title: Neutral evolution of snoRNA Host Gene long non-coding RNA affects cell fate control

city: London

first: Matteo

last: Vietri Rudan

address: Great Maze Pond

department: Centre for Gene Therapy and Regenerative Medicine

institute: King's College London

summary: A fundamental challenge in molecular biology is to understand how evolving genomes can acquire new functions. Several recent studies have underscored how non-conserved sequences can contribute to organismal diversification in the primate lineage. Actively transcribed, non-coding parts of the genome provide a potential platform for the development of new functional sequences, but their biological and evolutionary roles remain largely unexplored. Here we show that a set of neutrally evolving long non-coding RNAs (lncRNA) arising from small nucleolar RNA Host Genes (SNHGs) are highly expressed in skin and dysregulated in inflammatory conditions. Using SNHG7 and human epidermal keratinocytes as a model, we describe a mechanism by which these lncRNAs can increase self-renewal and inhibit differentiation. SNHG7 lncRNA’s activity has been acquired recently in the primate lineage and depends on a short sequence required for microRNA binding. Taken together, our results highlight the importance of understanding the role of fast-evolving transcripts in normal and diseased epithelia, and show how poorly conserved, actively transcribed non-coding sequences can participate in the evolution of genomic functionality.

overall_design: Human primary keratinocytes were transfected with siRNA targeting SNHG7 or Scramble controls in duplicate. Samples were collected after 24 and 48h from the start of transfection and analyzed by RNA-seq

first: Kalle

last: Sipilä

first: Christina

last: Philippeos

first: Clarisse

last: Gânier

first: Priyanka

last: Bhosale

first: Victor

last: Negri

first: Fiona

last: Watt


title: N2-alkyl-dG lesions trigger R-loop formation in genome

status: Public on May 01 2024

city: Riverside

first: feng

last: tang

state: CA

address: 26861 Campus Point Dr., Moreno Valley

department: chemistry

country: USA

institute: University of California, riverside

summary: Strand-specific kethoxal-assisted single-stranded DNA (ssDNA) sequencing (spKAS-seq) for mapping R-loop formation in HEK293T cells with/without the N2-heptynyl-dG treatment .

overall_design: spKAS-seq was conducted following previously published procedures (PMID: 36449625) with minor modifications, where N2-heptynyl-dG was added to the culture medium until its final concentration reached 10 μM. After a 3-h incubation, the cells were treated with 5 mM N3-kethoxal dissolved in the culture medium for 10 min at 37°C, then harvested the genomic DNA for mapping the R-loop formation.

first: Feng

last: Tang

first: Yinsheng

last: Wang


title: Expression data from adipose tissue macrophages of mice with or without moderate aerobic exercise

status: Public on Apr 17 2024

city: Guangzhou

first: Wenbai

last: Huang

state: Guangdong

address: 601 Huangpu Ave. Tianhe Dist.

department: School of Physical Education

country: China

institute: Jinan University

summary:
ATMs, which can constitute up to 50% of the cells in adipose tissue of obese mice 5, play a pivotal role in both metabolic and immune regulation of adipose tissue. This is particularly evident in both healthy states and in conditions associated with metabolic syndrome.
To delve into the precise mechanisms of the ATMs in response to exercise, we utilized exercise-induced primary ATMs and miRNAs microarray to investigate the effects of an 8-week aerobic exercise training on ATMs. Following the exercise regimen, ATMs were sorted using flow cytometer and subsequently analyzed through bioinformatics analysis to identify changes in miRNA expression.

overall_design: C57BL/6 mice were randomly assigned to either a sedentary (S) or an exercise (E) group. The S group remained inactive, while the E group underwent a one-week treadmill adaptation, followed by an 8-week aerobic treadmill exercise protocol (60 min/ day, 5 days/ week, at 65%-75% VO2max). Post-training, to investigate the effects of exercise in ATMs at the molecular level, miRNA microarray analysis was performed, followed by bioinformatic analysis.

first: Fei

last: Qin


title: Role of the TRIF-IFN-I pathway in Helicobacter-induced gastric cancer progression in an accelerated murine disease model

city: La Jolla

first: Christopher

last: Benner

state: California

address: 9500 Gilman Dr. MC 0640

department: Medicine

institute: University of California, San Diego (UCSD)

type: Expression profiling by high throughput sequencing

summary: Background: Helicobacter pylori (H. pylori) infection is a known cause of many digestive diseases, including gastritis, peptic ulcers, and gastric cancer. However, the underlying mechanism(s)by which H. pylori infection triggers these disorders are still not clearly understood.  Methods: We have developed an accelerated disease progression mouse model, which leverages mice deficient in the myeloid differentiation primary response 88 gene (Myd88-/-) infected with Helicobacter felis (H. felis) Findings: In this study, we found that H. felis-induced inflammation in Myd88-/- mice progressed to high-grade dysplasia, driven by activation of the type I interferon (IFN-I) signaling pathway and upregulation of its downstream targets, IFN-stimulated genes (ISGs). We also observed enrichment of IFN stimulated-response element (ISRE) motifs in the promoters of upregulated genes, further supporting the involvement of this pathway. In contrast, mice deficient in Toll/interleukin-1 receptor (TIR)-domain-containing adaptor inducing interferon-β (TRIF, TrifLps2) did not progress to severe gastric pathology after H. felis infection, implicating the TRIF signaling pathway in disease pathogenesis and progression. Additionally, analysis of gastric biopsy samples from human gastric cancer patients illustrated that low expression of Myd88 and high expression of Trif were both significantly correlated with poor survival. Interpretation: Our study using an accelerated animal model for gastric cancer and gastric biopsy samples from patients demonstrated that activation of the TRIF-IFN-I signaling pathway promotes Helicobacter-induced disease progression toward severe gastric pathology and gastric cancer development. This represents a potential target for therapeutic intervention, and further exploration may lead to the identification of novel treatment strategies.

overall_design: To investigate the role of Myd88 and Trif functions in Helicobacter-induced gastric cancer, RNA-seq expression profiling was conducted on gastric tissue from uninfected and infected tissue from WT, Myd88 KO, Trif KO, and Double KO mice.

first: Marygorret

last: Obonyo

first: Prerna

last: Bali

first: Ivonne

last: Lozano-Pope


title: Transcriptomic signature and pro-osteoclastic secreted factors of abnormal bone marrow stromal cells in fibrous dysplasia

status: Public on Apr 29 2024

city: Bethesda

first: Luis

middle: A

last: Fernandez de Castro Diaz

state: Maryland

address: 30 Convent Drive

department: SDMHS

institute: NIDCR/NIH

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Targeting an immunoregulatory dendritic cell-CCL22 program alleviates radioresistance

city: CHICAGO

first: Jason

last: Bugno

state: IL

institute: University of Chicago

summary:
Purpose: Radiation-mediated immune suppression limits efficacy and is a barrier in cancer therapy. Radiation induces negative regulators of tumor immunity including regulatory T cells (Treg). Mechanisms underlying Treg infiltration after radiotherapy (RT) are poorly defined. Given that dendritic cells (cDC) maintain Treg we sought to identify and target cDC signaling to block Treg infiltration after radiation.
Experimental Design: Transcriptomics and high dimensional flow cytometry revealed changes in murine tumor cDC that not only mediate Treg infiltration after RT, but associate with worse survival in human cancer datasets. Antibodies perturbing a cDC-CCL22-Treg axis were tested in syngeneic murine tumors. A prototype interferon-anti-epidermal growth factor receptor fusion protein (αEGFR-IFNα) was examined to block Treg infiltration and promote a CD8+ T cell response after RT.
Results: Radiation expands a population of mature cDC1 enriched in immunoregulatory markers that mediates Treg infiltration via the Treg-recruiting chemokine CCL22. Blocking CCL22 or Treg depletion both enhanced RT efficacy. αEGFR-IFNα blocked cDC1 CCL22 production while simultaneously inducing an antitumor CD8+ T cell response to enhance RT efficacy in multiple EGFR-expressing murine tumor models, including following systemic administration.
Conclusions: We identify a previously unappreciated cDC mechanism mediating Treg tumor infiltration after RT. Our findings suggest blocking the cDC1-CCL22-Treg axis augments RT efficacy. αEGFR-IFNα added to RT provided robust antitumor responses better than systemic free interferon administration, and may overcome clinical limitations to interferon therapy. Our findings highlight the complex behavior of cDC after RT and provide novel therapeutic strategies for overcoming RT-driven immunosuppression to improve RT efficacy.

overall_design: Live CD45+ CD11c+ cells were flow sorted from tumors 7 days after treatment with 20 Gy, fusion protein, or 20 Gy + fusion protein. The RNA library for sequencing was constructed using SMARTer® Stranded Total RNA-Seq Kit v2 - Pico Input Mammalian (Takara Bio) and sequencing performed at the University of Chicago Genomics Facility on an Illumina NovaSEQ machine in pair-read mode with 100 bp per read.

