title: An erythroid-specific enhancer of ATP2B4 mediates red blood cell hydration and malaria susceptibility [genotype]

city: Montreal

first: Guillaume

last: Lettre

state: Québec

address: 5000 rue Bélanger

institute: Montreal Heart Institute

summary: Few genotype-phenotype associations identified by genome-wide association studies (GWAS) have been defined mechanistically, precluding thorough assessment of their impact on human health. We conducted an expression quantitative trait loci (eQTL) mapping analysis in human erythroblasts and found erythroid-specific eQTLs for ATP2B4, the main calcium ATPase of red blood cells (RBC). The same SNPs were previously associated with mean corpuscular hemoglobin concentration (MCHC) and susceptibility to severe malaria infection. We showed that Atp2b4-/- mice demonstrate increased MCHC, confirming ATP2B4 as the causal gene at this GWAS locus. Using CRISPR-Cas9, we fine-mapped the genetic signal to an erythroid-specific enhancer bound by GATA1 and TAL1. These results illustrate the importance to combine transcriptome, epigenome, and genome editing approaches in phenotype-relevant cells to characterize non-coding regulatory elements associated with human complex diseases and traits. Our studies suggest ATP2B4 as a potential target to modulate RBC hydration in erythroid disorders and malaria infection.

overall_design: Genotypes of fetal (N=12) and adult (N=12) erythroblasts were obtained using the HumanOmniExpress-12 v1.1 BeadChip array

first: Samuel

last: Lessard

first: Emily

middle: N

last: Stern

first: Mélissa

last: Beaudoin

first: Patrick

last: Schupp

first: Falak

last: Sher

first: Syed

last: Ali

first: Sukhpal

last: Prehar

first: Ryo

last: Kurita

first: Yukio

last: Nakamura

first: Esther

last: Baena

first: Jonathan

last: Ledoux

first: Delvac

last: Oceandy

first: Daniel

last: Bauer


title: ChIP-seq from adrenal gland (ENCSR926NMC)

status: Public on Jul 16 2017

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

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


title: ChIP-seq from transverse colon (ENCSR933BVL)


title: ChIP-seq from gastrocnemius medialis (ENCSR899TDF)


title: ChIP-seq from esophagus squamous epithelium (ENCSR909UAG)


title: ChIP-seq from K562 (ENCSR915SJR)


title: ChIP-seq from thyroid gland (ENCSR908DTR)


title: ChIP-seq from body of pancreas (ENCSR903GLL)


title: ChIP-seq from limb (ENCSR890ACP)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse limb

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: ChIP-seq from stomach (ENCSR903QBX)


title: ChIP-seq from MCF-7 (ENCSR906IQU)


title: ChIP-seq from thyroid gland (ENCSR901BRV)


title: ChIP-seq from body of pancreas (ENCSR863TAL)


title: ChIP-seq from upper lobe of left lung (ENCSR859MXQ)


title: ChIP-seq from thyroid gland (ENCSR855XNQ)


title: ChIP-seq from sigmoid colon (ENCSR900UIP)


title: ChIP-seq from A549 (ENCSR892DRK)


title: ChIP-seq from heart left ventricle (ENCSR901SIL)


title: ChIP-seq from upper lobe of left lung (ENCSR869GBP)


title: ChIP-seq from heart left ventricle (ENCSR854OXF)


title: ChIP-seq from A549 (ENCSR933MHJ)


title: ChIP-seq from bipolar neuron (ENCSR886KKK)


title: ChIP-seq from B cell (ENCSR878JSF)


title: total RNA-seq from erythroid progenitor cell (ENCSR847AMQ)

type: Expression profiling by high throughput sequencing

summary:
PSU mouse CFU-E 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from sigmoid colon (ENCSR844YME)


title: ChIP-seq from transverse colon (ENCSR840VWD)


title: ChIP-seq from GM12878 (ENCSR849WCQ)


title: WGBS from forebrain (ENCSR888JFA)

type: Methylation profiling by high throughput sequencing

summary:
Whole genome bisulfite-seq on embryonic 10.5 day mouse forebrain

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: ChIP-seq from body of pancreas (ENCSR833HBT)


title: ChIP-seq from transverse colon (ENCSR828XQV)


title: ChIP-seq from Peyer's patch (ENCSR837SGJ)


title: WGBS from heart (ENCSR835OJU)

summary:
Whole genome bisulfite-seq on embryonic 10.5 day mouse heart

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: ChIP-seq from sigmoid colon (ENCSR812POE)


title: ChIP-seq from A549 (ENCSR817JZD)


title: WGBS from midbrain (ENCSR803ICQ)

summary:
Whole genome bisulfite-seq on embryonic 10.5 day mouse midbrain

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: Development of gene expression signatures for experimental lingual carcinogenesis

status: Public on Jul 15 2017

city: Kunming

first: XiaoMing

last: Dai

state: Yunnan

address: 293#,Xichang road

department: The maxillofacial service of the department of plastic surgery,

country: China

institute: The first affiliated hospital of Kunming Medical University

summary: To identification of gene expression profiling during lingual tumorigenesis, tongue cancer was induced by oral delivery of 4-nitroquinoline-1-oxide (4NQO) at a dose of 50mg/L for 16weeks in C57BL/6J female mice. Nine samples of lingual mucosa from 0th (encoded as C in experiment), 12th ((encoded as M in experiment) and 28th ((encoded as E in experiment) week which were supposed as normality, early stage and cancer during lingual tumorigenesis were harvested for microarray. 2339, 2539 and 2482 genes were significantly varied between M vs. C, E vs. M and E vs. C respectively.

overall_design: Chemical carcinogen 4-nitroquinoline-1-oxide induced gene expression in C57BL/6J female mice was measured at 0th (C), 12th (M) and 28th (E) week after oral delivery of 4-nitroquinoline-1-oxide (4NQO) at a dose of 50mg/L. Three independent experiments were performed at each time (0th ,12th ,28th week) using lingual mucosa.

first: Xiaoming

first: Hua

last: Liu


title: ChIP-seq from tibial nerve (ENCSR850RVA)


title: Type I IFN and not TNF, is essential for cyclic di-nucleotide-elicited CTL by a cytosolic cross-presentation pathway

city: Braunschweig

first: Robert

last: Geffers

address: Inhoffenstr. 7

department: Dep. Molecular Bacteriology

country: Germany

institute: HCI - Helmholtz Centre for Infection Research

summary:
Dendritic cells are the initiators of the adaptive immune response, therefore its gene expression allow us to predict the responses to vaccination. We used bone marrow derived dendritic cells (BMDC) to analyze the gene expression that result from the exposure to adjuvants. We use model antigen OVA and cyclic di-AMP (CDA) as an adjuvant in order to characterize the genes involved in the activation of dendritic cells by CDA alone or when the antigen is present.
Cyclic di-nucleotides (CDN) are potent stimulators of innate and adaptive immune responses. Cyclic di-AMP (CDA) is a promising adjuvant that generates humoral and cellular immunity. The strong STING-dependent stimulation of type I IFN represents a key feature of CDA. However, recent studies suggested that this is dispensable for adjuvanticity. Here we demonstrate that stimulation of IFN-γ-secreting CD8+ cytotoxic T lymphocytes (CTL) is significantly decreased after vaccination in the absence of type I IFN signaling. The biological significance of this CTL response was confirmed by the stimulation of MHC class I-restricted protection against influenza virus challenge. We show here that type I IFN (and not TNF-α) is essential for CDA-mediated cross-presentation by a cathepsin independent, TAP and proteosome dependent cytosolic antigen processing pathway, which promotes effective cross-priming and further CTL induction. Our data clearly demonstrate that type I IFN signaling is critical for CDN-mediated cross-presentation

overall_design: Cuadruplicates/Triplicates of different time points indicated below.

first: R

first: T

last: Ebensen

first: I

last: Liebich

first: D

last: Lirussi

first: Kai

last: Schulze

first: S

last: Tritel

first: C

middle: A

last: Guzman


title: Effect of the addition of corn DDGS and different sources of fat to the feedstuff of pigs on backfat transcriptome.

city: balice

first: Maria

last: Oczkowicz

state: malopolskie

address: krakowska 1

country: Poland

institute: National Reseach Institute of Animal Production

summary: We compared the transcriptomes of the backfat from pigs obtaining different diet. Animals were divided into four feeding groups The diet  differed among groups in terms of the presence of corn DDGS  as well as the type of fat used.  We observed upregulation of several genes engaged in metabolism of lipids, fatty acyl-CoA biosynthesis and  organization of lipid particles  in the samples from animals which did not obtain cDDGS in the feedstuff.

overall_design: RNA-seq was performed on 23 samples of backfat (7 samples -DDGS+rapeseed oil, 6 samples+DDGS+rapeseed oil, 5 samples +DDGS+beeftallow and 5 samples +DDGS+coconut oil) in two replicates on Illumina HiScanSQ 2000

first: Tomasz

last: Szmatoła


title: Entrainment of Breast Cell Lines Results in Rhythmic Fluctuations of MicroRNAs

city: Monterrey

first: Rafael

middle: Julián

last: Chacolla Huaringa

state: Nuevo León

address: 3000 Ignacio Morones Prieto ave., Col. Los Doctores

department: Medical School

country: Mexico

institute: Tec de Monterrey, campus Monterrey

summary: Circadian rhythms are essential for temporal (~24 h) regulation of molecular processes in diverse species. Dysregulation of circadian gene expression has been implicated in the pathogenesis of various disorders, including hypertension, diabetes, depression, and cancer. Recently, microRNAs (miRNAs) have been identified as critical modulators of gene expression post-transcriptionally, and perhaps involved in circadian clock architecture or their output functions. The aim of the present study is to explore the temporal expression of miRNAs among entrained breast cell lines. For this purpose, we evaluated the temporal (28 h) expression of 2006 miRNAs in MCF-10A, MCF-7, and MDA-MB-231 cells using microarrays after serum shock entrainment. We noted hundreds of miRNAs that exhibit rhythmic fluctuations in each breast cell line, and some of them across two or three cell lines. Afterwards, we validated the rhythmic profiles exhibited by miR-141-5p, miR-1225-5p, miR-17-5p, miR-222-5p, miR-769-3p, and miR-548ay-3p in the above cell lines, as well as in ZR-7530 and HCC-1954 using RT-qPCR. Our results show that serum shock entrainment in breast cells lines induces rhythmic fluctuations of distinct sets of miRNAs, which have the potential to be related to endogenous circadian clock, but extensive investigation is required to elucidate that connection.

overall_design: Temporal microarray expression (8-time points, 4-h intervals) of serum shock entrained cultured-cells, MCF-10A, MFC-7 and MDA-MB-231 human breast cell lines.

last: Chacolla-Huaringa

first: Jorge

last: Moreno-Cuevas

first: Victor

last: Trevino

first: Sean-Patrick

last: Scott


title: Binding of H2A.Z within gene bodies in cancer cells

city: Sherbrooke

first: Jean-Francois

last: Lucier

state: Quebec

address: 2500, boulevard de l'Université

department: Département de Biologie

country: Canada

institute: Université de Sherbrooke

summary: We used ChIP-seq to measure the binding of H2A.Z in cancer cells treated or not with alpha amanitin

overall_design: HCT116 cells were treated for 8h with 250 nM daunorubicin or with vehicle

first: Anahita

last: Lashgari

first: J

middle: F

last: Millau

first: L

last: Gaudreau


title: Modest static pressure suppresses columnar epithelial cell growth in association with cell shape and cytoskeletal modifications

