using a total of 853 cells in this experiment. Detection of mobile element expression at the locus-specific level requires high sequencing depth. Here, MCF7 and HEK293-ZRT single cells have been sequenced to a sufficient level to quanitfy LINE1 expression in single cells and compare expression differences between individual cells.
Single-cell RNA sequencing was carried out on individual cells using the 10X Genomics Chromium™ Single Cell 3’ Library & Gel Bead Kit v3 and 150 cycle kit. 750 cells were targeted for sequencing.

overall_design: scRNA-Seq of MCF7 and HEK293-ZRT cells with a combined total of 853 cells. HEK293-ZRT cells were used as an internal control to test for accurate cell clustering. HEK293-ZRT cell identiity was confirmed by aligning reads to the ZRT transgene sequence. Raw reads were demultiplexed using 10X Genomics bcl2fastq command. Gene expression analysis was performed using 10X Genomics cellranger.


title: TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq03, bulk-RNAseq)

summary: Different numbers of naive murine CD4+ T cells were cultured at different seeding cell densities and under different polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days in the presence of 2 or 5 ng/ml TGF-β (Tfh2 or Tfh5) or with anti-TGF-β (TfhA), sorted by flow cytometry, and subjected to bulk RNA-seq.


title: TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq01, bulk-RNAseq)

summary: Naive murine CD4+ T cells were cultured under different polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days, sorted by flow cytometry, and subjected to bulk RNA-seq.

overall_design: Seq01: bulk RNA-seq: Th1, Tfh(anti-TGF-β) = TfhA, Tfh(5 ng/ml TGF-β) = Tfh(5)


title: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and CRP-E182D Transcriptomes

city: Tianjin

first: Yangyang

last: Zheng

address: 135 Yaguan Road, Jinnan District, Tianjin

institute: Tianjin University

summary: Strain engineering for industrial production requires the improvement of tolerance to multiple unfavorable conditions. Here, we report using global regulator libraries based on the CRISPR-enabled trackable genome engineering (CREATE) method to engineer tolerance against multiple inhibitors in Escherichia coli. Deep mutagenesis libraries were rationally designed, constructed, and screened to target 34,340 mutations across 23 global regulators. A total of 69 specific mutations that respectively conferred tolerance to acetate, NaCl, furfural, and high temperature were isolated, confirmed, and evaluated. Among them, 32 novel reconstructed mutations exhibited better tolerance to the corresponding inhibitors, and the most dramatic mutation CRP-E182D conferred high cross-tolerance to acetate, NaCl and isobutanol. To further investigate the effects of this mutation in the CRP on acetate tolerance, whole-transcriptome sequencing (RNA-Seq) analysis was performed.

overall_design: Mutant strain CRP-E182D was grown in the presence of 20 g/L sodium acetate and collected for transcriptome analysis. The wild-type strain MG1655 grown with 20 g/L sodium acetate was used as control. Each strain was grown in three independent replicates. RNA sequencing of 6 samples was performed using an Illumina HiSeq platform. The samples were collected during the mid-logarithmic phase, quickly frozen in liquid nitrogen and stored at -80 °C. Total RNA was extracted using the RNeasy Mini Kit (Qiagen, Valencia, CA, USA). The quantity and quality of the isolated RNA were determined using an Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA, USA), Nano Drop (Thermo Fisher Scientific Inc.) and 1% agarose gel electrophoresis. The following library preparation required 1μg of total RNA with an RNA Integrity Number (RIN) value above 6.5. The NEBNext® Ultra™ RNA Library Prep Kit for Illumina® (New England BioLabs, Ipswich, MA, USA) was used to construct next-generation sequencing libraries. The libraries sequencing was carried out on an Illumina HiSeq platform using a 2×150 paired-end (PE) configuration. The sequences were processed and analyzed by GENEWIZ (Suzhou, China).

first: Xin

last: Song

first: Shuting

last: Li


title: Effects continuous and transient lurbinectedin exposure on the EWS-WT1 gene signature in DSRCT

city: Philadelphia

first: Patrick

last: Grohar

state: PA

address: 3501 Civic Center Blvd

institute: Children's Hospital of Philadelphia

summary: We report the effects of 6 and 12 hour 5 nM exposure vs 1 hour 25nM exposure of lurbinectedin on two DSRCT cell lines.