first: Ralph

middle: R

last: Weichselbaum


title: A fine kinetic balance of interactions directs transcription factor hubs to genes [ATAC-Seq]

status: Public on Apr 15 2024

city: philadelphia

first: Mustafa

last: Mir

state: PA

address: 3501 Civic Center Boulevard, CTRB 9030

institute: Children's Hospital of Philadelphia

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Eukaryotic gene regulation relies on the binding of sequence-specific transcription factors (TFs). TFs bind chromatin transiently yet occupy their target sites by forming high-local concentration microenvironments (hubs and condensates) that increase the frequency of binding events. Despite their ubiquity, such microenvironments have been difficult to study in endogenous contexts due to technical limitations. Here, we overcome these limitations and investigate how hubs drive TF occupancy at their targets. Using a DNA binding perturbation to a hub-forming TF, Zelda, in Drosophila embryos, we find that hub properties, including the stability and frequencies of associations to targets, are key determinants of TF occupancy. Our data suggest that hub targeting is driven not just by specific DNA motif recognition, but also by a fine-tuned kinetic balance of interactions between TFs and their co-binding partners.

overall_design: WT embryos were compared to embryos with the 5th Zinc Finger of Zelda deleted

first: Apratim

last: Mukherjee

first: Samantha

last: Fallacaro

first: Puttachai

last: Ratchasanmuang

first: Joseph

last: Zinski

first: Alan

last: Boka

first: Kareena

last: Shankta


title: Multi-target mode of action of Sulfodyne, a stabilized Sulforaphane, against pathogenic effects of SARS-CoV-2 infection

status: Public on Apr 10 2024

city: Fontenay aux roses

first: federica

last: ferri

address: 18 route du panorama

country: France

institute: cea

summary: The coronavirus disease 2019 (COVID-19) due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shown that, except vaccination, few therapeutics options for its treatment or prevention are available. Among the pathways that can be targeted for COVID-19 treatment, the Keap1/Nrf2 pathway seems of high interest as it regulates redox homeostasis and inflammation that are altered during SARS-CoV-2 infection. Here, we use three potent activators of the Keap1/Nrf2 pathway and showed that Sulfodyne, a stabilized natural Sulforaphane preparation with optimal bioavailability, had the highest antiviral activity in pulmonary or colonic epithelial cell lines even when added late after SARS-CoV-2 infection. This antiviral activity was not dependent on NRF2 activity but associated with action on ER stress and mTOR signaling that are activated during SARS-CoV-2 infection. Sulfodyne also decreased the inflammatory response of epithelial cell lines infected by SARS-CoV-2 independently of SARS-CoV-2 replication and reduced the activation of human monocytes that are recruited after infection of epithelial cells by SARS-CoV-2. Administration of Sulfodyne had little effects on SARS-CoV-2 replication in mice and hamsters infected with SARS-CoV-2 but significantly reduced weight loss and disease severity. Altogether, these results pinpoint the natural compound Sulfodyne as a potent therapeutic agent of COVID-19 symptomatology

overall_design: Calu-3 cells were infected with SARS-CoV-2 and treated or not with Sulfodyne at 12 hours post infection (hpi). Cells were harvested at 0hpi (mock), 12hpi, 18hpi and 36hpi for RNA-seq

first: Federica

last: Ferri


title: A fine kinetic balance of interactions directs transcription factor hubs to genes [RNA-Seq]


title: The impact of perinatal exposure to 2,4-BPS, BPSIP, BPS and E2 on the offspring of ICR mice

status: Public on Apr 06 2024

city: Fuyang

first: Qi

last: Wang

state: Anhui

address: 100 Qinghe West Road

institute: Fuyang Normal University

summary:
To investigate the effects of 2,4-BPS, BPSIP, BPS and E2 environmental hormones on offspring mice, we established a maternal exposure model from the first day of pregnancy until the end of lactation
We subsequently fed the progeny mice a standard diet until 10 weeks of age, harvested their livers, and conducted sequencing analysis

overall_design: Comparative gene expression profiling analysis of RNA seq data between offspring mice and normal mice after exposure to  2,4-BPS, BPSIP, BPS and E2

first: Shulin

last: Gao


title: Novel role of ALPI gene associated with constipation caused by complement component 3 deficiency

city: Miryang-si/Gyeongsangnam-do

first: Dae Youn

last: Hwang

address: 50 Cheonghak-ri, Samnangjin-eup

country: South Korea

institute: Pusan National University

summary:
To pinpoint a distinctive gene associated with constipation resulting from C3 deficiency, we conducted microarray hybridization using total RNA extracted from the mid colon of C3 knockout (C3 KO) mice.
Identification of causal genes through comparison of gene expression levels in mice induced with C3 deficiency.

overall_design: WT and C3 KO mice is 16 weeks old, and no other treatments.

first: Dae-Youn

last: Hwnag

first: Hee-Jin

last: Song


title: aChIP: efficient, sensitive, robust ChIP-seq for economically important plant organs [ChIP-Seq]

status: Public on Apr 28 2024

city: Wuhan

first: Wenying

last: Zhong

address: Lion Rock Street

institute: Huazhong Agricultural University

summary: Chromatin immunoprecipitation followed by sequencing (ChIP-seq) is a powerful method for profiling histone modifications and transcription factors binding throughout the genome. However, its application in economically important plant organs (EIPOs) such as seeds, fruits, tubers and flowers is challenging due to their sturdy cell walls and complex constituents. Here, we present advanced ChIP (aChIP), an optimized ChIP-seq strategy that efficiently isolates chromatin from plant tissues while simultaneously removing plant cell walls and cellular constituents. aChIP enables precise profiling of histone modifications in all tested EIPOs as well as transcription factors and chromatin-modifying enzymes. Notably, it significantly enhances ChIP efficiency and uncovers numerous novel modified sites compared to previous methods in vegetativetissues. Remarkably, aChIP unveils the first histone modification landscape of dry rapeseed seeds, illuminating the intricate roles of histone marks in EIPOs. Together, aChIP is a potent, efficient, and sensitive approach for comprehensive chromatin protein profiling across virtually all plant tissues, advancing plant epigenomics and functional genomics research, particularly within EIPOs.

sample_organism:
Citrus sinensis
Dianthus caryophyllus
Populus
Arabidopsis thaliana
Brassica napus
Glycine max
Solanum lycopersicum
Solanum tuberosum
Oryza sativa
Saccharum officinarum
Zea mays

overall_design: Chromatin Immunoprecipitation followed by seqencing (ChIP-seq) for histone modifications (H3K4me3 and H3K27me3), transcription factors (RNAPII and CAMTA3), DNA binding proteions (MBD7) and chromatin enzymes (DME) in different economically important plant organs (EIPOs) and vegetative tissues.

first: Qing

last: Zhang

first: Lun

last: Zhao


title: H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

city: Beijing

first: li

last: wang

institute: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital

summary: To investigate the distribution of H3.3B in VSMC phenotypic transition, we infect VSMCs with shNT or shH3f3b virus.

overall_design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone variants H3.3 in primary mouse VSMCs with shNT or shH3f3b.

first: Li

first: Xuelin


summary: To investigate the function H3f3b in the regulation of VSMC phenotypic transition, we infect VSMCs with shNT or shH3f3b virus.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for VSMCs and its KD derivatives (shH3f3b).


title: Whole-genome bisulfite sequencing of Mandarin fish ranavirus

status: Public on Apr 02 2024

city: Zhuhai

first: Mincong

last: Liang

address: No. 2 Daxue Road

department: School of Marine Sciences

institute: Sun Yat-sen University

type: Methylation profiling by high throughput sequencing

summary: To characterize the site-specific methylation landscape of the Mandarin fish ranavirus (MRV) genome, whole-genome bisulfite sequencing (WGBS) was conducted on an isolated MRV strain.

overall_design: After inoculating Mandarin fish fry (MFF-1) cells with MRV (MG941005.3) at 27°C and 5% carbon dioxide in Dulbecco's modified Eagle medium (DMEM) for 3 days, the sample was collected after repeated freeze-thaw cycles.  Virions were purified using a modified double sucrose gradient ultracentrifugation method.  Genomic DNA was extracted from the purified virions using the FastPure Cell/Tissue DNA Isolation Mini Kit (Vazyme, China), and whole-genome bisulfite sequencing (WGBS) was subsequently performed.

first: Weiqiang

last: Pan

first: Shaoping

last: Weng

first: Jianguo

last: He

first: Changjun

last: Guo


title: A chemogenetic screen for neuro-immune interactions in the gut: Trpv1+ nociceptor neurons control T regulatory cells

status: Public on Apr 01 2024

city: Boston

first: CBDM

last: Lab

state: MA

address: 77 Avenue Louis Pasteur

department: Microbiology and Immunobiology

institute: Harvard Medical School

summary: Neuroimmune crosstalk is critical for intestinal and tissue homeostasis. Yet the role of molecularly distinct subsets of gut-innervating neurons in regulating the activity of gut immunocytes, and the mechanisms of this neuroimmune signaling remain unclear. Here, we performed a chemogenetic and flow cytometry-based analysis of mice targeting eight different peripheral neuron subsets to assess how gut immunocytes are altered following neural activation. We found that distinct neurons modulated discreet anatomical populations of immunocytes in the gut in ileum, cecum, and colon. Nos1+ neuron activation decreased the percentage of RORg+ ileal conventional CD4+ T cells, whereas ChAT+ neuron activation decreased ileal neutrophils. Trpv1+ neuron activation displayed the most robust immunomodulatory phenotype, causing downregulation of RORg+ T regulatory cells in the colon and cecum. The immune cells exhibited decreased proliferation, enhanced cell stress, and altered cell activation markers. Further genetic and pharmacological approaches showed that spinal afferent Trpv1+ neurons specifically decreased Treg cells by signaling via the neuropeptide CGRP. Our study provided a comprehensive understanding of neuro-immune interactions, revealing a role for mechanisms by which Trpv1+ neurons regulate gut Treg cells.