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

country: Japan

institute: Osaka univ.

summary: Evidence is provided that columnar epithelial cells are growth suppressed by pressure load as low as 30 cmH2O, in association with cell shape flattening and cytoskeletal alterations.

overall_design: Comparison of gene expression in MDCK cells between 2- and 50-cm-high medium cultures

first: Man

last: Hagiyama

first: Akihiko

last: Ito


title: Expression data of ileal Peyer's patches from Salmonella Typhimurium infected pigs

city: Cordoba

first: Juan

middle: J

last: Garrido

address: Campus de Rabanales, Gregor Mendel building (C5), 1st floor

department: Genetica

country: Spain

institute: Universidad de Cordoba

summary:
This study couples a swine experimental model of non-typhoid salmonellosis to laser capture microdissection and microarray analysis to dissect the mechanisms carried out in the follicles of ileum Peyer’s Patches in response to Salmonella Typhimurium infection.
Affymetrix GeneChip® Porcine genome array was used to study the gene expression profiles of Peyer's Patches grom control and infected pigs at acute phase of infection.

overall_design: Eight crossbred weaned piglets of approximately four weeks of age and confirmed to be fecal-negative for Salmonella were randomly allocated to control or infected groups (four animals each). Control (0 day post-infection) pigs were necropsied 2 h before the experimental infection, whereas infected group was orally challenged with Salmonella Typhimurium phagetype DT104 and subsequently necropsied at 2 dpi. Ileum samples were collected from all experimental animals and immediately frozen in liquid nitrogen. Laser-capture microdissection was performed and RNA was hybridized to Affymetrix GeneChip® Porcine genome arrays. Results of infected samples were compared to those of controls to obtain differentially expressed genes.

first: Rodrigo

middle: P

last: Martins

first: Carmen

last: Aguilar

first: Valentina

last: Lorenzi

first: Ángeles

last: Jiménez-Marín

first: Sara

last: Zaldívar-López

first: Héctor

last: Argüello

first: Ana

last: Carvajal

first: Rocío

last: Bautista

first: M

middle: G

last: Claros


title: Zka virus (ZIKV) persistently infects primary human brain microvascular endothelial cells

city: Stony Brook

first: Erich

middle: R

last: Mackow

state: NY

address: 100 Nicholls Road

department: Molecular Genetics & Microbiology

institute: Stony Brook University

summary:
ZIKV alters transcriptional responses of infected cells to avoid immune detection. We have compared the transcriptional responses of ZIKV-infected hBMECs and mock-infected hBMECs.
Examination of transcriptional responses of ZIKV-infected hBMECs versus mock-infected hBMECs

overall_design: 10 total samples were analyzed twice. We generated the following measure of gene-level expression from >20,000 genes detected by Affymetric Clariom S chip arrays. Fold-changes between ZIKV-infected and mock-infected cells at each time point were determined using Affymetrix TAC software.

first: Megan

last: Mladinich

first: John

last: Schwedes


title: Expression data from human Esophageal squamous cell carcinoma (ESCC)

city: Hong Kong

first: Xiaoyan

last: Ming

address: 21 sassoon road, pokfulam, hong kong

country: Hong Kong

institute: the university of hong kong

summary:
Downregulation is a common feature of tumor suppressor gene (TSG), which can be caused by allele deletion, promoter hypermethylation, histone deacetylation and posttranscriptional silencing by microRNA. Therefore, comparison of expression profiles by cDNA microarray between tumor and non-tumor tissues and characterization of downregulated genes in tumor specimens is a useful strategy to identify TSGs.
To identify deregulated genes during ESCC development, Affemetrix cDNA microarray was applied to compare differentially expressed genes between 4 pairs of ESCC tumors and corresponding adjacent non-tumor tissues (#301, #327, #351 and #363), and one pair of esophageal dysplasia tissue and adjacent normal tissue (#314).

overall_design: Clinical specimens were collected from patients with ESCCs who underwent surgical resection of tumor tissues. Paired adjacent nontumor tissues from the proximal resection margins (>5 cm away from the ESCC sample) were also collected for RNA extraction and hybridization on affymetrix microarrays.

first: Xu

last: Zhang

first: Xiao-Yan


title: Understanding the structure/sequence preference of plant miRNA biogenesis machinery

city: Bengaluru

first: Shivaprasad

last: Padubidri V.

state: Karnataka

address: GKVK Campus, Bellary Road

country: India

institute: National Centre for Biological Sciences, TIFR

type: Non-coding RNA profiling by high throughput sequencing

summary: MicroRNAs (miRNAs) are ~21nt long endogenous non-coding RNAs that are involved in post-transcriptional silencing of target mRNAs. miRNAs are processed from precursors having a stem-loop structure that are recognized and cleaved by Dicer-like 1 (DCL1) with the help of dsRNA binding protein Hyponastic leaves 1 (HYL1) and a zinc finger protein named Serrate (SE). Plant miRNA stem-loops are very diverse in length and structure than animal miRNAs. Hence, mechanism of miRNA biogenesis from their precursors is poorly understood. Our bioinformatic analysis predicted that plant miRNAs have unique sequence signature. An artificial precursor with different predicted sequence signatures was constructed. This construct was expressed transiently in tobacco leaves and small RNAs were sequenced. Our analysis revealed that indeed the predicted sequence signature is prefered by plant miRNA biogenesis machinery.

overall_design: An artificial miRNA precursor with four stem loops, varying only in miRNA-miRNA* sequences, was infiltrated along with vector control in N. tabacum leaves. Small RNAs were sequenced from both vector and artificial miRNA precursor infiltrated tobacco leaves collected at 4dpi.

first: Padubidri

middle: V

last: Shivaprasad

first: Narjala

last: Anushree


title: Identification of cis-regulatory mutations generating de novo edges in personalized cancer gene regulatory networks

status: Public on Jul 14 2017

city: Leuven

first: Hana

last: Imrichova

address: Herestraat, 49

country: Belgium

institute: KU Leuven

summary: The identification of functional non-coding mutations is a key challenge in the field of genomics, where whole-genome re-sequencing can swiftly generate a set of all genomic variants in a sample, such as a tumor biopsy. The size of the human regulatory landscape places a challenge on finding recurrent cis-regulatory mutations across samples of the same cancer type. Therefore, powerful computational approaches are required to sift through the tens of thousands of non-coding variants, to identify potentially functional variants that have an impact on the gene expression profile of the sample. Here we introduce an integrative analysis pipeline, called μ-cisTarget, to filter, annotate and prioritize non-coding variants based on their putative effect on the underlying 'personal' gene regulatory network. We first validate μ-cisTarget by re-analyzing three cases of oncogenic non-coding mutations, namely the TAL1 and LMO1 enhancer mutations in T-ALL, and the TERT promoter mutation in melanoma. Next, we re-sequenced the full genome of ten cancer cell lines of six different cancer types, and used matched transcriptome data and motif discovery to infer master regulators for each sample. We identified candidate functional non-coding mutations that generate de novo binding sites for these master regulators, and that result in the up-regulation of nearby oncogenic drivers. We finally validated the predictions using tertiary data including matched epigenome data. Our approach is generally applicable to re-sequenced cancer genomes, or other genomes, when a disease- or sample-specific gene signature is available for network inference. μ-cisTarget is available from http://mucistarget.aertslab.org.

overall_design: Validation of predicted gain of function non-coding mutations in cancer cell lines, using ChIP against the chromatin marker H3K27ac. In this study, H3K27ac ChIP-seq experiments were performed on 4 cell lines (OVCAR-3, SKOV-3, DU-145, Colo-205).

first: Zeynep

last: Kalender-Atak

first: Valerie

last: Christiaens

first: Stein

last: Aerts


title: Transcriptome of Escherichia coli cells in coculture (Ile auxotroph and Leu auxotroph)

first: Kazufumi

last: Hosoda

address: Yamadaoka 1-5

institute: Osaka university

type: Expression profiling by genome tiling array

summary: We conducted experimental evolution of E. coli a mutual cross-feeding coculture, composed of two genetically-engineered Escherichia coli populations, I- and L-, which lack genes for biosynthesis of Ile (ilvE gene) and Leu (leuB gene), respectively. These two populations grew in a coculture by complementing required nutrients each other. After 883 generations of evolution experiments, we measured evolutionary changes in transcriptome, and we found ABC transporters for the branched chain amino acids (Ile, Leu, and Val) were significantly increased in both I- and L-. Also, we got other various results that would be interesting to discuss.

overall_design: In total, 20 samples.

first: Naoaki

last: Ono

first: Shingo

last: Suzuki


title: ChIP-seq from H1-hESC (ENCSR853NNZ)

first: ENCODE

last: DCC

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


title: Gene expression profiling of paracancerous tissues of human lung squamous cell carcinoma

city: Beijing

first: Li

last: Ping

address: 17# Panjiayuan Nanli, , Chaoyang District

institute: National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College

summary: Our group previously reported the gene expression profiles of four stages of human lung development, and the expression of one group of genes (PTN1 genes) steadily decreased during lung development, the data included four stages of human lung development and 69 lung adenocarcinoma (ADC) samples, and their gene expression profile data are available in the GEO (GSE43767). Our group has already performed another study with 69 lung squamous cell carcinoma (SCC) tissues, the gene expression profile data are available in the Gene Expression Omnibus (GSE67061). In the present study, we performed the whole genome gene expression mircroarray of 60 paracancerous tissues of human lung squamous cell carcinoma, we aim to show expression characteristics of PTN1 genes during the four lung developmental stages and in lung ADC, lung SCC and paracancerous samples. We examined the prognostic value of the PTN1 genes in five independent lung adenocarcinoma (ADC) and five squamous cell carcinoma (SCC) microarray datasets and revealed that the expression of PTN1 genes was associated with survival in lung ADC patients but had no prognostic value for lung SCC.

overall_design: A total of 60 paracancerous tissue samples from lung squamous cell carcinoma patients were profiled by Agilent Whole Human Genome Microarray 4x44K .

first: Ping

last: Li

first: Lin

last: Feng

first: Jun

middle: S

last: Cheng

first: Tai

middle: K


title: Arabidopsis inflorescence stems: wild type vs sgr1

status: Public on Jul 13 2017

city: Nagoya

first: Miyo

middle: Terao

last: Morita

address: Furocho, Chikusa

department: Graduate School of Bioagricultural Sciences

institute: Nagoya University

summary: Transcriptional profiling of wild type and sgr1 of Arabidopsis inflorescence stems. Candidate genes which were down-regulated in sgr1 relative to wild type were identified.

overall_design: Biological replicates: 2 replicates for each experiments and dye swapped for each sample

last: Terao Morita

first: Moritaka

last: Nakamura

first: Masatoshi

last: Taniguchi

first: Masao

last: Tasaka

first: Masahiko

last: Furutani

first: Takeshi

last: Nishimura

first: Toyohito

last: Fushita

first: Kota

last: Iijima

first: Kenichirou

last: Baba

first: Kazuhiro

last: Tanaka

first: Masatsugu

last: Toyota


title: Arabidopsis inflorescence stems: wild type vs eal1

summary: Transcriptional profiling of wild type and eal1 of Arabidopsis inflorescence stems. Candidate genes which were down-regulated in eal1 relative to wild type were identified.