overall_design: Evaluation of continuous 5nM and 25 nM transient exposure to lurbinectedin at 3 timepoints in 2 DSRCT cell lines

first: Jenna

last: Gedminas

first: Rebecca

last: Kaufman


title: chromatin Remodeling in Patient-Derived Colorectal Cancer Models

city: Durham

first: Ergang

last: Wang

state: NC

address: C215, LSRC

department: PCB

institute: Duke University

summary:
Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the epigenomes of different patient-derived models of colorectal cancer (PDO, PDX and PDOX) to the original patient tumor.
Methods: The Omni-ATAC protocol was utilized for ATAC library preparations. The nulcei were extracted from samples (PT, PDO, PDX and PDOX). For each sample set, three biological replicates were included. The libraries were sequenced using Illumina HiSeq 4000 PE 150bp.
Results: Using an optimized data analysis workflow, we achieved high quality ATAC-seq library. Data were mapped to hg19 with over 90% mapping rate, and relative low mitochondria fraction (<30%). We used Diffbind to assess the chromatin accessibility enrichment in each model with a strict threshold of p <0.05 and |logFC|>1.
Conclusions: Our study represents the first detailed analysis of CRC PDMC epigenome. CRC cells from all three models share chromatin alterations when compared to PT cells, representing a PT-PDMC epigenetic axis. Chromatin alterations in CRC cells are more similar betweeen PDOX and PDX than between PDOX and PDO, indicating that the growth environment of the model exerts strong influence on chraomtin adaptation in tumor cells.

overall_design: PT from 6 patients, PDO from 6 patients, PDOX from 6 patients, PDX from 3 patients

first: Kun

last: Xiang


title: Identification of differentially expressed genes in cisplatin-resistant and parental esophageal squamous cell carcinoma cells

city: Beijing

first: Qingyu

last: Luo

address: Panjiayuannanli No.17#, Chaoyang District

department: State Key Laboratory of Molecular Oncology

institute: Chinese Academy of Medical Sciences and Peking Union Medical College

summary: Drug resistance remains a main obstacle for cancer treatment. To reveal differentially expressed genes in chemoresistant cells, we established two pairs of resistant/parental esophageal squamous cell carcinoma (ESCC) cell lines, and performed whole transcriptome sequencing to identify both coding and noncoding RNAs that are significantly changed in chemoresistant cells. We identidied several important genes that contribute to the resistance of ESCC cells to chemotherapies.

overall_design: Whole transcriptome sequencing of KYSE450/DDP, KYSE450, YES2/DDP and YES2 cell lines. Two replicates for each arm.

first: Yabing

first: Xiaowei

last: Wu


title: Fenbutatin oxide resistance in the spider mite Tetranychus urticae

city: Ghent

first: Wannes

last: Dermauw

address: Coupure Links 653

department: Crop Protection

country: Belgium

institute: University Ghent

summary: Gene expression differences between MR-VL_FBO, a T. urticae strain highly resistant to fenbutatin oxide, and KOP8, a T. urticae strain susceptible to fenbutatin oxide, were determined.

overall_design: Four replicates for one comparison (MR-VL_FBO compared to KOP8)

first: Mousaalreza

last: Khalighi

first: Thomas

last: Van Leeuwen


title: Next generation sequencing facilitates quantitative analysis of wild type and overexpression of PuC3H35 transgenic lines Transcriptomes

city: Harbin City

first: Chenghao

state: HeiLongJiang Province

address: No. 51 HeXing Road,Xiangfang District

department: College of Forestry

institute: Northeast Forestry University

summary: For the RNA-seq experiments there week-old seedlings were cutting and subsequently transfer to 1/2 MS medium with or without 6% PEG6000 for 7 d and harvested roots. Samples were collected from there biological replicates (12 seedings each).