overall_design: We investigated the transcriptional status of cecum immunocytes upon Trpv1+ neuronal activation. To do so we purified CD45+ cecum immunocytes from Trpv1-ADC mice and littermate CTRL mice (2 replicates for each group). Each sample was tagged with DNA-coded anti-CD45 hashtag antibodies (BioLegend). Cells were encapsulated using the Chromium Single Cell 5’ v3 platform (10X Genomics).

first: Yangyang

last: Zhu

first: Kimberly

last: Meerschaert

first: Diane

last: Mathis

first: Isaac

last: Chiu

first: Christophe

last: Benoist


title: Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp2]

status: Public on Apr 04 2024

first: Jakub

last: Jankowski

state: MD

address: 8 Center DR.

department: NIDDK

institute: NIH

summary: Sexual dimorphism in kidney injury markers, such as Klotho, is frequently underestimated or disregarded, as most of the preclinical research is done in male animals. Klotho is well-linked to renal health and its deletion in mice results in a severe accelerated aging-like phenotype and premature death. Here, we identified candidate Klotho enhancers and discovered their function using mice carrying deletions in the enhancer loci. Candidate Klotho enhancers were deleted using CRISPR/Cas9 genome editing. Warm ischemia-reperfusion surgery (IRI) was performed bilaterally to induce acute kidney injury and unilaterally in a fibrosis model. Using ChIP-seq and RNA-seq, we analyzed renal chromatin features and gene expression. ELISA and colorimetric assays were used to measure serum FGF23 and serum component levels. Removal of the enhancer caused more substantial reduction in Klotho mRNA levels in female mice compared to males (90 vs. 50%), supported by gene promoter marks remaining more pronounced in males. Weight, lifespan, and fertility of mice lacking the enhancers were not impacted. Only male mutant mice displayed higher Havcr1 expression after IRI than controls (mean 1048 vs. 231.4, p=0.0016). 28 days after unilateral IRI, only males displayed increased fibrosis markers, but with no difference between genotypes. Our findings reveal sexual dimorphism of Klotho gene expression and its enhancer regulation. Only male mutant mice were more susceptible to acute injury and the enhancer deletion had no impact on fibrosis. Additional investigation into the mechanisms governing Klotho regulation is imperative to reassess its effectiveness as a kidney injury marker.

overall_design: Chromatin Immunoprecipitation and DNA Sequencing (ChIP-Seq) of histone modifications H3K27ac and H3K4me3 in mouse kidneys was used to assess efficacy of deletion of candidate Klotho gene enhancers and to assess it's effect on renal chromatin landscape. RNA-seq was used to investigate the effects of Klotho enhencer deletion on renal gene expression.


title: Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [RNA exp1]


title: Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury


title: Deletion of Klotho enhancer deepens sexual dimorphism of gene expression without impacting female resistance to kidney injury [ChIP]

overall_design: Chromatin Immunoprecipitation and DNA Sequencing (ChIP-Seq) of histone modifications H3K27ac and H3K4me3 and transcription factor HNF1b in mouse kidneys was used to assess efficacy of deletion of candidate Klotho gene enhancers and to assess its effect on renal chromatin landscape.

first: Julia

last: Wilflingseder


title: Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler

status: Public on Mar 31 2024

city: Parma

first: Giorgio

last: Dieci

address: Parco Area delle Scienze 23/A

department: Deparment of Life Sciences

country: Italy

institute: University of Parma


title: Selective Regulation of a Defined Subset of Inflammatory and Immunoregulatory Genes by an NF-kB p50-IkBz Pathway

status: Public on Apr 23 2024

city: Los Angeles

first: Stephen

last: Smale

state: Ca

address: 6-730 MRL 675 Charles E. Young Drive South

department: MIMG

institute: University of California Los Angeles

summary: The five NF-kB family members and three nuclear IkB proteins play diverse biological roles, but the mechanisms by which distinct NF-kB and NF-kB: IkB complexes contribute to selective gene transcription remain poorly understood. Using nascent transcript RNA-seq, we observed considerable overlap between p50-dependent and IkBz-dependent genes in Toll-like receptor 4 (TLR4)-activated macrophages. Key inflammatory and immunoregulatory genes, including Il6, Il1b, Nos2, Lcn2, and Batf, were among the p50-IkBz co-dependent genes. IkBz typically bound genomic sites occupied earlier by NF-kB dimers. However, p50-IkBz co-dependence did not coincide with preferential binding of either protein, as p50, IkBz, and RelA co-occupied thousands of sites. A common feature of p50-IkBz co-dependent genes was close proximity to a p50/RelA/IkBz co-bound site exhibiting p50-dependent binding of RelA and IkBz. This result and others suggest that IkBz function is not restricted to p50 homodimers. Notably, IkBz and the p50-IkBz target genes comprise a high percentage of genes that exhibited the greatest differential expression between TLR4-stimulated and tumor necrosis factor receptor (TNFR)-stimulated macrophages, with ectopic IkBz rescuing a subset of these genes. These results reveal a defined p50-IkBz pathway that selectively activates a set of key inflammatory and immunoregulatory genes and serves as an important contributor to the differential responses to TNFR and TLR4.

overall_design:
To understand the binding kinetics of p50 and IkBz we performed ChIP-seq experiments with Lipid A stimulation for 0, 0.5, 1.0, 2.0, and 6.0 hour timepoints.
To evaluate the dependence of IkBz and RelA on p50 for chromatin interactions, we performed IkBz and RelA ChIP-seq in p50-/- BMDMs stimulated with Lipid A for 2.0 hours.
To explore the binding interaction between p50, RelA, and IkBz on a global level, we employed sequential ChIP-seq. We first performed a RelA immunoprecipitation followed by sequential immunoprecipitation by either p50, IkBz, or p53.

first: Allison

last: Daly

first: George

last: Yeh


title: Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

summary: Alu retrotransposons, forming the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their bulk expression has long been known to increase in response to various types of stress, including viral infection. Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus, by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase and of the YAP1 and FOS transcription factors. The physical interaction of e1a with the chromatin remodeler EP400 turned out to be critical for Alu derepression, and upstream enrichment of EP400 was found to commonly demarcate expression-prone Alus. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, mediated by e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenovirus.

overall_design: Total RNA-seq of G1-arrested IMR90 cells infected with HAdV-C5 mutant dl1500 (which expresses the immediate early protein E1A with little or no expression of other viral genes), versus infection with HAdV-C5 mutant dl312, with deletion of the complete E1A coding region. Mock-infected cells taken through the same changes in medium, but without addition of virus, served as a further control. The experiment was performed in duplicate. A second round of total RNA-seq was performed in G1-arrested IMR90 cells infected with HAdV-C5 mutant strains expressing e1a mutants that are impaired in the ability to interact with either RB-family proteins, EP300 and its paralog CREB Binding Protein (CREBBP), or EP400, compared to cells infected in parallel with mock- or dl1500. The experiment was performed in triplicate, exept for RB binding mutant, which was performed in duplicate.

first: Simona

last: Cantarella

first: Davide

last: Carnevali

first: Roberto

last: Ferrari

first: Marco

last: Morselli

first: Nathan

last: Zemke

first: Barbara

last: Montanini

first: Martin

last: Teichmann

first: Matteo

last: Pellegrini

first: Arnold

middle: J

last: Berk


title: Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

overall_design: ChIP-seq of BDP1, Pol III and TFIIIC in G1-arrested IMR90 cells infected with HadV-C5 mutant dl1500 (which expresses the immediate early protein E1A with little or no expression of other viral genes). Mock-infected cells served as control.

last: Vezzoli

first: Corally

middle: F

last: Daussy

first: Harald

last: Wodrich


title: Alcaligenes faecalis corrects aberrant matrix metalloproteinase expression to promote re-epithelialization of diabetic wounds

status: Public on Mar 30 2024

city: Philadelphia

first: Ellen

last: White

address: 421 Curie Blvd

department: Dermatology

institute: Perelman School of Medicine

summary: Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here we focused onAlcaligenes faecalis, a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds withA. faecalisaccelerated healing during early stages. We investigated the underlying mechanisms and found thatA. faecalistreatment promotes re-epithelialization of diabetic keratinocytes, a process which is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found thatA. faecalistreatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.