title: ChIP-seq from thoracic aorta (ENCSR803IBD)

first: ENCODE

last: DCC


title: Spo11-oligo mapping of DSBs in an SK1 x S288C F1 hybrid strain

city: New York

first: Scott

last: Keeney

address: 1275 York Ave

department: Molecular Biology Program

institute: Memorial Sloan Kettering Cancer Center

summary: The Spo11-generated double-strand breaks (DSBs) that initiate meiotic recombination are non-randomly distributed across the genome. Here, we use Spo11-oligonucleotide complexes, a byproduct of DSB formation, to map the distribution of meiotic DSBs in an SK1 x S88C F1 hybrid strain of Saccharomyces cerevisiae.

overall_design: One sample, collected at 6 hr after transfer to sporulation medium

first: Xuan

last: Zhu


title: Gene expression profiling of idiopathic interstitial pneumonias (IIPs): identification of potential diagnostic markers and therapeutic targets

city: Hiroshima

first: Yasushi

last: Horimasu

address: 1-2-3 Kasumi, Minami-ku

institute: Hiroshima University

summary:
Chronic fibrosing idiopathic interstitial pneumonia (IIP) is characterized by alveolar epithelial damage, activation of fibroblast proliferation, and loss of normal pulmonary architecture and function.
This analysis was performed to investigate the genetic backgrounds of IIP and identify potential biomarkers that can aid in diagnosis and serve as novel therapeutic target.

overall_design: RNA extracted from lung specimens of 12 Japanese patients with chronic fibrosing IIP was profiled using Illumina Human WG-6 v3 BeadChips.

first: Nobuhisa

last: Ishikawa

first: Masaya

last: Taniwaki


title: Arabidopsis inflorescence stems: wild type vs eal1 and sgr1

first: Miyo

last: Morita

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

overall_design: Refer to individual Series


title: Gata4 and LMO3 balance angiocrine signaling and autocrine inflammatory activation by BMP2 in liver sinusoidal endothelial cells

city: Mannheim

first: Carsten

last: Sticht

address: Theodor-Kutzer-Ufer

department: ZMF

institute: University Heidelberg


title: Gata4 and LMO3 balance angiocrine signaling and autocrine inflammatory activation by BMP2 in liver sinusoidal endothelial cells [HLSEC]

summary: Liver sinusoidal endothelial cells (LSEC) represent a unique, organ-specific type of discontinuous endothelial  cells. LSEC instruct the hepatic vascular niche by paracrine-acting angiocrine factors. Recently, we have shown  that LSEC-specific transcriptional regulator GATA4 induces expression of BMP2 in cultured endothelial cells (EC)  in vitro. Furthermore, angiocrine Bmp2 signaling in the liver in vivo was demonstrated to control iron homeostasis.  Here, we investigated GATA4-dependent autocrine BMP2 signaling in endothelial cells by gene expression  profiling. GATA4 induced a large cluster of inflammatory endothelial response genes in cultured EC, which  is similar to previously identified virus-induced and interferon-associated responses. Treating the cells with the  BMP2 inhibitor Noggin counter-regulated the GATA4-dependent inflammatory phenotype of EC, indicating that  BMP2 is indeed the major driver. In contrast to continuous EC, LSEC were less prone to activation by BMP2.  Notably, GATA4-dependent induction of the inflammatory EC response gene cluster was attenuated by over-expression  of the LSEC-specific transcriptional modifier LMO3 while hepatocyte activation was fully preserved,  indicating conserved BMP2 synthesis. In summary, our data suggest that transcriptional counter-regulation by  GATA4 and LMO3 in LSEC prevents autocrine induction of an inflammatory phenotype, while maintaining angiocrine  BMP2-mediated cell communication in the liver vascular niche.

overall_design: HLSEC were transduced with human GATA4 and/or LMO3 or empty vector for RNA extraction and hybridization on Affymetrix microarrays.

first: Victor

last: Olsavszky

first: Philipp-Sebastian

last: Koch


title: Alveolar macrophages from tuberculosis patients display an altered inflammatory gene expression profile

city: Medellín

first: LELIA

last: LAVALETT

state: Antioquia

department: Antioquia

country: Colombia

institute: Universidad de antioquia

summary: Alveolar macrophages (AMs) are major targets of Mycobacterium tuberculosis (Mtb) infection, critical during the progression of active tuberculosis (TB). The complex immunopathology of TB generates diverse microenvironments in the lung, which shape immune responses by AMs. In the current study, we perform whole genome microarray transcriptional profiling on RNA isolated from AMs from TB patients (AMsTB) compared to AMs from control subjects (AMsCT) using bronchoalveolar lavage (BAL). Our hypothesis was that systemic effects on the local lung microenvironment during TB affect the transcriptional response of AMsTB. We found a unique gene expression profile of 51 genes, including up-regulated CHIT1, CHI3L1, CCL5, CCL22, CCL8, CXCL9, MMP9, MMP7 and MMP12, associated with a robust pro-inflammatory response, cell recruitment and tissue damage, and genes of the cyclin family (CCND1, CCND2, and CCNA1) associated with cell proliferation. These expression profiles may account for the inflammatory condition in the lungs of TB patients. CXCL5, IL1B, CAMP, and TGFB1 were down-regulated, suggesting an altered control of Mtb infection. Also, MARCO and COLEC12, affecting phagocytosis, and CES1, associated with an increase in free cholesterol, were down-regulated. The observed changes in mRNA expression profiles may partially account for the inability of AMsTB to effectively control Mtb infection, suggesting that a balanced control of pro- and anti-inflammatory immune responses is crucial for infection control.

overall_design: Total RNA obtained from AMsTB (n=3) compared to aAMsCT (n=4) from at least 3 replica wells was obtained with the RNeasy minikit (Qiagen). RNA (RIN>7.5) were used to prepare cRNAs. Biotinylated cRNAs were prepared from 0.55 µg of total RNA using the Illumina TotalPrep RNA Amplification kit (Ambion). Following fragmentation, 0.75 µg of cRNA were hybridized to the Illumina Expression Human HT-12v4 Expression Bead Chip, targeting 47,323 probes according to the protocols provided by the manufacturer. Raw data were extracted using the software provided by the manufacturer (Illumina GenomeStudio v2011.1 (Gene Expression Module v1.9.0). Probes signal values were transformed by logarithm method. The raw data were preprocessed by the Lumi Bioconductor package using the R software (www.r-project.org). Unsupervised methods with hierarchical clustering was calculated using complete Euclidean distance transformation. Gene-Enrichment and Functional Annotation analysis for significant probe list was performed using DAVID (http://david.abcc.ncifcrf.gov/).

first: Lelia

last: Lavalett

first: Hector

last: Rodriguez

last: Ortega

first: Sadee

last: Wolfgang

first: Larry

last: Schlesinger

first: Luis

last: Barrera


title: Gene expression profiling of continuous growth hormone infused (cGH) adult male mouse liver by RNA-seq analysis of liver RNA.

city: Boston

first: David

middle: J.

last: Waxman

state: MA

address: 5 Cummington Mall

department: Department of Biology and Bioinformatics Program

institute: Boston University


title: Gata4 and LMO3 balance angiocrine signaling and autocrine inflammatory activation by BMP2 in liver sinusoidal endothelial cells [HUVEC]

overall_design: HUVEC were transduced with human GATA4 or empty vector and stimulated with or without Noggin or BMP2 for RNA extraction and hybridization on Affymetrix microarrays.


title: Evidence that Mediator is essential for Pol II transcription but not a required component of the preinitiation complex in vivo

first: Natalia

last: Petrenko

address: 240 Longwood Ave

department: BCMP

institute: Harvard Medical School

summary: Mediator, a transcriptional co-activator complex, is recruited to enhancers by DNA-binding activators via its tail module, and it interacts with RNA polymerase (Pol) II as part of the preinitiation complex (PIC) via its head module.  Although Mediator has been described as a general transcription factor, it is unclear if it is essential for Pol II transcription and/or is a required component of the PIC in vivo.  We comprehensively analyze this issue by measuring Pol II transcription upon rapid depletion of individual or multiple Mediator subunits from the nucleus.  Depletion of individual subunits, even those essential for cell growth, causes a general but only modest decrease in Pol II transcription.  Transcriptional effects are stronger on SAGA-dependent genes as opposed to TFIID-dependent genes.  Thus, Mediator modules that associate either with the enhancer or with the core promoter confer partial transcriptional activity. Furthermore, Pol II transcription can occur when Mediator is not detected at core promoters.  In contrast, simultaneous depletion of all Mediator modules causes a drastic decrease in Pol II transcription that is roughly comparable to the effect observed upon anchor-away-mediated depletion of Pol II or TBP.  These results provide strong evidence that Mediator is essential for Pol II transcription in vivo, but that it is not a required component of the PIC.

overall_design: Chip-seq performed with 8WG14 antibodies before and after the anchor-away of 7 Mediator subunits, as well as in a WT strain, in a TBP anchor-away strain, an Rpb-1 anchor-away strain, and in the "Triple" mutant, where the Mediator tail is deleted and Med17 is anchored away.

first: Yi

last: Jin

first: Koon

middle: H

last: Wong

first: Kevin

last: Struhl


title: ChIP-seq from transverse colon (ENCSR791LZY)

status: Public on Jul 12 2017

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC


title: ChIP-seq from right atrium auricular region (ENCSR791KFQ)


title: ChIP-seq from gastrocnemius medialis (ENCSR785DJD)


title: ChIP-seq from A549 (ENCSR798EGJ)


title: ChIP-seq from embryonic facial prominence (ENCSR779MSI)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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: ChIP-seq from neutrophil (ENCSR785YRL)


title: ChIP-seq from breast epithelium (ENCSR770WSE)


title: ChIP-seq from thyroid gland (ENCSR761WVQ)


title: ChIP-seq from tibial nerve (ENCSR771YJT)


title: ChIP-seq from body of pancreas (ENCSR748TFF)


title: ChIP-seq from H1-hESC (ENCSR774YGM)


title: ChIP-seq from body of pancreas (ENCSR774CFO)


title: ChIP-seq from GM12878 (ENCSR751CJG)


title: ChIP-seq from gastrocnemius medialis (ENCSR776EAH)


title: ChIP-seq from upper lobe of left lung (ENCSR738SXD)


title: ChIP-seq from ACC112 (ENCSR741GJT)


title: ChIP-seq from right atrium auricular region (ENCSR793PLF)


title: ChIP-seq from ACC112 (ENCSR726ZZX)


title: ChIP-seq from A549 (ENCSR740DXC)


title: ChIP-seq from ascending aorta (ENCSR736PKV)


title: ChIP-seq from spleen (ENCSR726HTS)


title: ChIP-seq from thyroid gland (ENCSR716FUH)


title: ChIP-seq from esophagus muscularis mucosa (ENCSR743KZR)


title: ChIP-seq from K562 (ENCSR735JCD)


title: ChIP-seq from body of pancreas (ENCSR719COF)


title: ChIP-seq from A549 (ENCSR787VQB)


title: ChIP-seq from thyroid gland (ENCSR699FHH)


title: ChIP-seq from ascending aorta (ENCSR707AEW)