overall_design: RNA-seq of roots

first: Dandan


title: undetermined

first: Hao

last: Qi

address: No. 135 Yaguan Road, Haihe Educaton Park

summary: undetermined

overall_design: undetermined

first: Yang

first: Zhaoguan

first: Mengtong

last: Tang

first: Shurui

last: Liang

first: Peng

last: Yin

first: Hisashi

last: Tadakuma

first: Takuya

last: Ueda

first: Yan

last: Zhang


title: Generation of chemically induced totipotent cells through multi-parametric analysis of single-cells

city: Boston

first: Edroaldo

last: Lummertz da Rocha

state: MA

address: 1 Blackfan Circle

department: Hematology/Oncology

institute: Boston Children's Hospital

summary: Pluripotent stem cells fluctuate among distinct functional cell states. Such heterogeneity undermines the potential applications of stem cells in regenerative medicine. The heterogeneity of pluripotent cell states and their molecular nature remain less understood. Here, we utilized mass cytometry to dissect pluripotent cell states by simultaneously profiling multiple proteins and their modifications in single cells. Results indicated the role of extensive signaling cross-talk among multiple pathways in regulating cell state heterogeneity. By systematically dissecting the signals and their combinations, we identify conditions through which large portions of pluripotent cells can be chemically reprogrammed into totipotent cells which can be cultured. Unlike pluripotent cells, these chemically induced totipotent cells (CiTC) give rise to both embryonic and extra-embryonic cell types. In addition, CiTCs are molecularly distinct from pluripotent cells. CiTCs provide an in-vitro model to understand the nature of totipotent cells and the plasticity of pluripotent cells. Our quantitative and integrative approach provides general method to understand similar heterogenous cell systems such as cancer.

overall_design: Single-cell RNA-sequencing of a time-course of embryonic stem cells (ESC) under cell culture conditions to induce the totipotent-like cells

first: Mohan

last: Malleshaiah


title: (Pro)renin receptor inhibition reduces plasma cholesterol and triglycerides but does not attenuate atherosclerosis in atherosclerotic mice

city: Shenzhen

first: lu

middle: xi

last: feng

state: Guangdong

address: Taoyuan

institute: Shenzhen University

summary: Purpose: to clarify the transcriptomic changes in aortic arch of inhibiting the (pro)renin receptor using (P)RR G-ASOs

overall_design: Aortic arch isolated from non treated 8 week-old LDLR-/- mice (0 week control),  8-week-old LDLR-/- mice that received saline treatment and fed with WTD for 4 weeks, and 8-week-old LDLR-/- mice that received (P)RR G-ASOs treatment and fed with WTD for 4 weeks

first: Xifeng

last: Lu

first: Dien

last: Ye


title: ALKBH5 facilitates the progression of skin cutaneous melanoma through promoting ABCA1 demethylation and inhibiting autophagy in an m6A-dependent manner

status: Public on Feb 29 2024

city: Guangzhou

first: Julin

last: Xie

state: State...

address: Zhongshan 2nd Road, Yuexiu District, Guangzhou city, Guangdong Province, China

institute: First Affiliated Hospital of Sun Yat-sen University

summary: Background: N6-methyladenosine (m6A) is the most common and abundant mRNA modification, playing an essential role in biological processes and tumor development. However, the role of m6A methylation in skin cutaneous melanoma (SKCM) is not yet clear. This study analyzed the expression of m6A-related functional genes in SKCM and aimed to explore the key demethylase ALKBH5 mediated m6A modification and its potential mechanism in human SKCM. Methods: Based on public databases, the m6A-related gene expression landscape in SKCM was portrayed. MeRIP-Seq and RNA-Seq were used to recognize the downstream target of ALKBH5. In vivo and in vitro functional phenotype and rescue functional experiments were performed to explore the mechanism of the ALKBH5-ABCA1 axis in SKCM. Results: We found ALKBH5 upregulated in SKCM, associated with poor prognosis. ALKBH5 can promote melanoma cell proliferation, colony formation, migration, and invasion and inhibit autophagy in vitro, facilitating tumor growth and metastasis in vivo. We identified ABCA1, a membrane protein that assists cholesterol efflux, as a downstream target of ALKBH5-mediated m6A demethylation. Finally, our data demonstrated that ALKBH5 promoted SKCM via mediating ABCA1 downregulation by reducing ABCA1 mRNA stability in an m6A-dependent manner. Conclusion: Our findings exhibited the functional value of the key demethylase ALKBH5 mediated m6A modification in the progression of SKCM, suggesting ALKBH5 and its target ABCA1 as potential therapeutic targets in SKCM.