overall_design: Diabetic mouse wounds were treated with two different types of bacteria or vehicle control. At day 3, the skin was collected and processed for RNAsequencing. N = 4 mice per group

middle: K

first: Aayushi

last: Uberoi

first: Jamie

last: Ting-Chun Pan

first: Jordan

middle: T

last: Ort

first: Amy

middle: E

last: Campbell

first: Sofía

middle: M

last: Murga-Garrido

middle: C

last: Harris

first: Preeti

last: Bhanap

first: Monica

last: Wei

first: Nélida

last: Robles

first: Sue

last: Gardner

first: Elizabeth

last: Grice


title: Unveiling microbial dynamics in lung adenocarcinoma and adjacent nontumor tissues: Insights from nicotine exposure and diverse clinical stages via Nanopore Sequencing Technology

status: Public on Mar 25 2024

city: Zhengzhou

first: shuaifeng

last: wang

state: Henan

address: No.1 Jianshe East Road, Erqi District, Zhengzhou City, Henan Province

institute: The First Affiliated Hospital of Zhengzhou University

summary:
Background: Lung is the largest mucosal area of the human body and directly connected to the external environment, facing microbial exposure and environmental stimuli. Therefore, studying the internal microorganisms of the lung is crucial for a deeper understanding of the relationship between microorganisms and the occurrence and progression of lung cancer.
Methods: Tumor and adjacent nontumor tissues were collected from 38 lung adenocarcinoma patients and used nanopore sequencing technology to sequence the 16s full-length sequence of bacteria, and combining bioinformatics methods to identify and quantitatively analyze microorganisms in tissues, as well as to enrich the metabolic pathways of microorganisms.
Results: the microbial composition in lung adenocarcinoma tissues is highly similar to that in adjacent tissues, but the alpha diversity is significantly lower than that in adjacent tissues. The difference analysis results show that the bacterial communities of Streptococcaceae, Lactobacillaceae, and Neisseriales were significantly enriched in cancer tissues. The results of metabolic pathway analysis indicate that pathways related to cellular communication, transcription, and protein synthesis were significantly enriched in cancer tissue. In addition, clinical staging analysis of nicotine exposure and lung cancer found that Haemophilus, paralinfluenzae, Streptococcus gordonii were significantly enriched in the nicotine exposure group, while the microbiota of Cardiobactereae and Cardiobacterales were significantly enriched in stage II tumors. The microbiota significantly enriched in IA-II stages were Neisseriaeae, Enterobacteriales, and Cardiobacterales, respectively.
Conclusion Nanopore sequencing technology was performed on the full length 16s sequence, which preliminarily depicted the microbial changes and enrichment of microbial metabolic pathways in tumor and adjacent nontumor tissues. The relationship between nicotine exposure, tumor progression, and microorganisms was explored, providing a theoretical basis for the treatment of lung cancer through microbial targets.

overall_design: We collected tumor and adjacent nontumor samples from 37 lung cancer patients, sequenced microbial DNA within the tissues using Nanopore sequencing technology, and studied the microbial profile using bioinformatics analysis technology

first: Kangli

last: Yang

first: Shuaifeng

last: Wang

first: Zheng

last: Ding

first: Kai

last: Zhang

first: Weiwei

last: Zhu

first: Huifen

first: Mengshu

last: Pan

first: Xiangnan

last: Li

first: Hongmin

first: Zujiang

last: Yu


title: Impact of Multiple Antimicrobial Exposures on the Transfer Efficiency of Multidrug Resistance Plasmids in Salmonella enteric

city: Jefferson

first: Steven

last: Foley

state: AR

address: 3900 NCTR Road

department: Microbiology

institute: National Center for Toxicological Research, U.S. Food and Drug Administration

summary: Antimicrobial exposure can potentially lead to increased antimicrobial resistance plasmid transfer. RNA sequencing data was collected from conjugal pairs of Salmonella enterica and Escherichia coli exposed or not exposed to tetracycline over a time course to determine differences in transcript numbers associated with conjugation and tetracycline exposure. The samples were sequenced on the Illumina HiSeq X10 platform with the 150-bp paired-end kit. Among the most highly up-regulated genes in the tetracycline exposed samples were also  tetracycline efflux pump genes across the timepoints. In addition, some conjugal transfer-associated genes (e.g. traJ and traA) were upregulated in the tetracycline exposed samples.

sample_organism:
Salmonella enterica
Escherichia coli J53

overall_design:
To assess differential regulation of genes involved in plasmid transfer following tetracycline exposure, we mixed doner (Salmonella enterica 452) and recipient (E. coli J53) and exposed to different concentration of  tetracycline. Total RNA was isolated from mating pairs at different time points following tetracycline exposure.  A non-tetracycline exposed sample were in parallel with the exposed ones. Three RNA samples were isolates from each time point(triplicate).
The differential genes expression during mating experiment following tetracycline were analyzed by comparing it with non-exposed sample for each time points.


title: CITE-Seq analysis of immune populations in paired human epicardial adipose tissue and right atrial appendage tissue samples

status: Public on Apr 08 2024

city: London

first: Vishal

last: Vyas

address: Charterhouse Square

country: United Kingdom

institute: William Harvey Research Institute, Queen Mary University of London

summary: The primary aim of the study was to compare the immune repertoire of human epicardial adipose tissue with the underlying myocardium with a focus on T cell subsets and specifically tissue-resident memory T cell populations.

overall_design:
Two paired human epicardial adipose tissue and right atrial appendage tissue specimens were obtained during open chest cardiac surgery. The tissue specimens were enzymatically digested to isolate the stromal vascular fraction. CD45+ immune fraction was then isolated through PE bead enrichment using Nanobeads.  Cells were stained with CITE-Seq antibodies (antibody-derived tags) and further CD45+ enrichment was performed using fluorescence-activated cell sorting (FACS). The samples were maintained at a concentration of ~1000 cells/μL and processed as per the 10x Genomics CITE-Seq workflow with TotalSeq(TM)-C for cell surface protein and antigen specificity..
ADT Description                                                                  Barcode Sequence
TotalSeq™-C0138 anti-human CD5 Antibody                    CATTAACGGGATGCC
TotalSeq™-C0358 anti-human CD163 Antibody                   GCTTCTCCTTCCTTA
TotalSeq™-C0160 anti-human CD1c Antibody                   GAGCTACTTCACTCG
TotalSeq™-C0049 anti-human CD3 Antibody                    TATCCCTTGGGATGG
TotalSeq™-C0072 anti-human CD4 Antibody                    TGTTCCCGCTCAACT
TotalSeq™-C0080 anti-human CD8a Antibody                   GCTGCGCTTTCCATT
TotalSeq™-C0087 anti-human CD45RO Antibody                   CTCCGAATCATGTTG
TotalSeq™-C0148 anti-human CD197 (CCR7) Antibody                   AGTTCAGTCAACCGA
TotalSeq™-C0146 anti-human CD69 Antibody                   GTCTCTTGGCTTAAA
TotalSeq™-C0088 anti-human CD279 (PD-1) Antibody                   ACAGCGCCGTATTTA
TotalSeq™-C1046 anti-human CD88 (C5aR) Antibody                   GCCGCATGAGAAACA

first: M

middle: P

last: Longhi


title: Mycobacterium tuberculosis induced interferon pathways distinguish responses of Human Alveolar Macrophages from Monocyte-Derived Macrophages

status: Public on Mar 20 2024

city: Seattle

first: Kimberly

last: Dill-McFarland

state: WA

address: 750 Republican St

department: Allergy and Infectious Diseases

institute: University of Washington

summary: Alveolar macrophages (AMs) and recruited monocyte-derived macrophages (MDMs) mediate early lung immune responses to Mycobacterium tuberculosis (Mtb). Using paired human AMs and MDMs from 6 healthy volunteers, we investigated transcriptional profiles in responses to Mtb. We found 681 genes that were Mtb-dependent in AMs compared to MDMs, 107 that were induced in both cell types but in different directions, and 4538 that were Mtb-dependent in MDMs but not AMs (FDR < 0.05). We found that IFNA Response and IFNG Response were the top two gene sets selectively induced in Mtb-infected AM. Thus, a second experiment utilized MDMs treated with IFNA1, IFNA8, IFNE, or IFNL1 found that  IFNA8 modulated Mtb-induced pro-inflammatory cytokines and, compared to other interferons,stimulated unique transcriptional profiles.

overall_design: Using paired human AMs and 5-day MCSF-derived MDMs from 6 healthy volunteers, we infected cells for 6 hours with Mtb H37Rv, isolated RNA, and analyzed transcriptomic profiles with RNASeq. A second experiment utilized MDMs treated with IFNA1, IFNA8, IFNE, or IFNL1 for 6 hours.

first: Monica

last: Campo

first: Glenna

last: Peterson

first: Basilin

last: Benson

first: Shawn

last: Skerret

first: Thomas

last: Hawn


title: A bioinformatic pipeline for analysis of M.EcoGII methylation footprint PacBio long-read sequence data

status: Public on Mar 15 2024

city: Bethesda

first: David

middle: J.