title: ChIP-seq from PC-3 (ENCSR695SCQ)


title: ChIP-seq from gastroesophageal sphincter (ENCSR677LBH)


title: ChIP-seq from sigmoid colon (ENCSR682GOI)


title: ChIP-seq from fibroblast of arm (ENCSR673OPX)


title: ChIP-seq from spleen (ENCSR659RJP)


title: ChIP-seq from thyroid gland (ENCSR658VPF)


title: ChIP-seq from H1-hESC (ENCSR663WAR)


title: ChIP-seq from ascending aorta (ENCSR645FBM)


title: ChIP-seq from neural progenitor cell (ENCSR656MXA)


title: ChIP-seq from A549 (ENCSR659LJJ)


title: ChIP-seq from ascending aorta (ENCSR723IKM)


title: ChIP-seq from GM12878 (ENCSR649WUM)


title: ChIP-seq from A549 (ENCSR639GWS)


title: microRNA-seq from midbrain (ENCSR625ESQ)

summary:
miRNA-seq on embryonic 16.5 day mouse midbrain

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: ChIP-seq from right lobe of liver (ENCSR614JFD)


title: ChIP-seq from bipolar neuron (ENCSR592ETL)


title: ChIP-seq from body of pancreas (ENCSR596PFU)


title: ChIP-seq from right atrium auricular region (ENCSR593KDJ)


title: ChIP-seq from adrenal gland (ENCSR620TXL)


title: ChIP-seq from A549 (ENCSR616MOB)


title: ChIP-seq from ascending aorta (ENCSR589GII)


title: ChIP-seq from esophagus muscularis mucosa (ENCSR578MTT)


title: ChIP-seq from spleen (ENCSR589TCU)


title: ChIP-seq from Peyer's patch (ENCSR621BZD)


title: ChIP-seq from K562 (ENCSR583ACG)


title: microRNA-seq from hindbrain (ENCSR571RHM)

summary:
miRNA-seq on embryonic 16.5 day mouse hindbrain

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: ChIP-seq from H1-hESC (ENCSR591AOD)


title: microRNA-seq from forebrain (ENCSR552WPH)

summary:
miRNA-seq on embryonic 16.5 day mouse forebrain

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: ChIP-seq from breast epithelium (ENCSR553IAW)


title: ChIP-seq from DOHH2 (ENCSR562NOP)


title: ChIP-seq from neuroepithelial stem cell (ENCSR662PLB)


title: ChIP-seq from stomach (ENCSR546HZF)


title: ChIP-seq from breast epithelium (ENCSR543YQF)


title: ChIP-seq from tibial artery (ENCSR543DAS)


title: ChIP-seq from GM12878 (ENCSR549NPZ)


title: ChIP-seq from A549 (ENCSR550SCU)


title: total RNA-seq from G1E-ER4 (ENCSR538CVD)

summary:
PSU mouse G1E-ER4+E2 100ng rRNA-depeleted RNA-seq via ScriptSeq

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: ChIP-seq from A549 (ENCSR541AOQ)


title: ChIP-seq from stomach (ENCSR539HNK)


title: ChIP-seq from stomach (ENCSR489ZLL)


title: microRNA-seq from liver (ENCSR489FQD)

summary:
miRNA-seq  on embryonic 11.5 day mouse liver

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: ChIP-seq from right lobe of liver (ENCSR489DUV)


title: ChIP-seq from K562 (ENCSR530IUH)


title: ChIP-seq from ascending aorta (ENCSR494YJW)


title: ChIP-seq from HCT116 (ENCSR494CCN)


title: ChIP-seq from SK-N-MC (ENCSR526PZM)

summary:
ChIP-seq against H3K36me3 using SK-N-MC cell line which was previously described as a neuroepithelioma (ATCC HTB-10). However recent evidence reveals it is Ewing's Sarcoma (www.ncbi.nlm.nih.gov/pubmed/15548687, www.ncbi.nlm.nih.gov/biosample/3151999, www.ncbi.nlm.nih.gov/pubmed/25453903).

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: ChIP-seq from hepatocyte (ENCSR484MFB)

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


title: Yeast response to TFM exposure over time (YPD)

city: Northfield

first: Darlene

middle: M

last: Olsen

state: VT

address: 158 Harmon Drive

department: Mathematics

institute: Norwich University

summary: This time course microarray experiment was performed on Saccharomyces cerevisiae to determine the global gene expression alterations due to 3-trifluoromethyl-4-nitrophenol (TFM) exposure  over time. In this experiment,  yeast grown in standard, glucose-containing media were treated with 0.05mM TFM over a four hour period.

platform_organism:
Schizosaccharomyces pombe
Saccharomyces cerevisiae

overall_design: The wild type S. cerevisiae strain BY4741 were grown in yeast peptone dextrose (YPD), a fermentable medium (1% yeast extract, 2% peptone, and 2% dextrose), at 30°C to saturation and treated for 1h, 2h, or 4h with 0.05mM TFM in 2% isopropanol (TFM solvent). The two biological replicates taken immediately before treatment represented “time zero”, untreated (2% isopropanol only) controls. For each TFM treated time point, two independent RNA samples (two biological replicates) were isolated (except for at time 4h, only one RNA sample was isolated but two technical replicates were prepared and processed).

first: Karen

middle: L

last: Hinkle


title: microRNA-seq from heart (ENCSR481QIP)

summary:
miRNA-seq on embryonic 16.5 day mouse heart

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: ChIP-seq from tibial nerve (ENCSR479GPU)


title: ChIP-seq from thyroid gland (ENCSR475NOQ)


title: total RNA-seq from G1E (ENCSR475TDY)

summary:
PSU mouse G1E 100ng rRNA-depeleted RNA-seq via ScriptSeq

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: ChIP-seq from PC-3 (ENCSR461HUD)


title: ChIP-seq from A549 (ENCSR469WAO)


title: ChIP-seq from adrenal gland (ENCSR455JUO)


title: ChIP-seq from ascending aorta (ENCSR441YQA)


title: ChIP-seq from coronary artery (ENCSR443UYU)


title: ChIP-seq from body of pancreas (ENCSR429XBU)


title: Identify the expression of lncRNAs in peripheral blood mononuclear cells from rheumatoid arthritis

city: liaocheng

first: Min

last: Yuan

address: 67 dongchang xi road

institute: liaocheng people's hospital

type:
Expression profiling by array
Non-coding RNA profiling by array

summary: The expression profiles of lncRNAs in peripheral blood mononuclear cells (PBMCs) from rheumatoid arthritis (RA) patients have not been well researched. Therefore, we identified the lncRNA expression profiles in PBMCs from female patients with RA and explored the possible role of the abundantly expressed lncRNAs in RA.

overall_design: 3 pairs of samples were mixed with equivalent PBMCs from 27 female RA patients and 27 corresponding healthy controls, which were randomly divided into three groups according to age.

first: Huaxiang

last: Liu


title: ChIP-seq from MCF-7 (ENCSR460YHB)


title: ChIP-seq from upper lobe of left lung (ENCSR422TGJ)


title: ChIP-seq from heart left ventricle (ENCSR438QZN)


title: ChIP-seq from A673 (ENCSR435FGK)


title: Microarray expression data from leukemia cell lines RS4;11 and REH with CASC15 KD or KO respectively

city: Los Angeles

first: Norma

middle: Iris

last: Rodriguez-Malave

state: California

address: 8723 Alden Drive

institute: Cedars-Sinai Medical Center

summary:
Long non-coding RNAs play a variety of cellular roles, including regulation of transcription and translation, leading to alterations in gene expression. Here, we assess the role of lncRNA CASC15 in RUNX1/AML translocated leukemia. Differentially regulated genes following CASC15 knockdown were enriched for predicted transcriptional targets of the Yin and Yang-1 (YY1) transcription factor. Our findings represent the first characterization of this CASC15 in RUNX1-translocated leukemia, and point towards a mechanistic basis for its action.
We used microarrays to look at significantly differentally expressed genes and global effectes upon knockdown of knockout of CASC15 in two different leukemia cell lines

overall_design: RS4,11 cells were transduced with an empty vector (control) or with siRNAs (1, 2, 3) against CASC15. After confirmation of successful knockdown one replicate of each line was used. REH cells were transduced with an empty vector (control) or with a pair of guide RNAs against exon 1 and exon 9 of CASC15 (C1,9). After confirmation of successful knockout three replicates of each line was used. Cell lines were harvested for RNA extraction, DNAse treatment, and hybridization on Affymetrix HG-U133_Plus_2 microarrays.

first: Thilini

last: Fernando

middle: I


title: microRNA-seq from neural tube (ENCSR415KUB)

summary:
miRNA-seq on embryonic 15.5 day mouse neural tube

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: ChIP-seq from H1-hESC (ENCSR418RRF)


title: JAZi-mediated jasmonate signaling is invoved in floral defense in Nicotiana attenuata

city: Jena

first: Klaus

last: Gase

address: Hans-Knoell-Strasse 8

department: Molecular Ecology

institute: Max-Planck-Institute for Chemical Ecology

summary: Identification of transcripts that change expression in Nicotiana attenuata plants with reduced expression of JAZi in flowers

overall_design: Gene expression in floral stage 1 and 3 of JAZi-VIGS plants and VIGS control plants

first: Ran

last: Li

first: Ian

middle: T

last: Baldwin


title: ChIP-seq from GM12878 (ENCSR410HFN)


title: Amniotic fluid transcriptomics reflects novel disease mechanisms in fetuses with myelomeningocele

first: Tomo

last: Tarui

address: 800 Washington St.

department: Pediatric Neurology

institute: Tufts Medical Center

summary: To identify molecular pathophysiologic changes and novel disease mechanisms specific to myelomeningocele by analyzing AFS cfRNA in fetuses with open  myelomeningocele.

overall_design: AFS was collected from 10 pregnant women at the time of the open myelomeningocele repair in the second trimester (24.5+/-1.0 wks) and 10 archived AFS from sex and gestational age-matched euploid fetuses without myelomeningocele were used as controls (20.9+/-0.9 wks). Differentially regulated gene expression patterns were analyzed using Human Genome U133 Plus 2.0 arrays.

first: Aimee

last: Kim

first: Alan

last: Flake

first: Lauren

last: Mcclain

first: John

last: Stratigis

first: Inbar

last: Fried

first: Rebecca

last: Newman

first: Donna

last: Slonim

first: Diana

middle: W

last: Bianci


title: total RNA-seq from granulocyte monocyte progenitor cell (ENCSR277DPB)

first: ENCODE

last: DCC

summary:
PSU mouse GMP 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from sigmoid colon (ENCSR268ZCF)


title: Expression data from Zebrafish larvae at 4dpf

city: tianjin

first: shijiao

last: cai

address: Qixiangtai road

institute: Tianjin Medical University

summary:
Interleukin 7 receptor (IL7R) is a transmembrane receptor which belongs to the type I cytokine receptor family. Recent studies have indicated that the IL7R is involved in the pathogenesis of some neurodegenerative disorders, such as multiple sclerosis. Previously, we found that the retinal neuroregenation was delayed following the targeted knockdown of IL7R, highlighting the potential role of IL7R in the development of nervous system.
We used microarrays to detail the global programme of gene expression fllowing il7r knockout.