overall_design: To investigate the mechanism in regulating the progression and metastasis of skin cutaneous melanoma by demethylase ALKBH5, we established A375 cell lines in which target gene has been knocked down by shRNA. We then performed RNA-Seq and MeRIP-Seq using shALKBH5 and shCtrl A375 cell line, and the comparative expression analysis data was collected.

first: Hanwen

last: Wang

first: Shixin

last: Zhao

first: Hengdeng

last: Liu

first: Yiling

first: Zihui

first: Ziheng

last: Zhou

first: Shaohai


title: Patient-derived lymphoma spheroids integrating immune tumor microenvironment as preclinical follicular lymphoma models for personalized medicine

status: Public on Feb 28 2024

city: toulouse

first: gael

last: jalowicki

address: iuct

country: France

institute: iuct

summary: Background Follicular lymphoma (FL), the most common indolent non-Hodgkin’s Lymphoma, is a heterogeneous disease and a paradigm of the contribution of immune tumor microenvironment to disease onset, progression, and therapy resistance. Patient-derived models are scarce and fail to reproduce immune phenotypes and therapeutic responses. Methods To capture disease heterogeneity and microenvironment cues, we developed a patient-derived lymphoma spheroid (FL-PDLS) model culturing FL cells from lymph nodes (LN) with an optimized cytokine cocktail that mimics LN stimuli and maintains tumor cell viability. Results FL-PDLS, mainly composed of tumor B cells (60% on average) and autologous T cells (13% CD4 and 3% CD8 on average, respectively), rapidly organizes into patient-specific three-dimensional (3D) structures of three different morphotypes according to 3D imaging analysis. RNAseq analysis indicates that FL-PDLS reproduces FL hallmarks with the overexpression of cell cycle, BCR, or mTOR signaling related gene sets. FL-PDLS also recapitulates the exhausted immune phenotype typical of FL-LN, including expression of BTLA, TIGIT, PD-1, TIM-3, CD39 and CD73 on CD3+ T cells. These features render FL-PDLS an amenable system for immunotherapy testing. With this aim, we demonstrate that the combination of obinutuzumab (anti-CD20) and nivolumab (anti-PD1) reduces tumor load in a significant proportion of FL-PDLS. Interestingly, B cell depletion inversely correlates with the percentage of CD8+ cells positive for PD-1 and TIM-3. Conclusions In summary, FL-PDLS is a robust patient-derived 3D system that can be used as a tool to mimic FL pathology and to test novel immunotherapeutic approaches in a context of personalized medicine.

overall_design: 2D and 3D models from three patients are compared.

first: Carla

last: Faria

first: Fabien

last: Gava

first: Pauline

last: Gravelle

first: Juan

last: Garcia Valero

first: Celia

last: Dobaño-López

first: Nathalie

last: Van Acker

first: Cathy

last: Quelen

first: Gael

last: Jalowicki

first: Renaud

last: Morin

first: Cédric

last: Rossi

first: Jean-Michel

last: Lagarde

first: Jean-Jacques

last: Fournié

first: Loïc

last: Ysebaert

first: Camille

last: Laurent

first: Patricia

last: Pérez-Galán

first: Christine

last: Bezombes


title: Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a [Cut&Run]

city: Cambridge

first: Ce

last: Gao

address: 400 Technology Square

institute: Ragon Institute of MGH, MIT and Harvard

summary: CD4 T cells with latent HIV-1 infection persist despite treatment with currently available antiretroviral agents and represent the main barrier to a cure of HIV-1 infection. Pharmacological disruption of viral latency may increase the immunological vulnerability of HIV-1-infected cells, but the clinical efficacy of latency-reversing agents for reducing HIV-1 persistence remains to be proven. Here, we show in a randomized, controlled human clinical trial that the histone deacetylase inhibitor panobinostat, when administered in combination with pegylated interferon-a2a, induces a structural transformation of the HIV-1 reservoir cell pool, characterized by a disproportionate overrepresentation of HIV-1 proviruses integrated in ZNF genes and in chromatin regions with reduced H3K27ac marks, the molecular target site for panobinostat. In contrast, proviruses near H3K27ac marks appeared to be actively selected against, likely due to increased susceptibility to panobinostat. These data suggest that latency-reversing treatment with panobinostat can accelerate immune selection of HIV-1 proviruses.