last: Clark

address: 6 Center Drive

department: NICHD

summary: Recent studies have combined DNA methyltransferase footprinting of genomic DNA in nuclei with long-read sequencing, resulting in detailed chromatin maps for multi-kilobase stretches of genomic DNA from one cell. Nucleosome footprints and nucleosome-depleted regions can be identified, yielding unprecedented information concerning their degree of correlation within the same cell. The enzyme of choice is M.EcoGII, which methylates adenines in any sequence context, potentially resulting in very high resolution. However, in practice, the methylation efficiency (defined as the fraction of each genomic adenine that is methylated), is quite low, resulting in false footprints predicted by random unmethylated gaps between methylated adenines. We report PacBio long-read sequence data for budding yeast nuclei treated with M.EcoGII. We present a bioinformatic pipeline which accounts for methylation efficiency, as well as an observed bias against methylation as a function of increasing AT content. It also accounts for our observation that some methylation occurs within nucleosomes, breaking up their footprints. Comparison of long reads for each gene indicates the extent of chromatin heterogeneity within the cell population. Although the population average is consistent with that derived using other techniques, we observe a wide range of heterogeneity in nucleosome positions at the single-molecule level.

sample_organism:
Escherichia coli
Saccharomyces cerevisiae

overall_design: PacBio long-read sequences. Two biological replicate experiments comprised of 3 samples each: budding yeast nuclei treated with M.EcoGII, mock-treated nuclei (negative control) and genomic DNA treated with M.EcoGII (positive control) (6 samples). We also performed a test experiment for m6A identification by PacBio using pUC19 plasmid linearised with SmaI and treated in vitro with M.EcoGII methylase, or dam methylase, or untreated (6 samples). Total of 12 samples.

first: Allison

last: Dennis

first: Zhuwei

last: Xu


title: Multiomic Single Cell Sequencing Identifies Stemlike Nature of Mixed Phenotype Acute Leukemia and Provides Novel Risk Stratification  [normal bone marrrow PIP-Seq]

status: Public on Mar 13 2024

city: San Francisco

first: Catherine

last: Smith

address: 513 Parnassus Avenue

institute: University of California, San Francisco

summary: Mixed phenotype acute leukemia (MPAL) also known as acute leukemia of ambiguous lineage (ALAL), is characterized by leukemic blasts with both lymphoid and myeloid cell surface markers.  Here, we use SC multiomic profiling on newly diagnosed MPAL samples to characterize the immunophenotypic, genetic, and transcriptional landscapes of MPAL. This profiling allows us to definitively contradict the paradigm of MPAL as a disease on a continuum with myeloid and lymphoid lineage acute leukemias, and instead identifies MPAL as a distinct, stem-like disease that, unlike other leukemias, cannot be defined by genetics alone. We further describe a stem cell gene expression signature for MPAL that can predict patient survival. These results broaden our understanding of MPAL biology and suggest a path toward novel risk stratification for MPAL. Importantly, these findings have potential to direct treatment and, hopefully, ultimately improve the prognosis of this disease.

overall_design: Samples from 14 adult patients with de novo MPAL were analyzed for single cell DNA, RNA, protein.

first: Cheryl

last: Peretz

first: Vanessa

last: Kennedy

first: Anushka

last: Walia

first: Cyrille

last: Delley

first: Andrew

last: Koh

first: Elaine

last: Tran

first: Iain

first: Corey

last: Hayford

first: Chris

middle: D

last: Amato

first: Kristina

last: Fontanez

first: Ritu

last: Roy

first: Aaron

last: Logan

first: Alexander

last: Perl

first: Adam

last: Abate

last: Olshen


title: The impact of substrate stiffness on morphological, transcriptional and functional aspects in RPE

status: Public on Mar 11 2024

city: Tübingen

first: Lasse

last: Wolfram

address: Elfriede-Aulhorn-Straße 7

country: Germany

institute: Department for Ophthalmology, Eberhard Karls University of Tübingen

type: Non-coding RNA profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: The impact of substrate stiffness on morphological, transcriptional and functional aspects in RPE [miRNA-Seq]

summary:
To investigate the influence of stiffness as a major Bruch's membrane characteristic on the RPE transcriptome and morphology. ARPE-19 cells were plated on soft or stiff polyacrylamide gels (PA gels) or standard tissue culture plastic (TCP).
We then performed gene expression profiling analysis using data obtained from Next-generation sequencing of small RNAs of ARPE-19 cells cultured on 3 different biomechanical conditions.

overall_design: Comparative gene expression profiling analysis of Next-generation sequencing data for ARPE-19 cells cultured on soft or stiff polyacrylamide gels or standard tissue culture plastic.

first: Clara

last: Gimpel

first: Daniel

last: Böhringer

first: Günther

last: Schlunck


title: The impact of substrate stiffness on morphological, transcriptional and functional aspects in RPE [RNA-Seq]


title: A continuous ferroptosis-to-apoptosis landscape identifies ferroptosis biomarkers and repressors for cancer therapy

status: Public on Mar 07 2024

city: Rehovot

first: Sima

last: Lev

address: 234 Herzl St.

department: Molecular Cell Biology

country: Israel

institute: Weizmann Institute of Science

summary: Ferroptosis, a cell death pathway driven by lipid peroxidation, is implicated in several human diseases including cancer. Although ferroptosis is entwined with apoptosis, it currently has no   characteristic biomarkers or gene signature. In this project we established a continuous phenotypic gradient between ferroptosis and apoptosis and coupled it to transcriptomic and metabolomic landscapes. Omics and mechanistic studies revealed that ferroptosis was associated with enhanced MITF activity, lysosomal function, glutaminolysis, TCA cycle, and activation of ATF4, while its transition into apoptosis was attributed to enhanced ER-stress, ATF4/CHOP switch and PE/PC metabolic shift. The gradual ferroptosis-to-apoptosis transcriptomic landscape was used to generate a unique, unbiased transcriptomic predictor, the Gradient Gene Set (GGS), which classified ferroptosis and apoptosis with high accuracy. Further GGS optimization and datasets analysis of various ferroptotic and apoptotic responses revealed highly specific ferroptosis biomarkers, which were robustly validated in vitro and in vivo. A subset of the GGS was correlated with poor prognosis in breast cancer patients and in PDX models and was found to consist of different ferroptosis repressors, including PDAP1, whose knockdown suppressed breast tumor growth in a mouse model. Collectively, this study highlights molecular switches between ferroptosis and apoptosis, uncovering a highly prognostic predictive ferroptosis gene signature, pointing to a few ferroptosis repressors for targeted breast cancer therapy.

overall_design: In a previous project we identified a synthetic lethal drug combination, JQ1 (BRD4 inhibitor) and BTZ (proteasome inhibitor). We discovered that the combination of JQ1 (100nM) and BTZ (2nM) induces ferroptosis, while incresing the concentration of BTZ to 6nM (and maintining JQ1 at 100 nM) causes the combination to induce apoptosis. To study the underlying mechanism of these combinations, we treated two triple negative breast cancer cells, MDA-MB-468 and HCC70, with the different combinations (JB2: JQ1 100nM+BTZ 2nM; JB3: JQ1 100nM+BTZ 3nM; JB6: JQ1 100nM+BTZ 6nM). We also treated the cells with the single treatments (J: JQ1 100nM; B2: BTZ 2nM; B3: BTZ 3nM; B6: BTZ 6nM). DMSO was used as control (DMSO concentration is simillar in all samples). MDA-MB-468 cells were treated in 2 time points (24h and 6h), while HCC70 were treated with 24h. For comparisons to other ferroptosis inducers, MDA-MB-468 and HCC70 were also treated with the ferroptosis inducers Erastin and RSL3. We added another cell line, HCC38, treated with Erastin. Two independent repeats were done.

first: Yaron

last: Vinik

first: Avi

last: Maimon


title: New therapy for colorectal cancer targeting cancer metabolism through serotonin receptor HTR2B

status: Public on Mar 12 2024

city: Buk-gu, Gwangju

first: Suhyeon

last: Park

state: Gwangju

address: 광주광역시 북구 첨단과기로 123 다산빌딩 403호

institute: GIST

summary: Serotonin is important material in our body. 5-HT is synthesized by TPH1 starting with tryptophan and this compound exists on colorectal cancer. And serotonin combines with various receptors to conduct the metabolic pathway in colorectal cancer. Each receptor relates with various metabolism, such as lipid metabolism, growth, immunity, etc. In this way, medicine which inhibits these receptors can expect for therapy of colorectal cancer. Especially HTR 2B has correlation with growth factor and using the inhibitor of HTR2B, SB204741, can have effect on metabolic pathway in colorectal cancer. So, we set the hypothesis that HTR2B antagonist can have negative effect on growth of colorectal cancer.

overall_design: We treated the SB204741 in vitro on Colo 205, we isolated RNA from the cell and tissue and conducted the analysis of RNA sequence

first: Jeong-Yun

last: Lee

first: Chang-Myung

last: Oh


title: Effect of Replicative Aging on Cryptococcus neoformans

status: Public on Mar 06 2024

city: Stony Brook

first: Bettina

last: Fries

state: NY

address: HSC T 15 Room 080, 101 Nicholls Rd

institute: Stony Brook University

summary: Cryptococcus neoformans (Cn) is an opportunistic fungal microorganism that causes life-threatening meningoencephalitis. During the infection, the microbial population is heterogeneously composed of cells with varying generational ages, with older cells accumulating during chronic infections. This is attributed to their enhanced resistance to phagocytic killing and tolerance of antifungals like fluconazole (FLC). Using RNA-seq, we investigated how transcriptomic changes in different aspects of metabolism contribute to age-associated FLC tolerance in Cn.