overall_design: Zebrafish larvae of Tu and il7r-/- groups were collected at 4 days post hybridization (dpf) for RNA extraction and hybridization on Affymetrix microarrays. There are 3 duplicates in each group and homogeneous populations of larvae at each duplicate.

first: Yuhao

first: Shijiao

last: Cai


title: ChIP-seq from tibial nerve (ENCSR611YUJ)


title: Expression data from HUVECs with ADK shRNA knockdown

city: Augusta

first: Yiming

last: Xu

state: Georgia

address: 1459 Laney Walker Blvd

department: Vascular Biology Center

institute: Augusta University

summary:
The molecular mechanisms underlying vascular inflammation and associated inflammatory vascular diseases are not well defined. Here we show that endothelial intracellular adenosine and its key regulator adenosine kinase (ADK) play important roles in vascular inflammation. Pro-inflammatory stimuli lead to endothelial inflammation by increasing endothelial ADK expression, reducing the level of intracellular adenosine in endothelial cells, and activating the transmethylation pathway through increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH). Increasing intracellular adenosine by genetic ADK knockdown or exogenous adenosine reduces activation of the transmethylation pathway and attenuates the endothelial inflammatory response. In addition, loss of endothelial ADK in mice leads to reduced atherosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex. Taken together, these results demonstrate that intracellular adenosine, which is controlled by the key molecular regulator ADK, influences endothelial inflammation and vascular inflammatory diseases.
We knocked down the adenosine kinase (ADK) in human primary endothelial cells to study the endothelial inflammatory responses to ADK inactivation under static conditions.

overall_design: HUVECs were infected with human ADK shRNA or control adenovirus and RNA was processed for microarray analysis 30 h post infection. Three biological replicates were used for each condition.

first: Yuqing

last: Huo


title: ChIP-seq from SK-N-SH (ENCSR297MUV)


title: ChIP-seq from adrenal gland (ENCSR605QAV)


title: ChIP-seq from H1-hESC (ENCSR267YDT)


title: ChIP-seq from adrenal gland (ENCSR408ZEW)


title: ChIP-seq from GM12878 (ENCSR265MJJ)


title: ChIP-seq from hepatocyte (ENCSR252QYR)


title: ChIP-seq from spleen (ENCSR197QDK)


title: ChIP-seq from right atrium auricular region (ENCSR195BZZ)


title: ChIP-seq from spleen (ENCSR189UPU)


title: ChIP-seq from MM.1S (ENCSR402IDP)


title: ChIP-seq from adrenal gland (ENCSR189QAD)


title: ChIP-seq from esophagus muscularis mucosa (ENCSR177CGN)


title: ChIP-seq from uterus (ENCSR249INE)


title: Gene Expression Changes during embryo and seed maturation, quiescence and germination in soybean

city: Davis

last: Harada

address: One Shields Avenue

department: Plant Biology

institute: University of California

summary: To understand the molecular events underlying seed maturation, quiescence and germination, we performed transcriptome analysis of soybean (Glycine max) embryos at four seed developmental stages (cotyledon, early, mid and late maturation), mature dry seeds, and seedlings, eight days after seed sowing.

overall_design: mRNA profiling was performed on embryos at 4 stages of development, dry seeds and seedlings.  Three biological replicates were collected for each developmental stage.

first: Robert

middle: B

last: Goldberg

first: Ryan

last: Kirkbride

first: Julie

last: Pelletier

first: Tina

middle: Y

last: Wang

first: Russell

last: Baden

first: Alexander

last: Olson


title: Identification of LEC1 binding sites in Arabidopsis seedlings

first: John

type: Genome binding/occupancy profiling by genome tiling array

summary: LEAFY COTYLEDON1 (LEC1), an atypical subunit of the NF-Y CCAAT binding transcription factor, is a central regulator that controls many aspects of seed development including the maturation phase during which seeds accumulate storage macromolecules and embryos acquire the ability to withstand desiccation.    To define the gene network and developmental processes controlled by LEC1, genes regulated directly by and downstream of LEC1 were identified.  In this part of the study, we identified the genes bound by LEC1 by overexpressing a FLAG-tagged inducible form of LEC1 in Arabidopsis seedlings and inducing LEC1 activity for a short (4 hours) or long (8 days) period of time, to identify the genes bound  EARLY and LATE, respectively.

overall_design: LEC1 activity was induced in Arabidopsis 35S:FLAG-LEC1-GR plants, either by treating seedlings for 4h, or germinating seeds and growing seedlings for 8 days in the presence of dexamethasone (DEX).  Anti-FLAG antibodies (Sigma F1804) were used to immunoprecipitate LEC1-bound DNA fragments and compared to total fragmented chromatin from the same biological materials.  Two biological replicates per conditions were analyzed.

first: Raymond

last: Kwong

first: Anhthu

middle: Q

last: Bui

first: Brandon

last: Le

last: Golberg

middle: J


title: mRNA changes following induction of LEC1 activity in Arabidopsis seedlings

summary: LEAFY COTYLEDON1 (LEC1), an atypical subunit of the NF-Y CCAAT binding transcription factor, is a central regulator that controls many aspects of seed development including the maturation phase during which seeds accumulate storage macromolecules and embryos acquire the ability to withstand desiccation.    To define the gene network and developmental processes controlled by LEC1, genes regulated directly by and downstream of LEC1 were identified.   In this part of the study, we identified the genes regulated by LEC1 by overexpressing an inducible form of LEC1 in Arabidopsis seedlings and identifying the mRNAs induced EARLY (1h) after induction of LEC1 activity.

overall_design: Shoot apices from Arabidopsis thaliana 35S:LEC1-GR 8 day old seedlings were incubated for 1 h in the presence or absence of Dexamethasone to induce LEC1 activity.  Two biological replicates per treatment were analyzed.


title: Recombination at subtelomeres is regulated by physical distance, double strand break resection and chromatin status

city: Paris

first: Angela

last: Taddei

address: 26 rue d'Ulm

country: France

institute: Institut Curie

type: Genome binding/occupancy profiling by array

summary: Two conditions experiment, ChIP-chip anti-Sir3 comparing Sir3 occupancy in exponentially growing S.cerevisiae cells to Sir3 occupancy in strains overexpressing SIR3

overall_design: Two conditions experiment with biological duplicates

first: Antoine

last: Hocher


title: Gene Expression Changes in the Development of the Soybean Seed Mid-Maturation (B1) Stage

summary: We investigated soybean seed development because (1) soybean seeds are a major source of food and fuel, (2) soybean seeds have been an excellent system for studying the basic processes controlling seed development for over three decades, and (3) new soybean genomic resources, including the sequence of the soybean genome and the gene expression profiles for all seed compartments, tissues, and cell types, can be used to gain new insights into the regulatory processes required for seed differentiation. We sequenced messenger RNA populations of specific soybean seed compartments, which will provide new insights into gene expression that are important for “making a soybean seed.”

overall_design: Three compartments of the mid-maturation (B1) stage of the soybean seeds were analyzed. Three biological replicates were collected for each compartment.

first: Ssu-Wei

last: Hsu

first: Shu-Heng

last: Chang

first: Rie

last: Uzawa

first: Lourenz

last: Balayan

first: Erik

last: Garber

first: Meryl

last: Hashimoto

first: Uranus

last: Chau


title: Large-scale genomic reorganizations of topological domains (TADs) at the HoxD locus (4C-Seq)

city: Lausanne

first: Pierre

last: Fabre

address: Station 19

department: ISREC

country: Switzerland

institute: EPFL

summary: The transcriptional activation of Hoxd genes during mammalian limb development involves dynamic interactions with the two Topologically Associating Domains (TADs) flanking the HoxD cluster. In particular, the activation of the most posterior Hoxd genes in developing digits is controlled by regulatory elements located in the centromeric TAD (C-DOM) through long-range contacts. To assess the structure-function relationships underlying such interactions, we measured compaction levels and TAD discreteness using a combination of chromosome conformation capture (4C-seq) and DNA FISH. We challenged the robustness of the TAD architecture by using a series of genomic deletions and inversions that impact the integrity of this chromatin domain and that remodel the long-range contacts. We report multi-partite associations between Hoxd genes and up to three enhancers and show that breaking the native chromatin topology leads to the remodelling of TAD structure. Our results reveal that the re-composition of TADs architectures after severe genomic re-arrangements depends on a boundary-selection mechanism that uses CTCF-mediated gating of long-range contacts in combination with genomic distance and, to a certain extent, sequence specificity.

overall_design: 4C-seq analysis of Hoxd13 and Island-II 3D interactions in proximal and distal limbs from E12.5 wt or mutant embryos

first: P

first: M

last: Leleu

first: L

last: Lopez-Delisle

first: D

last: Duboule


title: ChIP-seq from breast epithelium (ENCSR403UOU)

first: ENCODE

last: DCC

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


title: Large-scale genomic reorganizations of topological domains (TADs) at the HoxD locus

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

overall_design: Refer to individual Series


title: LncRNA/mRNA expression  in pancreatic ductal adenocarcinoma (PDAC) and mached non-tumor tissues

status: Public on Jul 11 2017

city: Shanghai

first: Xing

last: Liang

state: Shanghai

address: No.415 Fengyang Road, Shanghai, China

department: Department of Pancreatic-biliary Surgery

institute: Shanghai Changzheng Hospital, China

summary: To determine the lncRNA and mRNA expression profile in PDAC and matched non-tumor tissues, we uesed lncRNA microArray analysis form Arraystar to examine the expression of lncRNAs and mRNAs in PDAC and matched non-tumor tissues.

overall_design: human tissues from PDAC surgery were distributed into two experimental groups: tumor tissue group and matched non-tumor tissues group, then perform lncRNAs chips by Arraystar Human lncRNAs chip (Arraystar)

first: Chenghao

last: Shao


title: RNAseq analysis between hepatocytes isolated from control livers,  β1-integrin mutant livers, P21 over-expressed livers and ductal cells.

city: Edinburgh

first: John

middle: Paterson

last: Thomson

address: Crewe Road

department: MRC Human Genetics Unit

country: United Kingdom

institute: University of Edinburgh

summary: RNAseq analysis between cell types. RNA extracted using Qiagen mini total RNA isolation protocols (Qiagen, Germany). Samples were treated with DNase (Ambion), and sample integrity verified on the Agilent Bioanalyser with the RNA Nano chip.  Illumina Tru-seq paired end strand specific sequencing (Illumina, USA) was carried out by on a NextSeq-550 sequencer (Edinburgh Clinical Research Facility, Western General Hospital, Edinburgh, Scotland, UK). 500ng of Total RNA underwent ribosomal RNA depletion (rRNA) prior to purification, fragmentation, random hexamer cDNA generation and purification with AMPure XP beads (Beckman-Coulter, USA). Multiple indexing adapters were ligated to ds cDNA with subsequent hybridisation onto flow cells, and DNA fragment enrichment by 15 cycle PCR for sequencing.  Completed libraries were quantified by qPCR using the KAPA Illumina Library Quantification Kit (Illumina, USA) before multiplexing in two equimolar pools and running on two flow cells on the Illumina NextSeq 550. The resulting FastQ files were mapped to the reference genome (mm9) using the Tophat alignment tool (V1) on Illumina Basespace software and reads per kilobase per million (RPKM) scores calculated.