overall_design: We performed CUT&RUNseq on isolated CD4T cells from PBMCs of 17 study participants in the ACTIVATE clinical trial to profile histone modifications in the genomic regions in response to the different study medications.

first: Marie

last: Armani-Tourret

first: Ciputra

last: Hartana

first: Isabelle

last: Roseto

first: Amy

last: Sbrolla

first: Katrina

last: Shea

first: Theresa

last: Flynn

first: Yelizaveta

last: Rassadkina

first: Liliana

last: Vela

first: Alexander

last: Hochroth

first: Carole

last: Lee

first: Francoise

last: Giguel

first: Rajeev

last: Malhotra

first: Frederic

middle: D

last: Bushman

first: Rajesh

last: Gandhi

first: Xu

middle: G

last: Yu

first: Daniel

middle: R

last: Kuritzkes

first: Mathias

last: Lichterfeld


title: Bulk-RNA seq in PC3shTIMP cell treated with Vehicle, Docetaxel , Adapelene or their combination (Combo)

city: Bellinzona

first: Andrea

last: Alimonti

address: Via vela 6

department: Molecular Oncology

institute: Institute of oncology research

summary: Cellular senescence, a stable cell growth arrest, can have dual effects in tumors, either suppressing or promoting tumor progression. The Senescence-Associated Secretory Phenotype (SASP), released by senescent cells, plays a crucial role in this dichotomy. Consequently, the clinical challenge lies in developing therapies that safely enhance senescence in cancer, promoting tumor-suppressive over tumor-promoting SASP factors.  Here, we identified the Retinoic-Acid-Receptor (RAR) agonist Adapalene as an effective pro-senescence compound in prostate cancer (PCa). The reactivation of the RARs triggers a strong senescence response and a tumor-suppressive SASP. In preclinical mouse models of PCa, the combination of Adapalene and Docetaxel, promotes a tumor-suppressive SASP that activates NK cell-mediated tumor clearance more effectively than either agent alone. This approach increases the efficacy of allogenic infusion of human NK cells in mice injected with human PCa cells, suggesting an alternative therapeutic strategy to stimulate the anti-tumor immune response in "immunologically cold" tumors.

overall_design: Bulk-RNA seq in PC3shTIMP cells treated with Vehicle, Docetaxel , Adapelene or their combination (Combo). Cells treated with Vehicle were used as internal controls. The analysis was performed on n=3 technical replicates for Vehicle, Adapalen and Combo samples, and on n=4 technical replicates for Docetaxel condition.

first: Troiani

last: Martina

first: Alimonti

last: Andrea


title: Transcriptome analyses of trophoblast upon hypoxia or normoxia

city: shanghai

first: ql

last: zheng

address: xiangyin

institute: immunity

summary: The hypoxia inducible molecules are proposed to be one of many key regulators of first trimester trophoblast behavior, but the key mechanism mediating invasion of trophoblast cells is not very clear.

overall_design: Transcriptome analyses of mRNAs from normoxia and hypoxia trophoblast cells

first: Qingliang

last: Zheng


title: Histone ChIP-seq from BLaER1 (ENCSR837LWL)

status: Public on Feb 27 2024

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Integrative analysis and risk model construction for super-enhancer-related immune genes in clear cell renal cell carcinoma

city: Guilin

first: Erlin

last: Song

address: No. 15 Lequn Road, Xiufeng District, Guilin, China

institute: Affiliated Hospital of Guilin Medical University

summary: To further development of SE-related lncRNA and mRNA expression differences, we have employed whole lncRNA microarray expression profiling as a discovery platform to identify SE-related immune genes with the potential to distinguish ccRCC.

overall_design: We selected five pairs of RCC and adjacent tissues (all specimens were pathologically confirmed as ccRCC after surgery) for microarray analysis.All experiment procedures were performed following the Arraystar standard protocol.

first: Zhenyu

last: Bi


title: Histone ChIP-seq from BLaER1 (ENCSR822ZAQ)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR524VDR)

summary:
H3K36me3 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR506IRD)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR999HNE)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Effects of mulberry (Morus alba L.) leaf ingestion on gene expression of peripheral whole blood [CvsQ]

city: Kanagawa

first: Asuka

last: Kamei

address: LiSE 4F C-4, 3-25-13 Tonomachi, Kawasaki-ku, Kawasaki-shi

department: Project for development of food functionality assessment methods

institute: Kanagawa Academy of Science and technology

summary: In the animal study, both a decrease of serum alanine aminotransferase level and whole blood gene expression changes were observed in rats fed a MLP-containing high-fat diet compared with rats fed a high-fat diet.