overall_design: To study the effects of replicative aging on the transcriptome of C. neoformans, we isolated young (0-3 generations) and old (10 generations) cells. Then, the transcriptomes of young and old cells were analyzed to identify ent gene expression.

first: Kyungyoon

last: Yoo

first: Natalia

last: Kronbauer Oliveira

first: Somanon

last: Bhattacharya


title: Factors governing cellular reprogramming competence in Arabidopsis adventitious root formation

city: Durham

first: Suresh

last: Damodaran

state: North Carolina

address: 124 Science Drive, 3332 French Family Science center

department: Biology

institute: Duke University

summary: To understand the molecular mechanisms regulating the competence to produce adventitious roots in wounded arabidopsis hypocotyl, we examined gene expression in the basal and medial zones of wild type (Col-0) and ahk3 ahk4 hypocotyl segments at early time points post-excision, prior to the appearance of adventitious root primordia.

overall_design: Comparative gene expression profiling analysis of QuantSeq data for basal and medial hypocotyl tissues of WT (Col-0) and ahk3 ahk4.

first: Lucia

last: Strader


title: Genes regulated by pharmacological Wnt activation by CHIR99021 in the embryonic mouse cochlea

status: Public on Mar 01 2024

city: West Lafayette

first: Vidhya

last: Munnamalai

address: 915 W State St

department: Biological Sciences

institute: Purdue

summary:
Our studies showed that Wnt activation influenced patterning of the mouse cochlea across the radial axis.
To identify genes responding to Wnt activation, mouse embryonic cochleas were treated in the presence and absence of the GSK 3beta inhibitor, CHIR99021.
Cochleas were harvested on E12.5 and cultured in vitro for 24 hours. On the next day (day 1), cochleas were treated with either DMSO vehicle control or CHIR99021.
The 6-hour treatment helped to identify the immediate genes transcribed following Wnt activation.

overall_design: Embryonic day 12.5 cochleas were cultured for 1 day and then were treated with vehicle (DMSO) or CHIR99021 for 6 hours. Bulk RNA-seq Includes 4 biological replicates from Control and CHIR treatment.


title: Anti-TIGIT antibody improves PD-L1 blockade through myeloid and Treg cells

status: Public on Mar 04 2024

city: South San Francisco

first: Xiangnan

last: Guan

address: 1 DNA WAY

institute: Genentech

summary: Tiragolumab, an anti-TIGIT antibody with an active IgG1κ Fc, demonstrated improved outcomes in the phase 2 CITYSCAPE trial (ClinicalTrials.gov: NCT03563716) when combined with atezolizumab (anti-PD-L1) versus atezolizumab alone. However, there remains little consensus on the mechanism(s) of response with this combination. Here we find that a high baseline of intratumoural macrophages and regulatory T cells is associated with better outcomes in patients treated with atezolizumab plus tiragolumab but not with atezolizumab alone. Serum sample analysis revealed that macrophage activation is associated with a clinical benefit in patients who received the combination treatment. In mouse tumour models, tiragolumab surrogate antibodies inflamed tumour-associated macrophages, monocytes and dendritic cells through Fcγ receptors (FcγR), in turn driving anti-tumour CD8+ T cells from an exhausted effector-like state to a more memory-like state. These results reveal a mechanism of action through which TIGIT checkpoint inhibitors can remodel immunosuppressive tumour microenvironments, and suggest that FcγR engagement is an important consideration in anti-TIGIT antibody development.

overall_design: The CT26 mouse colon carcinoma cell line was obtained from American Type Culture Collection. A total of 100,000 CT26 cells was inoculated subcutaneously into the right unilateral flank of the syngeneic BALB/c mice. All mice used were 6-8 week old and female. After approximately 10–12 days, mice bearing tumours of 150–200 mm3 were randomized into treatment groups on the basis of tumour size and treated with anti-mouse PD-L1 (6E11, isotype IgG2a LALAPG, 10 mg per kg), anti-mouse TIGIT (10A7, isotypes IgG2a, mIgG2b, and IgG2a LALAPG, 10 mg per kg), anti-mouse CSF-1R (Bioexcell, BP0213, 30 mg per kg) and/or anti-gp120 control antibodies (IgG2a isotype, to total 35 mg per kg overall antibody dosing). Antibodies were administered once intravenously, and 72 h after treatment, mice were euthanized by asphyxiation and CD45+ cells were collected for scRNA-seq analysis.

first: Ruozhen

last: Hu

first: Yoonha

last: Choi

first: Shyam

last: Srivats

first: Barzin

middle: Y

last: Nabet

first: John

last: Silva

first: Lisa

last: McGinnis

first: Robert

last: Hendricks

first: Katherine

last: Nutsch

first: Karl

middle: L

last: Banta

first: Ellen

last: Duong

first: Alexis

last: Dunkle

first: Patrick

middle: S

last: Chang

first: Chia-Jung

last: Han

first: Stephanie

last: Mittman

first: Nandini

last: Molden

first: Pallavi

last: Daggumati

first: Wendy

last: Connolly

first: Melissa

last: Johnson

first: Delvys Rodriguez

last: Abreu

first: Byoung Chul

last: Cho

first: Antoine

last: Italiano

first: Ignacio

last: Gil-Bazo

first: Enriqueta

last: Felip

first: Ira

last: Mellman

first: Sanjeev

last: Mariathasan

first: David

last: Shames

first: Raymond

last: Meng

first: Eugene

last: Chiang

last: Johnston

first: Namrata

last: Patil


title: ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [XMD RNA-seq]

city: macau

first: Chengcheng

last: SONG

address: universtiy of macau

department: fhs

country: Macau

institute: university of macau

summary: To investigate the function ERK5 in the regulation of hPSC pluripotency, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 12/24/48hr in H1 ESCs.

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of H1 ESCs at 4 time points.

last: Song

first: Guokai

last: Chen


title: Sequencing to determine the effect of neuronal IL-1 receptor knockout and microglia depletion on  stress-induced changes to the neuronal transcriptome

city: Columbus

first: Ethan

last: Goodman

state: Ohio

address: 460 Medical Center Drive

institute: Ohio State University

summary: Chronic stress is associated with increased anxiety, cognitive deficits, and post-traumatic stress disorder. Repeated social defeat (RSD) in mice causes long-term stress-sensitization associated with increased microglia activation, monocyte accumulation, and enhanced interleukin (IL)-1 signaling in endothelia and neurons. With stress-sensitization, mice have amplified neuronal, immune, and behavioral responses to acute stress 24d later. This is clinically relevant as it shares key aspects with post-traumatic-stress-disorder. The mechanisms underlying stress-sensitization are unclear, but enhanced fear memory may be critical. The purpose of this study was to determine the influence of microglia and IL-1R1 signaling in neurons in the development of sensitization and increased fear memory after RSD. The goal of this study was to sequence nuclei from the hippocampus to determine downstream pathways of neuronal IL-1R1 (nIL-1R1) and microglia reactivity.

overall_design:
Nuclei were isolated from hippocampi (n=3/pooled) 14hr after social defeat. 2x2: Control & Stress x Wildtype & nIL-1R1
snRNA-seq

first: Rebecca

last: Biltz

first: Jonathan

last: Packer

first: Damon

last: DiSabato

first: Samuel

last: Swanson

first: Braeden

last: Oliver

first: Ning

last: Quan

first: John

last: Sheridan

last: Godbout


title: ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [12h XMD RNA-seq]

summary: To investigate the function ERK5 in the regulation of hPSC pluripotency, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 12hr in H1 ESCs.

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of H1 ESCs for 12hr


title: ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [ChIP-seq]

summary: To investigate the function ERK5 in the regulation of hPSC histone modification, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 24hr in H1 ESCs. And H3K27ac and H3K4me3 ChIP-seq test

overall_design: We then performed gene expression profiling analysis using data obtained from ChIP-seq of H1 ESCs.


title: ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [MEK4DD RNA-seq]

summary: To investigate the function of MEK5/ERK5 in the regulation of hPSC pluripotency, we processed MAP2K5DD (MEK5DD) overexpression H1 ESC line.