overall_design: We carry out paired end, strand specific RNAseq prior to sequencing on NextSeq-550 sequencer to report on the transcriptional landscape control hepatocytes, wild type bile ducts, Biliray derived hepatocytes from Itgb1 fl/fl liver and Biliray derived hepatocytes from AAV8-p21 liver

middle: P

first: Alex

last: Raven

first: Wei-Yu

last: Lu

first: Stuart

last: Forbes


title: Analysis of gene expression in the distal forelimbs in 2.4Mb inversion adjacent to the HoxD cluster

summary: E12.5 mouse distal forelimb embryonic transcriptome

overall_design:
Data from inversion to compare with WT
RNA-Seq polyA on transcripts extracted from the dissection of three pairs of embryonic forelimbs at E12.5


title: Gene Expression during Model Dough Fermentation after Freezing Preservation of S. cerevisiae Baker’s Yeast Cells

city: Ikoma

first: Daisuke

last: Watanabe

state: Nara

address: 8916-5 Takayamacho

institute: Nara Institute of Science and Technology

summary: Freeze-thaw stress causes various cellular damages, survival and proliferation defects, and metabolic alterations, although how cells cope with it is poorly understood. In this study, model dough fermentations using two different strains of Saccharomyces cerevisiae baker’s yeast were compared after two-week cell preservation in the refrigerator or in the freezer. As a result, one strain specifically exhibited a decreased fermentation rate after exposed to freeze-thaw stress. A DNA microarray analysis of the cells during fermentation revealed that the genes involved in oxidative phosphorylation were upregulated after the freeze-thawing process in the stress-sensitive strain, suggesting a metabolism switching from glycolysis to respiration. In the identical strain, however, most of the genes that encode the components of the proteasome complex were commonly downregulated, and ubiquitinated proteins were highly accumulated by freeze-thaw stress. In the cells with a laboratory-strain background, treatment with a proteasome inhibitor MG132 or deletion of each transcriptional activator gene for the proteasomal genes (RPN4, PDR1, or PDR3) led to a marked decrease in the rate of model dough fermentation using the frozen cells. Based on these data, degradation of freeze-thaw damaged proteins by proteasome may guarantee the high fermentation performance. Furthermore, a heterozygous dominant-negative PDR3 allele (A148T/A229V/H336R/L541P) was found in the diploid genome of the stress-sensitive baker’s yeast strain, which may be associated with the decreased fermentation rate. Removal of such responsible mutations may improve the freeze-thaw stress tolerance and the fermentation performance of baker’s yeast strains, as well as other industrial S. cerevisiae yeast strains.

overall_design: We examined the effects of refrigerating or freezing preservation on gene expression of Saccharomyces cerevisiae yeast cells during model dough fermentation by using Agilent Technologies Yeast (v2) Gene Expression 8x15K Microarray. Total RNA samples were extracted from refrigerated cells and frozen cells of two strains (strains A and B) and were subjected for this DNA microarray analysis.

first: Hiroshi

last: Sekiguchi

first: Yukiko

last: Sugimoto

first: Atsushi

last: Nagasawa

first: Naotaka

last: Kida

last: Takagi


title: Murine triple negative breast cancer

city: Melbourne

first: Sathana

last: Dushyanthen

address: 305  Grattan St

country: Australia

institute: Peter MacCallum Cancer Centre

summary:
Differential gene expression analysis between Vehicle and Trametininb treatment in 4T1Ch9 in vivo.
GSEA  analysis between Vehicle and Trametininb treatment in 4T1Ch9 in vivo.

overall_design: 2 Vehicles (VEH), 2 Trametinib treated (MEK), in  vivo

first: S


title: Ionizing radiation induced changes of miRNA expression in A549 lung cancer cells

city: Seoul

first: Su

middle: Jae

last: Lee

state: Haengdang- Dong, Seongdong-Gu

address: 222, Wangsimni-ro

department: Life science

country: South Korea

institute: Hanyang University

summary: We have employed microarray expression profiling as a discovery platform to identify microRNAs induced by radiation. Human A549 lung cancer cells were irradiated (2Gy/day for consistent 3days) and miRNA signature was identified that distinguished between control and radiation treated samples.Irradiated and un-irradiated A549 cells were harvested after 48 hr of treatment and microarray analysis was performed. Expression of five miRNAs (miR-30a, miR-30b, miR-30c, miR-30d, and miR-30d) from this signature was quantified in the same RNA samples by real-time PCR, confirming variability between control and radiation treated A549 cells.

overall_design: Radiation induces miRNA expression in A549 cell line was measured at 48 hours after exposure to doses of  2Gy for 3days.

first: Su-Jae


title: mRNA expression after knockdowwn of UICLM in SW620 cells

city: Guangzhou

first: Dong-liang

last: Chen

address: No.651 Dong Feng East Road

institute: Sun Yat-sen University Cancer Center

summary: The purpose of this study is to identify the disregulated mRNAs after knockdown of UICLM (up-regulated in colorectal cancer liver metastasis, accession number: NR_033841) in SW620 cells. A total of 188 mRNAs were identified to be differentially expressed after knockdown of UICLM in SW620 cells

overall_design: SW620 cells (control) or SW620 cells knockdown of UICLM (siRNA) were subjected to microarray to select differentially expressed mRNAs

first: D

first: R

last: Xu


title: Open Chromatin and HIF-binding in renal tubular cells

city: Erlangen

first: Johannes

last: Schödel

address: Ulmenweg 18

institute: FAU Erlangen-Nürnberg


title: Acetylation on Histone H3 Lysine 9 Mediates a Switch from Transcription Initiation to Elongation

city: Irvine

first: Jiejun

last: Shi

address: 5270 California Ave

department: School of Medicine

country: USA

institute: University of California Irvine

summary: The transition from transcription initiation to elongation is a key regulatory step in gene expression, which requires RNA polymerase II (Pol II) to escape promoter proximal pausing on chromatin. While elongation factors promote pause release leading to transcription elongation, the role of epigenetic modifications during this critical transition step is poorly understood. Two histone marks on histone H3, lysine 4 trimethylation (H3K4me3) and lysine 9 acetylation (H3K9ac), co-localize on active gene promoters and are associated with active transcription. H3K4me3 can promote transcription initiation, yet the functional role of H3K9ac is much less understood. We hypothesized that H3K9ac may function downstream of transcription initiation by recruiting specific proteins important for the next step of transcription. Here, we describe a functional role for H3K9ac in promoting Pol II pause release by directly recruiting the super elongation complex (SEC) to chromatin. H3K9ac serves as a substrate for direct binding of the SEC, as does acetylation of histone H4 lysine 5 (H4K5ac), to a lesser extent. Furthermore, lysine 9 on histone H3 is necessary for maximal Pol II pause release through SEC action, and loss of H3K9ac increases the Pol II pausing index on a subset of genes in HeLa cells. At select gene promoters, loss of H3K9ac or depletion of the SEC reduces gene expression and increases paused Pol II occupancy. We therefore propose that an ordered histone code drives progression through the transcription cycle, providing new mechanistic insight that SEC recruitment to certain acetylated histones promotes the subsequent release of paused Pol II needed for transcription elongation.

overall_design: ChIP-seq analysis of Pol II in HeLa cells transfected with non-targeting control siRNAs or siRNAs targeting GCN5 (KAT2A) and PCAF (KAT2B) in duplicate

first: Bert

last: O'Malley

first: Wei

last: Li

first: Charles

middle: E

last: Foulds


title: Open Chromatin and HIF-binding in renal tubular cells [ChIP-seq]

summary: Un-physiological activation of hypoxia inducible factor (HIF) is an early event in most renal cell cancers (RCC) following inactivation of the von Hippel-Lindau tumor suppressor. Despite intense study, how this impinges on cancer development is incompletely understood. To test for the impact of genetic signals on this pathway, we aligned human RCC-susceptibility polymorphisms with genome-wide assays of HIF-binding and observed highly significant overlap. Allele-specific assays of HIF binding, chromatin conformation and gene expression together with eQTL analyses in human tumors were applied to mechanistic analysis of one such overlapping site at chromosome 12p12.1. This defined a novel stage-specific mechanism in which the risk polymorphism, rs12814794, directly creates a new HIF-binding site that mediates HIF-1? isoform specific upregulation of its target BHLHE41. The alignment of multiple sites in the HIF cis-acting apparatus with RCC-susceptibility polymorphisms strongly supports a causal model in which minor variation in this pathway exerts significant effects on RCC development.

overall_design: This study consists of HIF ChIP-seq samples (HIF-1a and HIF-1b) from one individual and FAIRE-seq samples from three individuals

first: Franziska

last: Kranz


title: Open Chromatin and HIF-binding in renal tubular cells [FAIRE-seq]


title: ChIP-seq from ascending aorta (ENCSR248PES)

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC


title: ChIP-seq from tibial artery (ENCSR166VXF)


title: ChIP-seq from spleen (ENCSR161FEJ)

status: Public on Jul 10 2017


title: ChIP-seq from PC-9 (ENCSR243INX)


title: Anti-inflammatory effect of indoleacrylic acid (IA)

city: Boston

first: Ramnik

last: Xavier

address: 55 Fruit Street

department: Gastroenterology

institute: Massachusetts General Hospital

summary: Host factors in the intestine, such as mucus secretion, play an important role in selecting for the colonization of bacteria that contribute to intestinal health. Here we characterized the capability of commensal species to cleave and transport mucin-associated monosaccharides and found that several members of the Clostridiales order can utilize intestinal mucins as an energy source. One such mucin utilizer, Peptostreptococcus russellii, reduces susceptibility to epithelial injury in mice. Several Peptostreptococcus species contain a gene cluster that enables the production of the tryptophan metabolite indoleacrylic acid (IA), which we show has a beneficial effect on intestinal epithelial barrier function and mitigates inflammatory responses. Furthermore, metagenomic analysis of human stool samples revealed that the genetic capability of microbes to utilize mucins and metabolize tryptophan was diminished in patients with inflammatory bowel disease. Our data suggest that stimulating the production of IA to promote anti-inflammatory responses could have therapeutic benefit.

overall_design:
Isolated hPBMCs treated with IA or 0.1% DMSO followed by LPS stimulation.
Comparisons of interest:
490_DMSO_vs_490_IA
1685_DMSO_vs_1685_IA
406_DMSO_vs_406_IA
ALL_DMSO_vs_ALL_IA

first: Marta

last: Wlodarska


title: Transcriptome analysis of virulence factors in Vibrio vulnificus FORC_036, isolated from a surf clam

first: Han Young

last: Chung

address: 1 Gwanak-ro, Gwanak-gu, Seoul 151-742

institute: Seoul National University

summary: Small octopus is one of the major source for V. vulnificus outbreak among aquatic products in Northeast Asian due to improperly cooking and wound infection by mishandling. However, there is no report on whole genome sequence of V. vulnificus isolated from contaminated surf clam, thus no information is available for major virulence factors about V. vulnificus obtained from small octopus. Therefore, the analysis of transcriptome of isolated V. vulnificus from  products are necessary to investigate potential risk of foodborne illness by contaminated products.

overall_design: The washed small octopus added to FORC_036 inoculated minimal medium, and incubated for 1 h, 4 h/Control group  (FORC_036 inoculated minimal medium, and incubated for 1 h, 4 h), in biological duplication, using Illumina HiSeq 2500.