overall_design: Male Wistar rats (7 weeks old) were purchased from Japan SLC, Inc. (Shizuoka, Japan) and housed in a room that was maintained at 21 ± 1°C and 50 ± 10% relative humidity with a 12-h light/dark cycle (light 08:00–20:00; dark 20:00–08:00). The rats were preliminary given a normal diet (CE-2, CLEA Japan, Kanagawa, Japan) for acclimation. After a week of acclimation, the rats were divided into three groups (n=10 each) and fed for 8 weeks on a high-fat diet (Quick fat, CLEA Japan, Kanagawa, Japan), a high-fat diet plus 1% mulberry leaf powder, or a normal diet. Mulberry leaf powder was obtained from Sagamihara chamber of commerce and industry (Kanagawa, Japan). The rats were given a specific diet and water for 24 h ad libitum. On day 56 after overnight fasting, the animals were euthanized under anesthesia to collect their blood.

first: Yuki

last: Watanabe

first: Fumika

last: Shinozaki

first: Akihito

last: Yasuoka

first: Kousuke

last: Shimada

first: Yukihiro

last: Kobayashi

first: Mie

last: Nishimura

first: Maki

last: Miyazawa

first: Jun

last: Nishihira

first: Takashi

last: Kondo

first: Keiko

last: Abe


title: Histone ChIP-seq from BLaER1 (ENCSR506FPQ)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: A high-content arrayed CRISPR screen reveals genetic requirements for dynein-based trafficking

first: Steven

middle: William

last: Wingett

state: Cambs

address: Francis Crick Avenue, Cambridge Biomedical Campus

department: Cell Biology

country: United Kingdom

institute: MRC Laboratory of Molecular Biology

summary: The RNA-binding protein SUGP1 was one of many proteins identified in a CRISPR-based screen for proteins that promote dynein-based cargo trafficking in U-2 OS cells. To elucidate how SUGP1 promotes transport, we investigated changes in gene expression caused by disrupting the SUGP1 gene in this cell line with CRISPR/Cas9. As controls, we disrupted the XCR1 gene, which is not expressed in U-2 OS cells, and treated cells with crRNAs that lack specific targets in the human genome. Sequences were quality trimmed by the commercial provider of the RNA-seq data before being provided to the contributors.

overall_design: 9 RNA-seq datasets for 3 biological replicates for each crRNA condition (SUGP1, XCR1 and non-targeting control (NTC)).

first: C

last: Wong

first: S

middle: W

last: Qian

first: J

middle: M

last: Taliaferro

first: D

last: Ross-Thriepland

last: Bullock


title: m6A-Seq analyses of trophoblast upon hypoxia or normoxia

first: ql

last: zheng

summary: N6-methyladenosine (m6A) is the most prevalent messenger RNA modification in eukaryotes, but the potential roles of m6A methylated mRNA in trophoblast upon hypoxia remain elusive.

overall_design: m6A-Seq analyses of mRNAs from normoxia and hypoxia trophoblast cells

first: Qingliang

last: Zheng


title: Effects of mulberry (Morus alba L.) leaf ingestion on gene expression of peripheral whole blood [QvsM]

first: Asuka

last: Kamei

first: Yuki

last: Watanabe

last: Shinozaki


title: Effects of mulberry (Morus alba L.) leaf ingestion on gene expression of peripheral whole blood