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of MEK5DD-OE H1 ESCs.


title: Selective translational control by PABPC1 phase separation regulates blast crisis and target therapy resistance of chronic myeloid leukemia

city: Beijing

first: Zhongyang

address: No.5, Dongdan Santiao, Dongcheng District

institute: School of Basic Medicine, Peking Union Medical College (PUMC)

summary: Tyrosine kinase inhibitors (TKIs) targeting the BCR-ABL1 fusion tyrosine kinase have revolutionized the treatment of chronic myeloid leukemia (CML). However, the development of TKI resistance and the subsequent transition from the chronic phase (CP) to blast crisis (BC) threaten CML patients. Accumulating evidence suggests that translational control is crucial for cancer development and progression. Here, we performed high throughput CRISPR/Cas9 screening and identified poly(A) binding protein cytoplasmic 1 (PABPC1) as a driver for CML-BC progression. PABPC1 preferentially improved the translation efficiency of multiple leukemogenic mRNAs with long and highly structured 5' untranslated regions, including BCR-ABL1 and its TKI-resistant mutants, through forming biomolecular condensates. Inhibiting PABPC1 significantly suppressed CML cell proliferation and attenuated disease progression, but did not affect normal hematopoiesis seriously. More importantly, we identified two novel PABPC1 inhibitors, 1,10-Phen and ML324, which inhibited BC progression and overcame TKI resistance in murine and human CML. Overall, our work identified PABPC1 as a selective translation enhancing factor in CML-BC, the genetic or pharmacological inhibition of which overcame TKI resistance and suppressed BC progression in CML.

overall_design: PABPC1-KD RNA-seq and PABPC1 eCLIP-seq datasets.

first: Chenguang

last: Sun

first: Yanni

last: Ma

first: Jia

last: Yu


title: ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells


title: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation [Slam-Seq]

first: Jernej

last: Ule

address: 10-12 Russell sq

department: Neuromuscular Diseases

institute: UCL Institute of Neurology

summary: The naïve pluripotent epiblast cells become polarized into a rosette-like structure, followed by irreversible transition into primed pluripotency during one of the fastest morphological switches termed lumenogenesis. This requires rapid decay of pluripotency-associated mRNAs, but the underlying mechanism remains unknown. Guided by machine learning and metabolic RNA sequencing, we identified RNA binding proteins (RBPs), especially LIN28A, as primary mRNA decay factors. To understand if RBP dynamics steer embryogenesis, we used mRNA-RBP interactome capture during naïve-rosette-epiblast-gastrulation progression. We identified a dramatic increase in LIN28A mRNA binding, driven by its nucleolus-to-cytoplasm translocation during the naïve-primed pluripotency transition. Cytoplasmic LIN28A binds to 3’UTRs of pluripotency-associated mRNAs to directly stimulate their decay, and thereby progression to lumenogenesis. Accordingly, forced nuclear retention of LIN28A impeded lumenogenesis, causing an unforeseen embryonic multiplication and impaired gastrulation. This reveals selective mRNA decay, driven by nucleo-cytoplasmic RBP translocation, as an intrinsic mechanism for cell identity switch that controls embryonic timing of lumenogenesis.

overall_design: Examination of Thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAMseq) in the differentiation and priming of mouse embryonic stem cells and in the presence or absence of LIN28A.

first: Miha

last: Modic

first: Igor

last: Ruiz de los Mozos


title: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation [RNA-Seq]

overall_design: Examination of RNA-seq in FACS sorted tetraploid complemented E7.5 embryo, Lin28a with or without NLS.


title: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation [Quant-Seq]

overall_design: Examination of QuantSeq in the differentiation and priming to rossete, epiblast and T-mesodermal prognitors of mouse embryonic stem cells and in the presence or absence of LIN28A


title: Single-cell multiomics reveals stage of differentiation and trajectory-dependent immunity-related gene expression patterns in human erythroid cells

city: Novosibirsk

first: Roman

middle: Yurievich

last: Perik-Zavodskii

state: Novosibirsk region

address: Yadrincevskaya 14

country: Russia

institute: "Research Institute of Fundamental and Clinical Immunology" (RIFCI)

summary: Erythroid cells, serving as progenitors and precursors to erythrocytes responsible for oxygen transport, exhibit a notable immunosuppressive and immunoregulatory phenotype. The present study CITE-seq reveals that erythroid cells have stage of differentiation-dependent immunity-related gene expression patterns. We also found that Erythroid cell differentiation is not linear and there is a bifurcation of polychromatophilic erythroblasts into ARG1 expressing polychromatophilic erythroblasts and orthochromatophilic erythroblasts. ARG1 expressing polychromatophilic erythroblasts account for almost all immunosuppressive ARG1 gene expression among erythroid cells. Thus, we infer the stepwise erythroid cells differentiation trajectory that has a branch that forms immunosuppressive erythroid cell population.

overall_design: Normal Bone Marrow mononuclear cells, B-cell ALL, T-cell ALL cells were acquired pre-treatment in the moment of diagnostic bone marrow biopsy, cells were extracted via Ficoll-paque density gradient centrifugation, barcoded with 28 AbSeq antibodies and 4 Sample Tag antibodies and loaded into BD Rhapsody Express apparatus


title: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation

overall_design: Refer to individual Series


title: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation [iCLIP]

overall_design: Examination of iCLIP in the differentiation and priming of mouse embryonic stem cells with a endogenous and exogenous Lin28a and a Lin28a NLS version


title: Single-cell atlas of the human brain vasculature across development, adulthood and disease (bulk RNA-Seq)

status: Public on Feb 29 2024

first: Thomas

last: Wälchli

state: London

address: Paul O'Gorman Building, 72 Huntley St

department: UCL Cancer Institute

institute: University College London

summary: A broad range of brain pathologies critically relies on the vasculature, and cerebrovascular disease is a leading cause of death worldwide. However, the cellular and molecular architecture of the human brain vasculature remains incompletely understood. Here, we performed single-cell RNA sequencing of 606,380 freshly isolated endothelial, perivascular and other tissue-derived cells from 117 samples, from 68 human fetuses and adult patients to construct a molecular atlas of the developing fetal, adult control and diseased human brain vasculature. We uncover extensive molecular heterogeneity of the vasculature of healthy fetal and adult human brains and across eight vascular-dependent Central Nervous System (CNS) pathologies including brain tumors and brain vascular malformations. We identify alteration of arteriovenous differentiation and reactivated fetal as well as conserved dysregulated genes and pathways in the diseased vasculature. Pathological endothelial cells display a loss of CNS-specific properties and reveal an upregulation of MHC class II molecules, indicating atypical features of CNS endothelial cells. Cell-cell interaction analyses predict numerous endothelial-to-perivascular cell ligand-receptor crosstalk including immune-related and angiogenic pathways, thereby unraveling a central role for the endothelium within brain neurovascular unit signaling networks. Our single-cell brain atlas provides insight into the molecular architecture and heterogeneity of the developing, adult/control and diseased human brain vasculature and serves as a powerful reference for future studies

overall_design: We constructed a human brain vasculature single-cell atlas using samples from fetal as well as adult control (undiseased atlas) and diseased brains, including adult brain vascular malformations and brain tumors (diseased atlas). We acquired freshly isolated cells (both FACS-sorted ECs and unsorted ECs and PVCs from 8 individual fetuses and from 61 adult brain specimens (from 61 individual patients), covering adult temporal lobe (TL) controls and adult vascular-dependent pathologies, namely, brain arteriovenous malformation (AVM), lower-grade glioma (LGG), glioblastoma (GBM), lung cancer brain metastasis (MET) and meningioma (MEN)

first: Moheb

last: Ghobrial

first: Marc

last: Schwab

last: Suntharalingham

first: Sandra

last: Vetiska

first: Daymé

last: Gonzalez

first: Hubert

last: Rehrauer

first: Jeroen

last: Bisschop

first: Luca

last: Regli

first: Karl

last: Schaller

last: Frei

first: Troy

last: Ketela

first: Mark

last: Bernstein

first: Paul

last: Kongkham

first: Taufik

last: Valiante

first: Gelareh

last: Zadeh

first: Ralph

last: Schlapbach

first: Katrien

last: De Bock

first: Philippe

last: Monnier

first: Gary

last: Bader

first: Ivan

last: Radovanovic


title: Single-cell atlas of the human brain vasculature across development, adulthood and disease (Extra Individuals)

first: Thomas

last: Wälchli

first: Moheb

last: Ghobrial

first: Marc

last: Schwab

first: Samuel

last: Suntharalingham

last: Vetiska


title: Single-cell atlas of the human brain vasculature across development, adulthood and disease (scRNA-Seq)

first: Sandra

first: Daymé

last: Gonzalez

first: Hubert

last: Rehrauer

first: Jeroen

last: Bisschop

last: Regli

last: Schaller


title: Control ChIP-seq from whole organism (ENCSR533CSZ)

status: Public on Feb 27 2024

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
This is the ChIP-seq control of transgenic worms expressing F49E8.2-eGFP fusion proteins.

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: Single-cell atlas of the human brain vasculature across development, adulthood and disease

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


title: Control ChIP-seq from whole organism (ENCSR530XBH)

summary:
This is the ChIP-seq control of transgenic worms expressing C08G9.2-eGFP fusion proteins.

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 whole organism (ENCSR533CXT)

summary:
ChIP-seq on transgenic flies expressing BEAF-32-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR837BBL)

summary:
Input control for ChIP-seq on transgenic flies expressing CG10565-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR524HLR)

summary:
Input control for ChIP-seq on transgenic flies expressing Ssrp-eGFP fusion proteins.

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 whole organism (ENCSR524LOH)

summary:
ChIP-seq on transgenic flies expressing Ravus-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR838HNJ)

summary:
Input control for ChIP-seq on transgenic flies expressing CG32264-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR528TJN)

summary:
This is the ChIP-seq control of transgenic worms expressing B0336.3-eGFP fusion proteins.

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 whole organism (ENCSR836LVI)

summary:
ChIP-seq of transgenic worms expressing ALY-1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR517WHP)

summary:
This is the ChIP-seq control of transgenic worms expressing tlf-1-eGFP fusion proteins.

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 whole organism (ENCSR529PIJ)

summary:
ChIP-seq of transgenic worms expressing F49E8.2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR506NPV)

summary:
Input control for ChIP-seq on transgenic flies expressing CG8216-eGFP fusion proteins.

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: Embryonic lumenogenesis is controlled by selective mRNA decay triggered by LIN28A relocation [miCLIP]

first: Jernej

last: Ule

overall_design: Examination of iCLIP, RNA-seq, QuantSeq in the differentiation and priming of mouse embryonic stem cells and in the presence or absence of LIN28A

first: Miha

last: Modic

first: Igor

last: Ruiz de los Mozos


title: TF ChIP-seq from whole organism (ENCSR517HVR)

summary:
ChIP-seq on transgenic flies expressing Mes4-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR826RWT)

summary:
Input control for ChIP-seq on transgenic flies expressing CG8632-eGFP fusion proteins.

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 whole organism (ENCSR517OKI)

summary:
ChIP-seq against eGFP-W03F9.2 in worms.

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 whole organism (ENCSR514BBN)

summary:
ChIP-seq on transgenic worms expressing ccch-3-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR992ICQ)

summary:
Input control for ChIP-seq on transgenic flies expressing mod(mdg4)-eGFP fusion proteins.

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 whole organism (ENCSR509XOC)

summary:
ChIP-seq against ama-1 in young adult worms.

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 whole organism (ENCSR998BRC)

summary:
ChIP-seq against eGFP-hpl-2 in starved L1 larva worms.

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 whole organism (ENCSR987LDU)

summary:
ChIP-seq on transgenic flies expressing CG6175-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR990RKL)

summary:
This is the ChIP-seq control of transgenic worms expressing akir-1-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR819KEO)

summary:
Input control for ChIP-seq on transgenic flies expressing tna-eGFP fusion proteins.

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 whole organism (ENCSR992BYJ)

summary:
ChIP-seq on transgenic flies expressing Ada2b-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR504CUV)

summary:
This is the ChIP-seq control of transgenic worms expressing T26A5.8-eGFP fusion proteins.

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 whole organism (ENCSR499IRC)

summary:
ChIP-seq against eGFP-lin-35 in young adult worms.

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: Control ChIP-seq from whole organism (ENCSR498NSZ)

summary:
This is the ChIP-seq control of transgenic worms expressing snpc-1.2-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR818AKL)

summary:
Input control for ChIP-seq on transgenic flies expressing E(z)-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR477IRP)

summary:
This is the ChIP-seq control of transgenic worms expressing set-16-eGFP fusion proteins.

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 whole organism (ENCSR816VQN)


title: TF ChIP-seq from whole organism (ENCSR978CMG)

summary:
ChIP-seq on transgenic flies expressing esn-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR475NRH)

summary:
This is the ChIP-seq control of transgenic worms expressing isw-1-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR671YDD)

summary:
This is the ChIP-seq control of transgenic worms expressing ALY-1-eGFP fusion proteins.

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 whole organism (ENCSR806QUX)

summary:
ChIP-seq of transgenic worms expressing REC-8-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR977VOU)

summary:
ChIP-seq of transgenic worms expressing MES-2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR981DLO)

summary:
ChIP-seq on transgenic flies expressing gro-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR668OMI)

summary:
ChIP-seq of transgenic worms expressing RPC-1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR666MXI)

summary:
ChIP-seq against eGFP-aly-2 in L1 larva worms.

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 whole organism (ENCSR672DJL)

summary:
ChIP-seq against eGFP-aly-2 in L3 larva worms.

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: Control ChIP-seq from whole organism (ENCSR665ROL)

summary:
Input control for ChIP-seq on transgenic flies expressing CG2875-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR661MKW)

summary:
This is the ChIP-seq control of transgenic worms expressing flt-1-eGFP fusion proteins.

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 whole organism (ENCSR798FMQ)

summary:
ChIP-seq on transgenic worms expressing unc-98-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR471YLT)

summary:
ChIP-seq on transgenic flies expressing -eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR972CCK)


title: TF ChIP-seq from whole organism (ENCSR472HTK)

summary:
ChIP-seq against eGFP-lin-35 in L1 larva worms.

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: Control ChIP-seq from whole organism (ENCSR662CJH)

summary:
This is the ChIP-seq control of transgenic worms expressing F57A8.1-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR470NLR)

summary:
Input control for ChIP-seq on transgenic flies expressing CG7839-eGFP fusion proteins.

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 whole organism (ENCSR812MWL)

summary:
ChIP-seq on transgenic worms expressing flt-1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR462RAG)

summary:
Input control for ChIP-seq on transgenic flies expressing Lhr-eGFP fusion proteins.

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 whole organism (ENCSR969UGO)

summary:
ChIP-seq on transgenic flies expressing Dad-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR797CVA)

summary:
Input control for ChIP-seq on transgenic flies expressing CG34422-eGFP fusion proteins.

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 whole organism (ENCSR665UXV)

summary:
ChIP-seq of transgenic worms expressing MES-4-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR456YDF)

summary:
ChIP-seq of transgenic worms expressing CEY-2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR454PLL)

summary:
Input ChIP-seq in L2 larva worms.

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 whole organism (ENCSR461AXL)

summary:
ChIP-seq on transgenic flies expressing h-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR454PPJ)

summary:
ChIP-seq on transgenic worms expressing hmg-1.2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR655QMD)

summary:
Input control for ChIP-seq on transgenic flies expressing Chrac-16-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR782TWP)

summary:
This is the ChIP-seq control of transgenic worms expressing HIM-1-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR959KFB)

summary:
Input ChIP-seq in young adult worms.

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: Control ChIP-seq from whole organism (ENCSR780YWP)

summary:
Input ChIP-seq in early embryonic worms.

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 whole organism (ENCSR961MUW)


title: TF ChIP-seq from whole organism (ENCSR957HDY)

summary:
ChIP-seq on transgenic flies expressing ADD1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR791IKU)

summary:
ChIP-seq against AMA-1 in YA worms.

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: Control ChIP-seq from whole organism (ENCSR951GLF)


title: Control ChIP-seq from whole organism (ENCSR778CNK)

summary:
This is the ChIP-seq control of transgenic worms expressing CHD-7-eGFP fusion proteins.

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 whole organism (ENCSR453UOF)

summary:
ChIP-seq on transgenic flies expressing Pif1B-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR776AID)

summary:
This is the ChIP-seq control of transgenic worms expressing zfp-3-eGFP fusion proteins.

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 whole organism (ENCSR948RHA)

summary:
ChIP-seq on transgenic flies expressing mam-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR449ROG)

summary:
This is the ChIP-seq control of transgenic worms expressing MES-2-eGFP fusion proteins.

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 whole organism (ENCSR949XGL)

summary:
ChIP-seq on transgenic flies expressing chif-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR463EQY)


title: Control ChIP-seq from whole organism (ENCSR438SMK)

summary:
Input control for ChIP-seq on transgenic flies expressing Taf1-eGFP fusion proteins.

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 whole organism (ENCSR945XEH)

summary:
ChIP-seq on transgenic flies expressing Pif1A-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR441OGV)

summary:
Input control for ChIP-seq on transgenic flies expressing pum-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR435DMG)

summary:
This is the ChIP-seq control of transgenic worms expressing unc-98-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR761BHV)

summary:
ChIP-seq on transgenic flies expressing -eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR650IGG)

summary:
Input ChIP-seq in L2 larva worms.

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 whole organism (ENCSR438PSB)

summary:
ChIP-seq of transgenic worms expressing SDC-2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR636YHR)

summary:
Input control for ChIP-seq on transgenic flies expressing Mes4-eGFP fusion proteins.

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: Control ChIP-seq from whole organism (ENCSR757RQP)

summary:
Input control for ChIP-seq on transgenic flies expressing Su(var)2-10-eGFP fusion proteins.

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 whole organism (ENCSR637GDK)

summary:
ChIP-seq on transgenic flies expressing Su(var)2-10-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR934OMU)

summary:
ChIP-seq on transgenic worms expressing B0336.3-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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 whole organism (ENCSR424CLY)

summary:
ChIP-seq against ama-1 in late embryonic worms.

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 whole organism (ENCSR934KZU)

summary:
ChIP-seq against ama-1 in early embryonic worms.

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: Control ChIP-seq from whole organism (ENCSR633YHP)

summary:
This is the ChIP-seq control of transgenic worms expressing tbp1-eGFP fusion proteins.

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 whole organism (ENCSR934WJF)

summary:
ChIP-seq on transgenic flies expressing tna-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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: Control ChIP-seq from whole organism (ENCSR626XZR)

summary:
This is the ChIP-seq control of transgenic worms expressing MES-4-eGFP fusion proteins.

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 whole organism (ENCSR748DYJ)

summary:
ChIP-seq on transgenic worms expressing Y53F4B.3-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

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