first: Han-Young

first: So-Jeong

last: Gil


title: Allelic reprogramming of 3D chromatin architecture during early mammalian development

city: Beijing

first: Zhenhai

last: Du

address: Qinghua Yuan, Haidian District

country: China

institute: Tsinghua University

summary: In mammals, chromatin organization undergoes drastic reprogramming after fertilization. However, the three-dimensional structure of chromatin and its reprogramming in preimplantation development remain poorly understood. Here, by developing a low-input Hi-C (genomewide chromosome conformation capture) approach, we examined the reprogramming of chromatin organization during early development in mice. We found that oocytes in metaphase II show homogeneous chromatin folding that lacks detectable topologically associating domains (TADs) and chromatin compartments. Strikingly, chromatin shows greatly diminished higher-order structure after fertilization. Unexpectedly, the subsequent establishment of chromatin organization is a prolonged process that extends through preimplantation development, as characterized by slow consolidation of TADs and segregation of chromatin compartments. The two sets of parental chromosomes are spatially separated from each other and display distinct compartmentalization in zygotes. Such allele separation and allelic compartmentalization can be found as late as the 8-cell stage. Finally, we show that chromatin compaction in preimplantation embryos can partially proceed in the absence of zygotic transcription and is a multi-level hierarchical process. Taken together, our data suggest that chromatin may exist in a markedly relaxed state after fertilization, followed by progressive maturation of higher-order chromatin architecture during early development.

overall_design: Mouse preimplantation embryos were obtained from crosses of C57BL/6N and PWK/PhJ. Hi-C were performed on these embryos at various stages in preimplantation development.

last: Xie


title: total RNA-seq from erythroblast (ENCSR247IMK)

summary:
PSU mouse ERY 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from H1-hESC (ENCSR157EOE)


title: ChIP-seq from stomach (ENCSR166CNR)


title: ChIP-seq from tibial nerve (ENCSR157ZVP)


title: ChIP-seq from OCI-LY1 (ENCSR155XXB)


title: ChIP-seq from tibial nerve (ENCSR154SJE)


title: microRNA-seq from midbrain (ENCSR152ETW)

summary:
miRNA-seq  on embryonic 11.5 day mouse midbrain

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: ChIP-seq from sigmoid colon (ENCSR150YAU)


title: ChIP-seq from esophagus muscularis mucosa (ENCSR229KWP)


title: ChIP-seq from gastrocnemius medialis (ENCSR148FWR)


title: ChIP-seq from GM12878 (ENCSR228DTL)


title: total RNA-seq from common myeloid progenitor (ENCSR133SAI)

summary:
PSU mouse CMP 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from upper lobe of left lung (ENCSR208WDY)

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


title: ChIP-seq from tibial artery (ENCSR127ZSP)


title: ChIP-seq from fibroblast of arm (ENCSR124MTJ)


title: ChIP-seq from tibial artery (ENCSR233LCT)


title: ChIP-seq from ascending aorta (ENCSR122LOZ)


title: ChIP-seq from transverse colon (ENCSR208QRN)


title: ChIP-seq from GM12878 (ENCSR391IWM)


title: ChIP-seq from ascending aorta (ENCSR202XTW)


title: ChIP-seq from adrenal gland (ENCSR204DMS)


title: ChIP-seq from esophagus squamous epithelium (ENCSR121RSS)


title: ChIP-seq from hepatocyte (ENCSR384LYW)


title: ChIP-seq from adrenal gland (ENCSR094VJC)


title: WGBS from limb (ENCSR377CZO)

summary:
Whole genome bisulfite-seq on embryonic 10.5 day mouse limb

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: total RNA-seq from hematopoietic stem cell (ENCSR085AJX)

summary:
PSU mouse HSC 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from DOHH2 (ENCSR084RDK)


title: ChIP-seq from A549 (ENCSR368ZHR)


title: ChIP-seq from GM12878 (ENCSR120IIK)


title: ChIP-seq from Peyer's patch (ENCSR363CJF)


title: ChIP-seq from thoracic aorta (ENCSR083MAZ)


title: ChIP-seq from stomach (ENCSR133NBJ)


title: ChIP-seq from stomach (ENCSR357ROS)


title: ChIP-seq from spleen (ENCSR105URN)


title: ChIP-seq from body of pancreas (ENCSR348TQM)


title: ChIP-seq from GM12878 (ENCSR330EXS)


title: ChIP-seq from ascending aorta (ENCSR103QHX)


title: ChIP-seq from gastrocnemius medialis (ENCSR201OSX)


title: total RNA-seq from megakaryocyte-erythroid progenitor cell (ENCSR121HYR)

summary:
PSU mouse MEP 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from esophagus muscularis mucosa (ENCSR095YMD)


title: ChIP-seq from esophagus squamous epithelium (ENCSR078ZGC)


title: ChIP-seq from gastrocnemius medialis (ENCSR101NFY)


title: WGBS from hindbrain (ENCSR324XQF)

summary:
Whole genome bisulfite-seq on embryonic 10.5 day mouse hindbrain

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: ChIP-seq from H1-hESC (ENCSR882AWL)


title: ChIP-seq from thoracic aorta (ENCSR318HUC)


title: ChIP-seq from ascending aorta (ENCSR069UMW)


title: ChIP-seq from ACC112 (ENCSR311DQO)


title: ChIP-seq from tibial nerve (ENCSR314SPW)


title: ChIP-seq from neutrophil (ENCSR373WCB)


title: ChIP-seq from esophagus squamous epithelium (ENCSR057YVO)


title: ChIP-seq from esophagus squamous epithelium (ENCSR057BFO)


title: ChIP-seq from B cell (ENCSR051VDI)


title: ChIP-seq from bipolar neuron (ENCSR066BZZ)


title: ChIP-seq from breast epithelium (ENCSR034ZKE)


title: total RNA-seq from megakaryocyte progenitor cell (ENCSR027FCH)

summary:
PSU mouse CFU-Mk 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from adrenal gland (ENCSR043UWF)


title: total RNA-seq from megakaryocyte (ENCSR025JRA)

summary:
PSU mouse MEG 100ng rRNA-depleted RNA-seq via ScriptSeq

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: ChIP-seq from right lobe of liver (ENCSR080QVO)


title: ChIP-seq from OCI-LY7 (ENCSR027HML)


title: ChIP-seq from gastroesophageal sphincter (ENCSR025CGR)


title: ChIP-seq from B cell (ENCSR005WWZ)


title: ChIP-seq from Peyer's patch (ENCSR005UXZ)


title: PLC/PRF/5 cells ChIP on CHIP

city: New Orleans

first: HUA

last: LU

state: LA

address: 1430 Tulane Ave

department: Biochemistry and Molecular Biology

institute: TULANE UNIVERSITY

summary: PLC/PRF/5 cells were harvested for chromatin immunoprecipitation followed by CHIP analysis performed on Aligent platform.

overall_design: PLC/PRF/5 harbors p53 R249S mutation that was utilized for ChIP on CHIP analysis to identify p53-R249S specific DNA sequence.

first: Peng

last: Liao

first: Hua

last: Lu


title: ChIP-seq from heart left ventricle (ENCSR000XAA)

state: CA


title: ChIP-seq from ascending aorta (ENCSR007WYC)


title: Histone acetylation, not stoichiometry, regulates linker histone binding in S. cerevisiae

city: Vancouver

first: Benjamin

last: Martin

state: BC

address: 2350 Health Sciences Mall

department: Biochemistry

institute: UBC

summary: Linker histones play a fundamental role in shaping chromatin structure, but how their interaction with chromatin is controlled not well understood. In this study we used a combination of genetic and genomic approaches to explore the regulation of linker histone binding in the yeast, Saccharomyces cerevisiae. Despite the tight correlation between linker-to-core histone ratio and nucleosome repeat length (NRL) observed in many organisms, we found that increasing Hho1 levels did not change the overall NRL in yeast chromatin. While over-expression of Hho1 did not alter nucleosome spacing, it did result in a severe growth defect, which could be rescued by mutations that increased histone acetylation in the cell. Consistent with this, genome-wide analysis of linker histone occupancy revealed an inverse correlation with histone tail acetylation in both yeast and mouse embryonic stem cells. Collectively these results suggest that histone acetylation negatively regulates linker histone binding in S. cerevisiae and other organisms.

overall_design: Sonication-based ChIP-seq for H3 and Hho1

first: Nicolas

last: Coutin

first: LeAnn

last: Howe


title: Combining theoretical analysis and experimental data generation reveals IRF9 as a crucial factor for accelerating interferon a-induced early antiviral signalling

status: Public on Jul 08 2017

city: Lübeck

first: Hauke

last: Busch

state: Schleswig-Holstein

address: Ratzeburger Allee 160

department: Lübeck Institute of Experimental Dermatology

country: Germany

institute: University of Lübeck

summary: Type I interferons (IFN) are important components of the innate antiviral response. A key signalling pathway activated by IFNa is the Janus kinase ⁄ signal transducer and activator of transcription (JAK⁄STAT) pathway. Major components of the pathway have been identified. However, critical kinetic properties that facilitate accelerated initiation of intracellular antiviral signalling and thereby promote virus elimination remain to be determined. By combining mathematical modelling with experimental analysis, we show that control of dynamic behaviour is not distributed among several pathway components but can be primarily attributed to interferon regulatory factor 9 (IRF9), constituting a positive feedback loop. Model simulations revealed that increasing the initial IRF9 concentration reduced the time to peak, increased the amplitude and enhanced termina- tion of pathway activation. These model predictions were experimentally verified by IRF9 over-expression studies. Furthermore, acceleration of signal processing was linked to more rapid and enhanced expression of IFNa target genes. Thus, the amount of cellular IRF9 is a crucial determinant for amplification of early dynamics of IFNa-mediated signal transduction.

overall_design: Huh7.5 wild-type cells or cells over-expressing IRF9 were starved for 3 h and stimulated using IFNa for 0, 1, 2, 3, 4, 8, 12 or 24 h, or left untreated as a control.

first: Annette

last: Schneider

first: Norbert

last: Gretz

first: Ursula

last: Klingmüller


title: RNAseq analysis of chemotherapy and radiation therapy-naïve breast tumors

city: Portland

first: Lisa

last: Coussens

state: Oregon

address: SW Sam Jackson Park Rd

institute: OHSU

summary: Assessment of chemo- and radiation therapy-naïve biopsy-confirmed invasive human breast tumors by RNAseq.

overall_design: 103 total samples from 63 unique patients. Clinical details were provided only for the 50 samples in current publication. However, all 103 samples were analyzed together.

first: E

middle: S

last: Hwang

first: Hope

last: Rugo


title: Injury-inducible stem cell potential of the intestinal enteroendocrine lineage: single-cell mRNA-seq profiling

city: New York

first: Kelley

last: Yan

department: Medicine

institute: Columbia University

summary: We report the single-cell transcriptomic profiles of Bmi1-GFP+ and Prox1-GFP+ cells in comparison to Lgr5-eGFP+ and Lgr5-eGFP- cells

overall_design: Primary epithelial cells were isolated from Bmi1-GFP, Prox1-GFP or Lgr5-eGFP reporter mice and subjected to single-cell mRNA-seq

first: K

first: C

last: Kuo

first: G

last: Zheng


title: Transcription factor Foxo1 is essential for IL-9 induction in T helper cells

status: Public on Jul 09 2017

first: Manoj

last: Bhasin

address: 330 Brookline Avenue  RN 380E

institute: Beth Israel Deaconess Medical Center

summary: Interleukin 9 (IL-9) producing helper T (Th9) cells play a crucial role in allergic inflammation, autoimmunity, immunity to extracellular pathogens and anti-tumor immune response. In addition to Th9, Th2, Th17 and Foxp3+ Treg cells produce IL-9.  Transcription factor that is critical for IL-9 induction in Th2, Th9 and Th17 cells has not been identified. Here we show that Foxo1, a forkhead family transcription factor, requires for IL-9 induction in Th9 and Th17 cells. We further show that inhibition of AKT enhances IL-9 induction in Th9 cells while it reciprocally regulates IL-9 and IL-17 in Th17 cells via Foxo1. Mechanistically, Foxo1 binds and transactivates IL-9 and IRF4 promoters in Th9, Th17 and iTregs. Furthermore, loss of Foxo1 attenuates IL-9 in mouse and human Th9 and Th17 cells, and ameliorates allergic inflammation in asthma. Our findings thus identify that Foxo1 is essential for IL-9 induction in Th9 and Th17 cells.

overall_design: Transcriptional analysis of Th0 and TGF-beta 1 + IL-4 induced Th9 cells

first: Amit

last: Awasthi


title: Extensive overlap of the STAT6 and RXR cistromes in the active enhancer repertoire of human CD14+ monocyte-derived differentiating macrophages

status: Public on Jul 07 2017

city: Debrecen

first: Gergely

last: Nagy

address: Egyetem ter 1.

department: Department of Biochemistry and Molecular Biology

country: Hungary

institute: University of Debrecen

summary: Macrophages are able to differentiate into classically polarized (M1) or alternatively polarized (M2) states upon encountering pro-inflammatory cytokines such as interferon (IFN) g or anti-inflammatory cytokines such as interleukin (IL) -4/IL-13, respectively. Moreover, macrophages are known to regulate lipid metabolism via multiple members of the nuclear hormone receptor family, including the retinoid X receptors (RXR). It has been also documented that cytokines are able to modulate macrophage responses to lipid signals but the nature of these interactions and the underlying mechanisms of these processes especially at the level of the chromatinized genome are not well understood. Previous work from our laboratory suggested that STAT6 is a facilitator of nuclear receptor mediated transcriptional activity acting at the genome level. This prompted us to investigate genome-wide DNA binding events and the development of cistromes in human CD14+ monocyte-derived macrophages upon exposure to IL-4. We determined the impact of IL-4 on the PU.1, RXR and STAT6 cistromes within the active enhancer regions marked by H3K27-acetylation using chromatin immunoprecipitation followed by deep sequencing and integrated bioinformatics analyses. We found that about 2/3rd of the IL-4 induced STAT6 peaks co-localized with RXR peaks.  These STAT6/RXR co-peaks differed at least in part from the non-overlapping RXR peaks regarding the most enriched de novo transcription factor binding motifs. Interestingly, RXR-binding was not regulated at the STAT6/RXR co-bound enhancers following IL-4 stimulation, but differential enhancer interactions were observed between the IL-4/STAT6 and RXR signaling pathways acting in a gene selective manner. Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.

overall_design: RNA-seq and ChIP-seq-based characterization of the interaction between IL-4/STAT6 and RXR signaling pathways in differentiating human macrophages

first: Laszlo


title: Omics analysis of transgenic chickens compared with non-transgenic chickens [gender]

city: Koganei

first: Taira

last: Miyahara

state: Tokyo

address: 2-24-16 Nakacho

institute: Tokyo university of agriculture and technology

summary:
To investigate food safety made from genetically modified organisms and genome editing organism, we researched the difference of the metabolic substances between wild type and transformant in chicken blood by using transcriptome, proteome and metabolome analysis.
In this study, for the first basic research, we compared the difference of gene expression by sexual difference in leukocyte extracted from 1-2 month old wild type chickens.

overall_design: To compare gene expressions between sexual differece in leukocytes of 1-2 month old chickens. Compare male vs female with each triplet samples in brute force.

first: Hiroyuki

last: Horiuchi

first: Yoshihiro

last: Ozeki

first: Reiko

last: Teshima

first: Daisaku

last: Ohta

first: Ryo

last: Ezaki

first: Takumi

last: Ogawa


title: Gene expression profiling of HepG2 cells treated with extracts of R.coptidis from different growing regions vs. DMSO-treated control group

first: Juan

last: Feng

address: No.30, Shuangqing Road, Haidian District

summary: Rhizoma coptidis (R.coptidis) is a widely cultivated traditional Chinese herb. Although the chemical profiles of R.coptidis have been established previously, the biological profiling of R.coptidis has not been conducted yet. Here, we collected R.coptidis varieties from four different regions as well as its analogue, Rabdosia serra (R.serra) were  and performed genome-wide biological response fingerprinting (BioReF) on HepG2 cells using a gene expression array.

overall_design: Analysis used DMSO-treated RNA as control samples for comparison to the experimental samples treated with R.coptidis from Dayi, Lichuan, Shizhu, Yaan and R.serra from Yunnan. Indirect comparisons were made across multiple arrays with raw data pulled from different channels for data analysis and comparison to the control data.

first: Long

last: Zhao

first: Lan

last: Xie

first: Xun

last: Li


title: Omics analysis of transgenic chickens compared with non-transgenic chickens [genotypes]

summary:
To investigate food safety made from genetically modified organisms and genome editing organism, we researched the difference of the metabolic substances between wild type and transformant in chicken blood by using transcriptome, proteome and metabolome analysis.
In this study, we compared the difference of gene expression between wild type and GFP hetero transformant in leukocyte extracted from 1-2 month old female chickens.

overall_design: To compare gene expressions between transformant and wild type in leukocyte of 1-2 month old chickens. Compare hetero GFP transformants vs wild type with each triplet samples in brute force.


title: Omics analysis of transgenic chickens compared with non-transgenic chickens

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

overall_design: Refer to individual Series


title: ChIP-seq from A549 (ENCSR321BJQ)

first: ENCODE

last: DCC

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


title: Genome-wide profiling of microRNAs revealing novel insights into mutual interactions mechanism between H9N2 avian influenza virus and avian dendritic cells

city: nanjing

first: Jian

last: Lin

state: jiangsu

address: tongwei road N0.1

department: Life Science

institute: nanjing agricultural university

summary:
Background：Dendritic cells (DCs), have the most important antigen presenting ability and played an irreplaceable role in recognizing and clearing virus. Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. MicroRNA, small non-coding RNAs, that can regulate dendritic cells to inhibit the infection and replication of avian influenza virus. Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication.
Results： Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. First, we found that both active and inactive H9N2 AIV enhance the ability of DCs to present antigens and activate T lymphocytes. Next, total microarray analyses suggested that H9N2 AIV stimulation involved in protein localization, nucleotide binding and leukocyte transendothelial migration and MAPK signal pathways.  Moreover, we construct 551 transcription factor (TF)-microRNA-mRNA loops based on the above analyses. Furthermore, we found that HA fragment could not activate DCs, while truncated HA highly increased the immune function of DCs by activating ERK and STAT3 signal pathway. Last, our insight research not only gained that gga-miR1644 might target to MBNL2 to enhanced avian DCs in inhibiting virus replication, but also suggested that gga-miR6675 target to the NLS of PB1 to trigger the silencing of PB1 genes and lead to inhibition of H9N2 avian influenza viral replication. All together, our innovative research will shed new light on the roles of avian microRNA in evoking avian DCs and inhibiting virus replication, which will suggest new strategies to combat avian influenza virus.

overall_design: In the study presented here,cultured avian BMDCs were randomly divided into control group and AIV stimulated group. Each group consisted of three wells of BMDCs from three chickens.

first: Jing

last: Xia

first: Tian

last: Zhang

first: Keyun

first: Qian

last: Yang


title: Transcriptional Consequences of XPA Disruption in Human Cell Lines

city: Houston

first: Yue

last: Lu

state: TX

address: 1881 East Road

department: Epigenetics & Molecular Carcinogenesis

institute: The University of Texas MD Anderson Cancer Center

summary:
Purpose: Nucleotide excision repair (NER) in mammalian cells requires the xeroderma pigmentosum group A protein (XPA) as a core factor. Remarkably, XPA and other NER proteins have been detected by chromatin immunoprecipitation at some active promoters, and NER deficiency is reported to influence the activated transcription of selected genes. However, the global influence of XPA on transcription in human cells has not been determined.
Methods: We analyzed the human transcriptome by RNA sequencing (RNA-Seq). Four genetically matched human cell line pairs deficient or proficient in XPA were analyzed
Results: Of the ~14,000 genes transcribed in each cell line, 325 genes (2%) had a significant XPA-dependent directional change in gene expression that was common to all four pairs (with a false discovery rate of 0.05). These genes were enriched in pathways for the maintenance of mitochondria. Only 27 genes were different by more than 1.5-fold. The most significant hits were AKR1C1 and AKR1C2, involved in steroid hormone metabolism. AKR1C2  protein was lower in all of the immortalized XPA-deficient cells. Retinoic acid treatment led to modest XPA-dependent activation of some genes with transcription-related functions.
Conclusions: We conclude that XPA status does not globally influence human gene transcription. However, XPA significantly influences expression of a small subset of genes important for mitochondrial functions and steroid hormone metabolism. The results may help explain defects in neurological function and sterility in individuals with xeroderma pigmentosum.

overall_design: Eight cell lines were used as follows. For HeLa-derived cells, HeLa S3 (XPA+, two cultures), HeLa KO38 (XPA-), and HeLa KO142 (XPA-), XPA2OS (XPA-). A fibroblast cell pair was XP2OS (XPA-) and an XPA complemented clone XPA/XPA2OS (XPA+). A second fibroblast cell pair was XP12RO (XPA-) and an XPA complemented clone XPA/XPA12RO (XPA+). Each culture was treated with a DMSO control or with retinoic acid in DMSO. Independent cultures and libraries were prepared and analyzed in triplicate, for a total of 48 samples.

first: Mandira

last: Manandhar

first: Megan

middle: G

last: Lowery

first: Karen

last: Boulware

first: Kevin

first: Richard

middle: D

last: Wood


title: Effects of PPARgamma-inactive Delta-2-TGZ on breast cancer cells MCF-7

city: Illkirch

first: Doulaye

last: Dembele

address: 1 rue Laurent Fries

department: Biopuces

institute: IGBMC

summary:
TGZ is an agonist of the nuclear receptor PPARgamma. This synthetic compound displays anticancer effects on breast cancer cells but some of them are PPARgamma independent. Delta-2-TGZ (delta-2-troglotazone) is a PPARgamma inactive TGZ derivative possessing a double bond adjoining the thiazolidinedione ring. This compound still displays anticancer efefcts. It is an interesting tool to study the PPARgamma-independent mechanisms.
We used microarrays to examine the global programme of gene expression in response to Delta-2-TGZ treatment in MCF7 cell line.

overall_design: We compare global gene expression levels between untreated and delta-2-troglitazone treated MCF7 cells at 12H. Each data point was realized in triplicate

first: Xiao

last: Yao

first: Isabelle

last: Grillier-Vuissoz

first: Stéphane

last: Flament