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Histone ChIP-seq from BLaER1 (ENCSR839YFS)

first: ENCODE

last: DCC

summary:
H4K20me1 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR987EKG)

summary:
H3K27me3 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR992WXP)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Comprehensive characterisation of HNF4A and HNF1A genomic targets in pancreatic beta cells and hepatic cells reveals common and tissue-specific pathways and genes

city: Singapore

first: Adrian

middle: Kee Keong

last: Teo

state: Singapore

address: 61 Biopolis Drive, Proteos

department: Stem Cells and Diabetes Laboratory

country: Singapore

institute: IMCB, A*STAR

summary: To determine the downstream regulatory network of HNF4A and HNF1A, two transcription factors that play important roles in the pancreas and liver and that are associated with diabetes, we generated a comprehensive genome-wide map of the binding targets of HNF4A and HNF1A in hiPSC-derived pancreatic and hepatic cells and relevant cell lines using ChIP-Seq and molecular validation. We report binding targets of HNF4A and HNF1A that map to both known and novel gene promoters, that are common or differentially bound across different cell types and developmental stages. Overall, the detailed characterisation of the regulatory roles of HNF4A and HNF1A in pancreatic beta cells and hepatic cells will potentially shed light on how dysregulation of these factors can contribute to altered tissue development and function, and thus pathogenesis of both monogenic diabetes and T2D.

overall_design: Chromatin immunoprecipitation and sequencing (ChIP-Seq) was performed using antibodies against HNF4A and HNF1A in multiple cell types (EndoC-βH1 cells, human islets, hiPSC-derived pancreatic progenitors, hiPSC-derived endocrine progenitors, hiPSC-derived beta-like cells, hiPSC-derived hepatoblasts and HepG2 cells). ChIP-Seq was also conducted using the antibody against FLAG in EndoC-βH1 cells stably overexpressing FLAG-tagged HNF4A8 WT or T117I variant. Validation by ChIP-qPCR confirmed binding at selected targets.

first: Natasha

middle: H

last: NG

first: Soumita

last: GHOSH

middle: K

last: TEO


title: Histone ChIP-seq from brain (ENCSR817LUF)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR820DOR)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR477ATR)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR980ZJN)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR490DXW)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR827TOM)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR808DPZ)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR472CMR)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR972GGW)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR660WMS)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR797ELD)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR659KFN)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR451WXC)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR452JBP)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR660TLD)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR938FQG)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR642PBI)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR649DTM)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from Patski (ENCSR942RCG)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR939VQF)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR763VEJ)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR653NOJ)

summary:
H3K4me3 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR433GMU)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR638YPP)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR440PPG)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR422YCP)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR747ZAI)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR421YVG)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR921OXE)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR634UTP)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR754WUX)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR927XFE)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR632VNI)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR421CEE)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR420KZB)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR615ECV)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR917FJW)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR415ACV)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR612WDG)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR413YCI)

summary:
H3K27ac ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR911ONC)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR598XDA)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR597XRK)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR706VZI)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR595IZX)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR881ZMP)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 12 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR705USK)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR714QUE)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from Patski (ENCSR419OOD)

summary: For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR698XRC)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR400XSW)

summary:
H3K27ac ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR867ARL)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 48 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR872ROW)

summary:
H3K9ac ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR693KAX)

summary:
H3K4me2 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR863PSM)

summary:
H3K4me1 ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR380KTU)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR389TOA)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR548ADW)

summary:
CEBPA ChIP-Seq on untreated BLaER1 cell line.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR716KBL)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR687MPF)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR598CRA)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR371LUA)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR393ZOI)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR374JBS)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR368EZK)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR266SKT)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR261LYD)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR265LGX)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR355XNF)

summary:
H3K4me1 ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR256YSL)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 6 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR377IMJ)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR251DKX)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR258TUP)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 72 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR377EZA)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR337RFQ)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR056CYG)

summary:
H3K4me3 ChIP-Seq on BLaER1 cell line after 18 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR039WOA)

summary:
H3K9me3 ChIP-Seq on BLaER1 cell line after 24 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR326VRD)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR351OAC)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from BLaER1 (ENCSR400YGT)

summary:
CEBPA ChIP-Seq on BLaER1 cell line after 36 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR039CNL)

summary:
H4K20me1 ChIP-Seq on BLaER1 cell line after 168 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR056PCC)

summary:
H3K9ac ChIP-Seq on BLaER1 cell line after 9 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR174YDU)

summary:
H3K36me3 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR250YFT)

summary:
H3K4me2 ChIP-Seq on BLaER1 cell line after 120 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Histone ChIP-seq from BLaER1 (ENCSR266RKE)

summary:
H3K27me3 ChIP-Seq on BLaER1 cell line after 3 h treatment with 100 nM 17β-estradiol, 10 ng/mL Interleukin-3, 10 ng/mL CSF1.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf