title: Identification of genetic variants affecting vitamin D receptor binding and associations with autoimmune disease

city: Hinxton

first: Giuseppe

last: Gallone

state: Cambridgeshire

address: Wellcome Trust Genome Campus

institute: Wellcome Trust Sanger Institute

summary: Large numbers of statistically significant associations between sentinel SNPs and case-control status have been replicated by genome-wide association studies (GWAS). Nevertheless, currently few underlying molecular mechanisms of complex disease are known. Our approach has been to investigate whether variation in binding of a transcription factor, the vitamin D receptor (VDR) whose activating ligand vitamin D has often been proposed as a modifiable factor in multiple disorders, could explain any of these associations. VDR modifies gene expression by binding DNA as a heterodimer with the Retinoid X receptor (RXR). We identified 43,332 genetic variants significantly associated with altered VDR binding affinity (VDR-BVs) using a high-resolution (ChIP-exo) genome-wide analysis of 27 HapMap lymphoblastoid cell lines (LCLs). The VDR-BVs are over-represented in well conserved consensus RXR:VDR binding motifs. However, most fell outside of recognisable RXR:VDR motifs, implying that genetic variation often affects RXR:VDR binding affinity only indirectly. Finally, we compared 341 VDR-BVs replicating by position in multiple individuals against background sets of variants lying within VDR-binding regions that had been matched in allele frequency and were independent with respect to linkage disequilibrium. In this stringent test, these replicated VDR-BVs were significantly (q < 0.1) and substantially (> 2-fold) enriched in GWAS intervals associated with autoimmune and other diseases, including inflammatory bowel disease, Crohn's disease and rheumatoid arthritis. Replicated VDR-BVs associated with these disorders could represent causal disease risk alleles whose effect is modifiable by vitamin D levels.

overall_design: Genome-wide analysis of the impact of genetic variation on vitamin D receptor binding using ChIP-exo on 27 Hapmap cell lines (3 additional samples failed analytical QC).

first: Wilfried

last: Haerty

first: Giulio

last: Disanto

first: Sreeram

last: Ramagopalan

first: Chris

middle: P

last: Ponting

first: Antonio

middle: J

last: Berlanga-Taylor


title: RNA-seq Analysis of 15q Duplication and AS Deletion DPSC derived neurons.

status: Public on Mar 17 2017

city: Memphis

first: Quynh

last: Tran

state: TN

address: 262 Danny Thomas Place, C4029, Mail Stop 250

department: Pathology

country: USA

institute: St. Jude Children's Research Hospital

type: Expression profiling by high throughput sequencing

summary: A major problem in studying neurogenetic syndromes is obtaining live neurons from people with these disorders.  We have taken a novel approach to studying gene expression in neurons from Angelman or Dup15q syndrome subjects using dental pulp stem cells (DPSC). Shed teeth were collected to generate DPSC lines from 3 AS deletion, 3 15q Duplication and three neurotypical subjects. mRNAseq was performed on DPSC and DPSC derived neurons. We identified 20 genes in AS, 120 genes in 15q duplication and 3 genes in both groups (DPT, MED12L and AKRIC1) that were significantly different from control DPSC-neurons. Copy number correlated to gene expression for most genes across the 15q11.2-q13.1 critical region. Two thirds of the genes differentially regulated in 15q duplication were down-regulated compared to controls including the transcription factors FOXO1 and HAND2, while in AS the genes did not show a clear trend except in the 15q region.  Pathway analysis revealed increased cytokine activity related genes including four genes that increased in 15q duplication samples: CCL7, CCL2, MMP2 and MMP3; while steroid hormone biosynthesis genes were slightly enriched in both 15q duplication and AS neurons.  Overall there were more dramatic changes in gene expression in the 15q) duplication than AS deletion cell lines, perhaps because the mechanism of AS may be through protein targeting by UBE3A.  Nonetheless, the finding of a significant increase in both HERC2 and UBE3A in 15q duplication neurons and significant decrease in these two genes in AS deletion neurons may impact the AS phenotype, at least in deletion cases.

overall_design: RNA-seq Analysis of 3 15q Duplication, 3 Angelman syndrome deletion and 3 neurotypical control DPSC derived neurons (~3 weeks post maturation)

first: Norra

last: Urraca

middle: T

first: Grant

last: Belgard

first: Rawaha

last: Memon

first: Sarita

last: Goorha

first: Colleen

last: Valdez

first: Silvia

last: Sanchez

first: Juanma

last: Ramirez

first: Martin

last: Donaldson

first: Dave

last: Bridges

first: Lawrence

last: Reiter


title: Differentiation-dependent changes in the epigenomic landscape of human myeloid leukemia cells implicate signaling pathways and highlight chromosomal amplifications

status: Public on Mar 16 2017

city: West Lafayette

first: Joseph

last: Irudayaraj

state: IN

address: 225 S. University Street

department: Bindley Bioscience Center

institute: Purdue University

type: Methylation profiling by high throughput sequencing

summary: To assess how DNA modification patterns are influenced by myelopoesis, we have mapped regions enriched for 5mC or 5hmC throughout the genome during promyelocyte to granulocyte differentiation in the HL-60 cell model.

overall_design: MeDIP-seq and hMeDIP-seq were performed on undifferentiated and 1.5% DMSO differentiated HL-60 cells.

first: Ann

last: Kirchmaier

first: Basudev

last: Chowdhury


title: A Mouse Model of Epstein-Barr virus LMP1 and LMP2A Driven Germinal Center B-cell Lymphoproliferative Disease

city: Boston

first: Benjamin

last: Gewurz

state: Massachusetts

address: 181 Longwood Ave

department: Medicine

institute: Brigham and Women's Hospital

summary: Epstein-Barr virus (EBV) is a major cause of immunosuppression-related lymphomas.   EB-driven lymphoproliferative disease complicates up to 20% of transplants, and EBV is a major cause of human immunodeficieciency virus associated lymphomas.  Despite successful antiretroviral therapy, the incidence of EBV-associated Hodgkin lymphoma continues to increase in HIV+ individuals.  To gain insights into  EBV membrane oncoprotein effects on B-cell growth, survival and pathogenesis in vivo, we generated transgenic mouse models, in which knock-in mice transgenically express control GFP or EBV latent membrane proteins (LMP) 1 and 2A under the control of the AICDA promoter. Upon T and NK-cell depletion by antibody cocktail, LMP1 and 2A co-expression drove explosive growth of plasmablastic lymphoma-like cells, which proliferated in  the spleen, caused severe end-organ damage and death.  RNAseq profiling identified genome-wide LMP1 and 2A effects on B-cell gene expression, including dramatic effects on chemokine and cytokine production.  While cells exhibited plasmablast features, LMP1 and 2A co-expression also induced mixed hematopoietic lineage markers, a well described but incompletely understood feature of Hodgkin lymphoma.  Collectively, our results identify synergistic effects of EBV membrane oncoprotein expression, and highlight their role in lymphoproliferative diseases of immunocompromised hosts.

overall_design: B220 positive B splenocytes were isolated from GFP and LMP1/2a transgenic mice, which are T/NK cell depleted by antibody cocktails, and subjected to RNA-seq analysis to compare the transcriptomic changes in LMP1/2a transgenic mice compared to GFP transgenic mice. Two mice from each transgenic group were used.

first: Yijie

last: Ma

first: Takeharu

last: Minamatani

first: Elliott

last: Kieff

first: Hitoshi

last: Kikutani

first: Hufeng

last: Zhou

first: Bo

last: Zhao

middle: E

first: Yasui

last: Teruhito


title: Expression data from different B cell subsets in peripheral blood

status: Public on Mar 15 2017

city: shanghai

first: zhicui

last: liu

address: No. 197 Rui Jin Er Road

department: Department of Dermatology

country: China

institute: Ruijin Hospital, Shanghai Jiao Tong University School of Medicine

summary:
We found the presence of CD19hi and CD19lo B cell populations in the periphery of SLE and pemphigus patients，as well as human secondary lymphoid organs. In addition, CD19hi B cells and CD19lo B cells can be induced in vitro with the help of activated CD4+T cells.
We used microarrays to detail the global programme of gene expression of CD19hi and CD19lo B cells and identified distinct classes of up-regulated genes between them.

overall_design: we established an in vitro CD4+ T and B cells co-culture system to mimic the bilateral T-B cell interaction. Purified human CD4+ T cells were stimulated in vitro with anti-CD3/CD28 Dynabeads for 24 hrs and co-cultured with autologous B cells. After 3 days, CD19hi and CD19lo B cells were purified.

first: Zhicui

last: Liu

first: Ying

last: Wang


title: Different Temporal Effects of Ebola Virus VP35 and VP24 Proteins on Global Gene Expression in Human Dendritic Cells

city: Galveston

first: Alexander

last: Bukreyev

state: Texas

address: 301 University Boulevard

institute: University of Texas Medical Branch at Galveston

summary:
Purpose: The goal of this study is to investigate the effect on gene exression of mutations in Ebola virus inate immune response antagonizing  domains (IRAD).
Methods: RNA-Seq transcriptome analysis of dendritic cells 8 and 24 hours post infection

overall_design: Human dendritic cells are infected with wild-type Ebola viruses and viruses  harboring mutations in IRADs. Gene expression levels at 8 and 24 hours post infections were compared to mock infected cells.

first: Philipp

middle: A

last: Ilinykh

first: Ndongala

middle: M

last: Lubaki

first: Steven

middle: G

last: Widen

first: Lynnsey

last: Renn

first: Terence

middle: C

last: Theisen

first: Ronald

middle: L

last: Rabin

first: Thomas

last: Wood


title: The evolution of CHROMOMETHYLTRANSFERASES and gene body DNA methylation in plants

city: Athens

first: Robert

last: Schmitz

state: GA

address: B416 Davison Life Sciences

department: Genetics

institute: University of Georgia

summary: The evolution of gene body methylation (gbM) and the underlying mechanism is poorly understood. By pairing the largest collection of CHROMOMETHYLTRANSFERASE (CMT) sequences (773) and methylomes (72) across land plants and green algae we provide novel insights into the evolution of gbM and its underlying mechanism. The angiosperm- and eudicot-specific whole genome duplication events gave rise to what are now referred to as CMT1, 2 and 3 lineages. CMTε, which includes the eudicot-specific CMT1 and 3, and orthologous angiosperm clades, is essential for the perpetuation of gbM in angiosperms, implying that gbM evolved at least 236 MYA. Independent losses of CMT1, 2 and 3 in eudicots, and CMT2 and CMTmonocot+magnoliid in monocots suggests overlapping or fluid functional evolution. The resulting gene family phylogeny of CMT transcripts from the most diverse sampling of plants to date redefines our understanding of CMT evolution and its evolutionary consequences on DNA methylation.

sample_organism:
Psilotum
Equisetum
Gnetum gnemon
Urtica dioica
Synsepalum dulcificum
Lupinus angustifolius
Cyathea
Amentotaxus argotaenia
Araucaria
Aloe vera
Juniperus virginiana
Pereskia grandiflora
Amentotaxus formosana
Cephalotaxus harringtonia
Hypericum perforatum
Cyperus papyrus
Kalanchoe tomentosa
Selaginella kraussiana
Diplazium proliferum
Chamaecyparis hodginsii
Yucca brevifolia
Papuacedrus papuana
Dacrydium balansae
Manoao colensoi
Aristolochia grandiflora
Torreya taxifolia
Cissus quadrangularis
Encephalartos horridus
Microsorum punctatum
Dacrycarpus compactus
Celtis occidentalis
Impatiens niamniamensis
Thuja sutchuenensis
Nepenthes bicalcarata

overall_design:
MethylC-Seq collected from leaves of a diverse collection of land plants.

The assembled transcriptomes used in this study were not publicly available at the time of submission since they are part of the on-going 1KP initiative (www.onekp.com). They will be made available upon release of the 1KP capstone paper.


title: Type 2 Innate Lymphoid Cells Treat and Prevent GI Tract GvHD Through Enhanced Accumulation of Myeloid Derived Suppressor Cells

city: Chapel Hill

first: Jonathan

middle: S

last: Serody

state: NC

address: 125 Mason Farm Rd.

department: Lineberger Comprehensive Cancer Center

institute: University of North Carolina at Chapel Hill

summary: Transcriptome analysis of in vitro expanded murine type 2 innate lymphoid cells

overall_design: Examination of CD90+ and CD90- populations of cultured ILC2s

first: Danny

last: Bruce

first: Jon


title: Myocardial infarction (MI) primes autoreactive T cells through activation of dendritic cells

city: Zwijnaarde

first: Liesbet

last: Martens

address: Technologiepark 927

department: VIB Inflammation Research Center

country: Belgium

institute: VIB-University of Ghent

summary: DC subsets of the murine healthy heart consisted of IRF8-dependent conventional (c)DC1,  IRF4-dependent cDC2 and monocyte-derived DCs. In steady state, cardiac self-antigen α-myosin was presented in heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4+ TCR-M T cells, and their differentiation into Tregs. Following MI, all DC subsets infiltrated the heart, while only cDCs migrated to the mLN. Here, cDC2s induced TCR-M proliferation and differentiation into IL-17/IFNγ producing effector cells. Thus, cardiac specific autoreactive T cells get activated by mature DCs following myocardial infarction.

overall_design: cDC1s, cDC2s, MFs and moDCs were isolated and sorted from steady state or infarcted hearts in four independent replicates. 31 samples (RNA-Seq) in total. RNA was isolated, amplified by SMARTer amplification, converted to cDNA and then sequenced using Illumina NextSeq.

first: Katrien

last: Van der Borght

first: Charlotte

last: Scott

first: Veronica

last: Nindl

first: Ann

last: Bouché

first: Dorine

last: Sichien

first: Justine

last: Van Moorleghem

first: Manon

last: Vanheerswynghels

first: Sofie

last: De Prijck

first: Burkhard

last: Ludewig

first: Thierry

last: Gillebert

first: Martin

last: Guilliams

first: Peter

last: Carmeliet

first: Bart

last: N Lambrecht


title: Lymphocyte Activation Gene-3 limits regulatory T cell proliferation and function in autoimmune diabetes

city: Pittsburgh

first: Maria

last: Chikina

state: PA

address: 3501 5th ave

institute: University of Pittsburgh

summary: Inhibitory receptors (Irs) are pivotal in controlling T cell homeostasis because of their intrinsic regulation of conventional T (Tconv) cell proliferation, viability and function.  However, the role of Irs on regulatory T (Treg) cells remains obscure, as they could be required for suppressive activity and/or limit Treg cell function.  We evaluated the role of Lymphocyte Activation Gene-3 (LAG3, CD223) on Treg cells by generating mice in which LAG3 is absent on the cell surface of Treg cells in a murine model of Type 1 Diabetes.  Surprisingly, mice that lacked LAG3 expression on Treg cells exhibited reduced autoimmune diabetes, consistent with enhanced Treg cell proliferation and function.  Whereas the transcriptional landscape of peripheral wild-type (WT) and Lag3-deficient Treg cells was largely comparable, substantial differences between intra-islet Treg cells were evident and involved a subset of genes and pathways that promote Treg cell maintenance and function.  Consistent with these observations, Lag3-deficient Treg cells out-competed WT Treg cells in the islets but not in the periphery in co-transfer experiments due to enhanced IL2-Stat5 signaling and Eos expression.  Our study suggests that LAG3 intrinsically limits Treg cell proliferation and function at inflamed pancreas, promotes autoimmunity in a chronic autoimmune-prone environment and may contribute to Treg cell insufficiency in autoimmune disease

overall_design: Wt and Lag3 deficient Tregs from islets and non-draining lymph nodes NDLN in an autoimmune diabetes model.


title: Activation of the LMO2 oncogene through a somatically acquired neomorphic promoter in T-Cell Acute Lymphoblastic Leukemia

city: Cambridge

first: Richard

last: Young

state: MA

address: 9 Cambridge Center

institute: Whitehead Institute for Biomedical Research

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Somatic mutations within non-coding genomic regions that aberrantly activate oncogenes have remained poorly characterized. Here we describe recurrent activating intronic mutations of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukaemia (T-ALL). Heterozygous mutations were identified in PF-382 and DU.528 T-ALL cell lines, in addition to 3.7% (6/160) of paediatric and 5.5% (9/163) of adult T-ALL patient samples. The majority of indels harbor de novo MYB, ETS1 or RUNX1 consensus binding sites. Analysis of 5’-capped RNA transcripts in mutant cell lines identified the usage of an intermediate promoter site, with consequential monoallelic LMO2 overexpression. CRISPR/Cas9-mediated disruption of the mutant allele in PF-382 cells markedly downregulated LMO2 expression, establishing clear causality between the mutation and oncogene dysregulation. Furthermore, the spectrum of CRISPR/Cas9-derived mutations provide important insights into the interconnected contributions of functional transcription factor binding. Finally, these mutations occur in the same intron as retroviral integration sites in gene therapy induced T-ALL, suggesting that such events occur at preferential sites in the non-coding genome.

overall_design: ChIP-Seq for MYB in T cell leukemia (T-ALL) cell lines

first: Sunniyat

last: Rahman

first: Michael

last: Magnussen

first: Theresa

last: León

first: Nadine

last: Farah

first: Zhaodong

last: Li

first: Brian

last: Abraham

first: Krisztina

middle: Z

last: Alapi

first: Rachel

last: Mitchell

first: Tom

last: Naughton

first: Adele

middle: K

last: Fielding

first: Arnold

last: Pizzey

first: Sophia

last: Bustraan

first: Christopher

last: Allen

first: Teodora

last: Popa

first: Karin

last: Pike-Overzet

first: Laura

last: Garcia-Perez

first: Rosemary

last: Gale

first: David

last: Linch

first: Frank

last: Staal

first: A

last: Look

first: Marc

middle: R

last: Mansour


title: CDK12 regulates alternative last exon mRNA splicing and promotes invasion of a breast cancer cell line

city: Vancouver

first: Gregg

last: Morin

state: BC

address: 675 W 10th Ave

country: Canada

institute: University of British Columbia

summary: We performed mRNA sequencing on 184-hTert and SK-BR-3 and MDA-MB-231 cell lines treated with siRNA directed to CDK12 (Cyclin dependent kinase 12) or a scrambled siRNA control. For each cell line, we generated 6 RNA-seq libraries (3 treatment replicates and 3 control replicates) to study the differential expression and the differential splicing patterns regulated by CDK12.

overall_design: Examination of differential mRNA abundance and splicing patterns between the CDK12 siRNA treated samples and control samples for SK-BR-3 and 184-hTert and MDA-MB-231 cell lines.

middle: B


title: Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (ChIP-seq)

city: Madrid

first: Carlos

last: Martinez

state: Madrid

address: C/Darwin 3

department: Inmunology and Oncology

country: Spain

institute: Centro Nacional de Biotecnologia

summary: Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.

overall_design: Study of HADido3 DNA binding by chipseq technology in mouse embryonic stem cells Dido3deltaCT reconstituted with HADido3

first: Agnes

last: Futterer

first: Jesus

last: De-Celis


title: Modeling bias and variation in the stochastic processes of small RNA sequencing

city: Albuquerque

first: Christos

last: Argyropoulos

state: New Mexico

address: 901 University Blvd SE, Suite 150

department: Department of Internal Medicine

institute: University of New Mexico School of Medicine

type: Non-coding RNA profiling by high throughput sequencing

summary: The use of RNA-seq as the preferred method for the discovery and validation of small RNA biomarkers is hindered by high variability and biased sequence counts. In this paper we develop a statistical model for sequence counts  that accounts for ligase bias and stochastic variation  in library amplification steps and sequencing depth variation.  Our analytical contributions are the description of the Linear Quadratic (LQ) relation between the mean and variance of the sequence counts in an RNA-seq experiment and the derivation of the Poisson truncated mixture as the underlying probability distribution for RNA-seq data.  Using a large number of sequencing datasets, we demonstrate here how one can use this modeling framework to calculate empirical correction factors for ligase bias, while accounting for random variation in sequence counts. Bias correction may remove the majority of bias in the absence of differential expression and more than 40% of the bias in the presence of variable expression of miRNAs. Empirical bias correction factors appear to be nearly constant over at least one and up to four orders of magnitude of total RNA input and independent of sample composition.

overall_design: Small RNA libraries were prepared from equimolar or ratiometric mixes of two synthetic RNA pools at the indicated input concentrations using various protocol variations.

first: Alton

last: Etheridge

first: Nikita

last: Sakhanenko

last: Galas


title: Genetic influences on gene expression in Arabidopsis thaliana

city: Salt Lake City

first: Richard

last: Clark

state: Utah

department: Department of Biology

institute: University of Utah

summary: In this study, we describe the impact of genetic variation on transcript abundance in an F2 population of Arabidopsis thaliana. The RNA-seq resource generated by this study is suitable for expression quantitative trait locus (eQTL) mapping. From the aligned RNA-seq reads, and available genomic data for each of the parents of the cross, we imputed the genomes of each F2 individual (to allow genetic mapping of RNA abundance traits; briefly, genetic differences in aligned RNA-seq reads were used to impute each F2 genome). Our results show that heritable differences on gene expression can be detected using F2 populations (that is, single F2 plants), and shed light on the control of expression differences among strains of this reference plant.

overall_design: 183 samples consisting of single F2 plants of a cross between Arabidopsis thaliana accessions 8230 and 6195 were generated. For each sample, RNA was collected from the aerial shoot at the 9th true leaf stage, and Illumina mRNA-seq libraries were constructed. Using these libraries, 50 bp single end RNA-seq Illumina reads were generated for each sample, and used to quantify gene expresison in each individual. The resulting expression phenotypes are suitable for genetic mapping of the control of gene expression differences in the species.

first: Edward

last: Osborne

last: Parrott

first: Robert

last: Greenhalgh


title: ChIP-seq analysis of coronavirus-infected human cells

city: Giessen

first: Marek

last: Bartkuhn

state: Hessen

address: Aulweg 132

department: Biomedical Informatics and Systems Medicine

country: Germany

institute: Justus-Liebig-University Giessen

summary: The aim of the experiment is to identify chromatin and transcription factor binding dynamics in host gene expression upon infection of human Huh7 hepatoma carcinoma cells  with human coronavirus HCoV-229E as compared to uninfected cells and in comparison to cells stimulated by  IL-1alpha (10ng/ml) for 1h. All experiments have been performed at 33°C which is required for sufficient viral entry/replication.

overall_design: ChIP-seq

first: Michael

last: Kracht


title: Spemann organizer transcriptome induction by early β-Catenin, Wnt, Nodal and Siamois signals in Xenopus laevis

city: Los Angeles

last: De Robertis

state: CA

address: 615 Charles E. Young Drive South

department: Biological chemistry

institute: HHMI/UCLA

summary: During Xenopus gastrulation, dorsal stabilization of β-Catenin at the earliest stage and subsequent target genes expression are critical for dorsal-ventral axis determination. However, many β-Catenin targets that mediate this process are still unkown.  Here through RNA-seq analysis of β-Catenin knockdown embryos and self-regulating dorsal and ventral half embryos at early gastrula, we define an early β-Catenin gene signature that is downregulated by β-Catenin MO and enriched in dorsal gastrula tissues. This gene signature includes classic Spemann organizer genes, as well as other novel genes. Further analyses revealed that the early β-Catenin gene signature is positively correlated with LiCl treated, Wnt8 and Siamois mRNA-induced genes, consistent with their early role in dorsal-ventral axis formation. Our results also show that St 10.5 is the appropriate stage to uncover β-Catenin target genes that regulate dorsal-ventral patterning than St 9. Meanwhile, the multi-growth factor antagonist Cerberus inhibits part of the early β-Catenin gene signature and also controls the expression of a unique set of genes. Our findings provide new insight into the pivotal role of β-catenin in dorsal-ventral axis determination and can serve a fruitful resource for this field.

overall_design: A genome-wide study of the effects of depleting the early dorsal b-Catenin signal which is responsible for the induction of the body axis.

first: Yi

last: Ding

first: Diego

last: Ploper

first: Eric

last: Sosa

first: Gabriele

last: Colozza

first: Yuki

last: Moriyama

first: Maria

middle: D

last: Benitez

first: Kelvin

last: Zhang

first: Daria

last: Merkurjev


title: Modeling of WGBS data from normal and cancer tissues, young and old cells, passaged fibroblasts and stem cells

city: Baltimore

first: Andrew

last: Feinberg

state: MD

address: 855 N. Wolfe St., Rangos 570

department: Center for Epigenetics

institute: Johns Hopkins

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

overall_design: Refer to individual Series


title: Modeling of WGBS data from normal and cancer tissues, young and old cells, passaged fibroblasts and stem cells IV

summary: We develop a novel analysis method for WGBS data that allows us to measure diverse aspects of methylation information genome-wide.

overall_design: modeling of WGBS data for a diverse set of samples. BAM files for data generated in this study can be found in SRP072078 (PRJNA315696), SRP072071 (PRJNA315694), SRP072075 (PRJNA315695) and SRP072141 (PRJNA315903). The rest of the data was downloaded from other studies: GSE46644, GSE49629, GSE52972, GSE31742. For the latter, N/As have been used in BioSample and instrument model fields.

first: Garrett

last: Jenkinson

first: Elisabet

last: Pujadas

first: John

last: Goutsias


title: Modeling of WGBS data from normal and cancer tissues, young and old cells, passaged fibroblasts and stem cells III


title: Modeling of WGBS data from normal and cancer tissues, young and old cells, passaged fibroblasts and stem cells I


title: DHX9 suppresses spurious RNA processing defects originating from the Alu invasion of the human genome

status: Public on Mar 28 2017

city: Freiburg

first: Asifa

last: Akhtar

address: Stuebeweg 51

department: Chromatin Regulation

institute: Max Planck Institute of Immunobiology and Epigenetics

summary:
Transposable elements are viewed as ‘selfish genetic elements’, yet they contribute to gene regulation and genome evolution in diverse ways. More than half of the human genome consists of transposable elements. With over 1 million insertions, Alu elements belong to the short interspersed nuclear element (SINE) family of repetitive elements, and with over 1 million insertions they make up more than 10% of the human genome. Despite their abundance and the potential evolutionary advantages they confer, Alu elements can be mutagenic to the host as they can act as splice acceptors, inhibit translation of mRNAs and cause genomic instability. Alu elements are the main targets of the RNA-editing enzyme ADAR and the formation of Alu exons is suppressed by the nuclear ribonucleoprotein HNRNPC, but the broad effect of massive secondary structures formed by inverted-repeat Alu elements on RNA processing in the nucleus remains unknown. Here we show that DHX9, an abundant nuclear RNA helicase, binds specifically to inverted-repeat Alu elements that are transcribed as parts of genes. Loss of DHX9 leads to an increase in the number and amount of circular RNAs, translational repression of reporters containing inverted-repeat Alu elements, and transcriptional rewiring (the creation of mostly nonsensical novel connections between exons) of susceptible loci. Biochemical purifications of DHX9 identify the interferon-inducible isoform of ADAR (p150), but not the constitutively expressed ADAR isoform (p110), as an RNA-independent interaction partner. Co-depletion of ADAR and DHX9 augments the double-stranded RNA accumulation defects, leading to higher levels of circular RNA production, revealing a functional link between these two enzymes. Our work uncovers an evolutionarily conserved function of DHX9. We propose that it acts as a nuclear RNA resolvase that neutralizes the immediate threat posed by transposon insertions and allows these elements to evolve as tools for the post-transcriptional regulation of gene expression.

This SuperSeries is composed of the SubSeries listed below.

sample_organism:
Drosophila melanogaster
Homo sapiens
Mus musculus


title: Modeling of WGBS data from normal and cancer tissues, young and old cells, passaged fibroblasts and stem cells II


title: Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (RNA-seq shRNA)

city: Montreal

first: Magalie

last: Celton

state: Quebec

address: 2950, Chemin de Polytechnique

institute: IRIC

summary: Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donor’s genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs .

overall_design: Transcriptome of MLL-AF9 AML pediatric patients


title: Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (RNA-seq B-ALL)

overall_design: study of transcriptome during the development of MLL-AF9 B-ALL


title: Expression data that were specifically regulated by lncRNA-LFAR1 in mouse primary HSCs

status: Public on Mar 14 2017

city: Tianjin

first: Kun

address: Qixiangtai Road NO.22

department: Department of Histology and Embryology

institute: Tianjin medical university

summary: Long noncoding RNAs (lncRNAs) play important roles in various biological processes; however, few have been identified that regulate hepatic stellate cells (HSCs) activation and the progression of liver fibrosis. Through a detailed analysis of the expression of lncRNAs in various tissues, we discovered the existence of a liver enriched lncRNA-LFAR1 (lncRNA-Liver Fibrosis Associated RNA1). To identify the roles of  lncRNA-LFAR1 in liver fiboris, we systematically analyzed the regulation of mRNAs in primary HSCs infected with two separated lnc-LFAR1-shRNAs by RNA-seq, which revealed a panel of mRNAs that were specifically regulated by lncRNA-LFAR1 in mouse primary HSCs.

overall_design: To identify the roles of  lncRNA-LFAR1 in liver fibrosis, we systematically analyzed the regulation of mRNAs in primary HSCs infected with shRNA-control (n=2), lncRNA-shRNA1 (n=2) and lncRNA-shRNA3 (n=2) by RNA-seq.

first: Wei

last: Hong

first: Tao

last: Han


title: Transcriptomic Insights into Genetic Diversity of  Protein-Coding Genes in X. laevis

city: Boston

first: Leonid

last: Peshkin

address: 200 Longwood Ave

department: Systems Biology

institute: Harvard Medical School

summary: We characterize the genetic diversity of Xenopus laevis strains using allele-specific RNA-seq data analysis and provide a catalogue of coding variation which can be used for improving the genomic sequence, as well as for better sequence alignment, probe design, and proteomic analysis.  In addition, we paint a broad picture of the genetic landscape of the species by functionally annotating different classes of mutations with a well-established prediction tool (PolyPhen-2). Further, we specifically compare the variation in the progeny of a cross from the inbred genomic (J)-strain, a cross from the popular occasionally outbred albino (B)-strain, and two hybrid crosses. We use the comparison to identify a subset of mutations specific to the B-strain, which allows us to investigate the specific selection pressures affecting duplicated genes in this pseudo-tetraploid. We find the ratio of non-synonymous to synonymous mutations is lower in duplicated genes, which therefore appear to be under greater purifying selection. Surprisingly, we also find that function-altering ("damaging") mutations constitute a greater fraction of the non-synonymous variants in this group, which may suggest a role for subfunctionalization in coding variation affecting duplicated genes.

overall_design: We successfully performed natural mating of the two Xenopus strains: two reciprocal (BxJ, JxB) and two straight self (JxJ, BxB) crosses. We then collected tadpoles at a single developmental timepoint (stage NF 42), pooled ten tadpoles per cross, and isolated RNA from each pool. After RiboZero treatment, we constructed Illumina libraries, and performed RNAseq on HiSeq 2000, resulting in approximately 30 to 47 million reads per library with paired-end 100 base reads.

first: Virginia

last: Savova

first: Esther

last: Pearl

first: Elvan

last: Boke

first: Marko

last: Horb

first: Sasha

last: Gimelbrant


title: m6A-seq in glioblastoma stem cells

city: Chicago

first: zhike

last: lu

state: IL

address: 5801 South Ellis Avenue

department: department of chemistry

institute: University of Chicago

summary: m6A RNA methylation plays an important role in regulating the self-renewal and tumorigenesis of glioblastoma stem cells. We performed m6A-seq analysis in glioblastoma stem cells with m6A levels modulated by knocking down METTL3 or METTL14 and identified m6A regulated genes in glioblastoma stem cells.

overall_design: Glioblastoma stem cells were treated with lentivurs expressing constrol shRNA or target (METTL3 or METTL14) shRNA to knockdown the expression of METTL3 or METTL14. RNAs were extracted and m6A-seq analysis was performed using m6A specific antibody immunoprecipitation followed by RNA-seq.

first: Qi

last: Cui

first: Hailing

last: Shi

first: Zhike

last: Lu

first: Chuan

last: He

first: Yanhong


title: Genome-wide analysis of RNA polymerase II termination at protein-coding genes

city: Göttingen

first: Carlo

last: Bäjen

address: Am Fassberg 11

department: Molecular Biology

institute: Max Planck Institute for Biophysical Chemistry

summary: At the end of protein-coding genes, RNA polymerase (Pol) II undergoes a concerted transition that involves 3’-processing of the pre-mRNA and transcription termination. Here we conduct a genome-wide analysis of this 3’-transition in yeast. We find that the 3’-transition globally requires the Pol II elongation factor Spt5 and factors involved in the recognition of the poly-adenylation (pA) site and in endonucleolytic RNA cleavage. Pol II release from DNA occurs in a narrow termination window downstream of the pA site and generally requires the ‘torpedo’ exonuclease Rat1 (human XRN2). The Rat1-interacting factor Rai1 contributes to RNA degradation downstream of the pA site. Defects in the 3’-transition result in transcription interference at downstream genes, which is attenuated by a back-up termination mechanism.

overall_design: In this study, we depleted the main termination factors of the Rat1–Rai1–Rtt103 exonuclease complex as well as the CFIA factor Pcf11 from the nucleus and monitored changes in RNA synthesis using the anchor-away (aa) technique and 4-thiouracil (4tU) sequencing, respectively. We applied ChIP-seq and PAR-CLIP to obtain high-confidence genome and transcriptome maps, respectively. Additionally, we assayed the effects after nuclear depletion of Spt4/5 as well as for Spt5 mutants lacking both the C-terminal repeat (CTR) and fifth KOW domain. We show that Rat1 is needed for termination of the transcribing RNA Polymerase (Pol) II by comparing the ChIP-seq profiles of Rpb1 before (Rat1no) and after nuclear depletion (Rat1aa) of the exonculease Rat1.

last: Baejen

first: Jessica

last: Andreani

first: Phillipp

last: Torkler

first: Sofia

last: Battaglia

first: Bjoern

last: Schwalb

first: Michael

last: Lidschreiber

first: Kerstin

last: Maier

first: Andrea

last: Boltendahl

first: Petra

last: Rus

first: Stephanie

last: Esslinger

first: Johannes

last: Soeding

first: Patrick

last: Cramer


title: Transcriptome analysis of thymic APC subsets, mTECs and thymic DCs in comparison to splenic DCs

city: Braunschweig

last: Beckstette

state: Lower Saxony

address: Inhoffenstrase 7

department: Molecular Infection Biology

institute: Helmholtz Centre for Infection Research

summary: Thymic antigen-presenting cells (APCs), including thymic dendritic cells (t-DCs) and medullary thymic epithelial cells (mTECs) have been described to play a critical role in thymic Treg generation. Our findings could show that both these thymic APCs can induce a more pronounced demethylation of Foxp3 and other Treg-specific epigenetic signature genes in developing Tregs when compared to splenic DCs. In order to elucidate the unique properties of thymic APCs, gene expression profiling was performed in comparison to splenic DCs. Transcriptome analysis of thymic APCs revealed differential expression of costimulatory molecules that could be involved in stable Treg generation. Importantly, both mTEC- and t-DC- induced alloantigen-specific Tregs displayed significantly higher efficacy in prolonging skin allograft acceptance when compared to alloantigen-specific Tregs generated by splenic DCs.

overall_design: Thymic APCs, including mTECs and t-DCs and splenic DCs were isolated ex vivo from thymus as CD45-EpCAM+Ly51- (mTECs) and CD45+EpCAM-CD11chiLin- (t-DCs) and from spleen as CD11chiLin- (splenic DCs) (Lin is defined as CD90, CD49b, F4/80 and CD19), respectively.

first: Garima

last: Garg

first: Jochen

last: Huehn


title: Hyper- and hypo- nutrition studies of the hepatic transcriptome and epigenome suggest that PPARα regulates anaerobic glycolysis

first: Shmulik

last: Motola

address: 77 Mass Ave.

institute: MIT

summary: Diet plays a crucial role in shaping human health and disease. Diets promoting obesity and insulin resistance can lead to severe metabolic diseases, while calorie-restricted (CR) diets can improve health and extend lifespan. In this work, we fed mice either a chow diet (CD), a 16 week high-fat diet (HFD), or a CR diet to compare and contrast the effects of these diets on mouse liver biology. We collected transcriptomic and epigenomic datasets from these mice using RNA-Seq and DNase-Seq. We found that both CR and HFD induce extensive transcriptional changes, in some cases altering the same genes in the same direction. We used our epigenomic data to infer transcriptional regulatory proteins bound near these genes that likely influence their expression levels. In particular, we found evidence for critical roles played by PPARα and RXRα. We used ChIP-Seq to profile the binding locations for these factors in HFD and CR livers. We found extensive binding of PPARα near genes involved in glycolysis/gluconeogenesis and uncovered a role for this factor in regulating anaerobic glycolysis. Overall, we generated extensive transcriptional and epigenomic datasets from livers of mice fed these diets and uncovered new functions and gene targets for PPARα.

overall_design: RNA-seq analysis of mouse liver maintained on normal chow diet, high-fat diet or calorie restricted diet, ChIP-seq on RXRα and PPARα from mouse liver maintained on calorie restricted or high-fat diets, DNase-seq on mouse liver maintained on normal chow, high-fat, or calorie restricted diets.

first: Anthony

last: Slotis

first: Santiago

last: Vernia

first: Christopher

middle: W

last: Ng

first: Norman

last: Kennedy

first: Simona

last: Dalin

first: Bryan

last: Matthews

first: Roger

last: Davis

first: Ernest

last: Fraenkel


title: Expression analysis of Mebendazole treated THP-1 cells in three paired samples

city: London

first: Jasper

middle: de

last: de Boer

state: Greater London

address: 30 Guilford Street

department: Developmental Biology and Cancer Programme

country: United Kingdom

institute: UCL Great Ormond Street Institute of Child Health

summary: Mebendazole treatment of MLL rearanged cell line THP-1

overall_design: 3 pairs of THP-1 cells were either treated with Mebendazole or vehicle control

first: Owen

last: Williams


title: Mex3a Marks a Slowly Dividing Subpopulation of Lgr5+ Intestinal Stem Cells

city: Barcelona

first: Gustavo

last: Rodriguez-Esteban

state: Catalonia

address: C. Baldiri Reixac, 4; Barcelona Science Park

department: Development

institute: Centro Nacional de Análisis Genómico

summary: The intestinal epithelium is continuously regenerated by highly proliferative Lgr5+ intestinal stem cells (ISCs). The existence of a population of quiescent ISCs has been suggested yet its identity and features remain controversial. Here we describe that the expression of the RNA-binding protein Mex3a labels a subpopulation of Lgr5+ cells that divide less frequently and contribute to regenerate all intestinal lineages with slow kinetics. Single cell transcriptomic analysis revealed two classes of Lgr5-high cells, one of them defined by the Mex3a-expression program and by low levels of proliferation genes. Lineage tracing experiments show that large fraction of Mex3a+ cell population is continuously recalled into the rapidly dividing self-renewing ISC pool in homeostatic conditions. Chemotherapy and radiation target preferentially rapidly dividing Lgr5+ cells but spare the Mex3a-high/Lgr5+ population, which helps sustain the renewal of the intestinal epithelium during treatment.

overall_design: Single cell transcriptomes of 400 Lgr5+ murine small intestinal epithelial stem cells.

last: Rodríguez-Esteban

first: Holger

last: Heyn


title: Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition

city: Goettingen

first: Steven

middle: A.

last: Johnsen

address: Robert-Koch-Straße 40

department: Department of General, Visceral and Pediatric Surgery

institute: University Medical Center Goettingen


title: Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines


title: Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition [RNA-Seq]

summary: We examined transcriptome-wide effects of pertrurbation in KLF10 function (siKLF10) on TGFβ-regulated genes and EMT in two different cells lines: A549 and Panc1.

overall_design: We performed  mRNA sequencing from A549 and Panc1 cells following following  TGFβ treatment and KLF10 knockdown. The mRNA-Seq includes following conditions: siControl, siKLF10, TGFβ, siKLF10+TGFβ (A549 and Panc1 cells). mRNA-sequencing was performed in duplicates for A549 and triplicates for Panc1 cells.

first: Vivek

last: Mishra


title: Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFβ-Induced Epithelial-to-Mesenchymal Transition [ChIP-Seq]

summary: We have elucidated the potential role of KLF10 in inhbiting TGFβ-induced EMT. Further, we show that KLF10 directly binds to SNAI2 and recruit HDAC1 to inhbit the expression of SNAI2.

overall_design: We performed ChIP-sequencing from A549 cells and generated ChIP-Seq data for KLF10. Furthermore, we also geneerated ChIP-Seq data for H3K27ac and H3K9ac (+/- siKLF10 and +/- TGFβ). Consistently, Input DNA was also included.


title: Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines [ChIP-seq]

summary: We have utilized a  HDAC class-I specific inhbitor 4SC-202 and revealed a potential involvement of BRD4 and MYC in regulating the expression of induced genes in response to 4SC-202 treatment.

overall_design: We performed ChIP-sequencing from L3.6 cells (treated with DMSO or 4SC-202 for 24 hours) .  We generated ChIP-Seq data for H3K27ac and H3K4me3 from DMSO and 4SC-202 treated L3.6 cells. Consistently, Input DNA from all the two conditions was included as well.


title: Functional genomics of HDAC class-I specific inhbitor 4SC-202 in pancreatic cell lines  [RNA-seq]

summary: We examined transcriptome-wide effects of 4SC-202 in L3.6, BXPC3 and PANC1 cells as well as its effect on TGFβ signaling

overall_design: We performed  mRNA sequencing from L3.6, BXPC3 and PANC1 cells following following DMSO, 4SC-202 and/or TGFβ treatment. The mRNA-Seq includes following conditions: 4SC-202 vs DMSO (for L3.6, BXPC3 and PANC1 cells), TGFβ vs DMSO and 4SC-202+TGFβ vs TGFβ (for PANC1  cells). The libraries were performed in triplicates.


title: Age-related alterations in Wnt-signaling in paneth and stem cells isolated from intestinal crypts.

city: Cincinnati

first: Rebekah

last: Karns

state: OH

address: 3333 Burnet Ave

department: Gastroenterology, Hepatology, & Nutrition

institute: Cincinnati Children's Hospital Medical Center

summary:
Purpose: Characterize functional alterations in stem cells and paneth cells obtained from young and aged mice, focusing on age-based impairment of intestinal regeneration due to a decline in canonical Wnt signaling.
Methods: mRNA profiles of young and aged stem and paneth cells were generated in triplicate (with one additional young paneth sample) using the Illumina HiSeq 2500.  Reads that passed quality filters were aligned to the mm10 mouse genome with annotations provided by UCSC.
Results:  Approximately 10 millions reads were aligned per sample, corresponding to 36186 transcripts -- of these, 19574 exhibited reasonable expression.  The effect of age was tested wtihin paneth and stem cells, using unpaired t-tests with a p-value cutoff of 0.05 and fold change cutoff of 1.5. Within paneth cells, 1025 genes were significant; within stem cells, 750 genes exhibited differential regulation.  Among the downregulated genes in paneth and stem cells, we observed significant enrichment of canonical Wnt signaling genes.
Conclusion: Age-related downregulation of canonical Wnt signaling is involved in the impairment of intestinal regulation upon aging.

overall_design: mRNA profiles of paneth and stem cells obtained from proximal intestinal crypts from aged and young male Lgr5 mice were generated using RNAsequencing in triplicate, using Illumina HiSeq 2500.

first: Hartmut

last: Geiger

first: Kodanda

last: Reddy


title: Integrative epigenomic analysis in MLL-AF9 acute myeloid leukemia (AML) and B-acute lymphoblastic leukemia (B-ALL)

first: Magalie

last: Celton

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

overall_design: Refer to individual Series


title: Hepatic differentiation of liver organoids

summary: We analyzed gene expression profiles of self-organizing, multi-cellular, 3D liver organoids derived by co-culture of induced Pluripotent Stem Cell and stromal progenitors. We report the RNA-seq results of liver organoid at day0, day2, day4, day6 of co-culture. We also report RNA-seq results of constituent of the liver organoid, which are human iPSC at hepatic specification stage, human Mesenchymal stem cells derived from bone marrow, human umbilical vein endothelial cell. As controls, we also report RNS-seq results of un-differentiated human iPSC, human iPSC at definitive endoderm stage, human liver tissue, and primary cultured human hepatocytes isolated from unused donor livers.

overall_design: mRNA profiles of  liver organoids and their constituents were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500.

first: Akihiro

last: Asai

first: Reena

last: Mourya


title: Identification of intrinsic growth modulators for intact CNS neurons after injury

status: Public on Mar 13 2017

city: West Haven

first: Francesc

last: Lopez

state: CT

department: Department of Genetics

institute: Yale University

summary: Functional deficits persist after spinal cord injury (SCI) because axons in the adult mammalian central nervous system (CNS) fail to regenerate. However, modest levels of spontaneous functional recovery are typically observed after trauma, and are thought to be mediated by the plasticity of intact circuits. The mechanisms underlying intact circuit plasticity are not delineated. Here, we characterize the in vivo transcriptome of sprouting intact neurons from ngr1 null mice after partial SCI. We identify the lysophosphatidic acid signaling modulators Lppr1 and Lpar1 as intrinsic axon growth modulators for intact corticospinal motor neurons after adjacent injury. Furthermore, in vivo Lpar1 inhibition or Lppr1 overexpression enhances sprouting of intact corticospinal tract axons and yields greater functional recovery after unilateral brainstem lesion in wild type mice. Thus, the transcriptional profile of injury-induced sprouting of intact neurons reveals targets for therapeutic enhancement of axon growth initiation and new synapse formation.

overall_design: GFP labeled Corticospinal motor neurons (CSMNs) were harvetsed via laser capture microdissection to assess gene expression between populations that were quiescent and those that initated a functional axon growth response.

first: William

last: Cafferty

last: Lopez-Giraldez


title: Stable Polycomb-dependent transgenerational inheritance of chromatin states in Drosophila

city: Taipei

first: Jia-Ming

last: Chang

address: NO.64, Sec. 2, ZhiNan Rd., Wenshan District

department: Department of Computer Science

country: Taiwan

institute: National Chengchi University

summary: Transgenerational epigenetic inheritance entails transmission of epigenetically determined phenotypic traits through multiple generations. However, very little is known on the principles and the mechanisms governing this type of inheritance. Here, we established stable and isogenic Drosophila epilines by transiently enhancing long-range chromatin interactions. Such epilines display two opposing chromatin states, which depend on differential levels of the H3K27me3 histone mark. Once established, both the active and the repressed epialleles can dominantly be transmitted to naïve flies and can induce paramutation. Importantly, both epilines can be reset to an intermediate naïve state by disrupting chromatin interactions. Finally, we show that the environment can modulate the expressivity of the epialleles and we extend our paradigm to naturally occurring genetic makeups. Our work sheds light on how nuclear organization contributes to epigenetically heritable phenotypic variability and therefore to evolution.

overall_design: genomic DNA sequencing and RNA sequencing of Drosophila melanogaster epilines

first: Filippo

last: Ciabrelli

first: Federico

last: Comoglio

first: Simon

last: Fellous

first: Boyan

last: Bonev

first: Maria

last: Ninova

first: Quentin

last: Szabo

first: Anne

last: Xuereb

first: Christophe

last: Klopp

first: Alexei

last: Aravin

first: Renato

last: Paro

first: Frederic

last: Bantignies

first: Giacomo

last: Cavalli


title: Differentially expressed genes between SPOPmut and control in mouse prostate organoids

city: New York

first: Deli

last: Liu

state: New York

address: 1300 York Ave

institute: Weill Cornell Medicine

summary:
To provide further insight to the signaling pathways deregulated by SPOP mutation and determine the relevance of these models to human prostate cancer, we performed RNA-seq on SPOP mutant organoids and controls. RNA-seq reads mapped to human and mouse SPOP confirmed appropriate expression of the F133V transgenic transcript without overexpression compared to endogenous mouse Spop. Quantification of gene expression was performed via RSEQtools using GENCODE as reference gene–annotation set.

Both SPOPmut and SPOPwt were done in the same run. S0 was done in first run; S1 and S2 were done in second run. S3, S4 and S5 were done in third run.

S5mut and S5wt were excluded from differentially expressed genes analysis, due to the different mouse line.

overall_design: Differentially expressed genes between mouse SPOPmut organoids and control by RNA-seq.

first: Mirjam

last: Blattner

first: Christopher

last: Barbieri

first: Mark

last: Rubin

first: Andrea

last: Sboner


title: H3.Y discriminates between HIRA and DAXX chaperone complexes and reveals unexpected insights into human DAXX-H3.3-H4 binding and deposition requirements

city: Giessen

first: Marek

last: Bartkuhn

address: Aulweg 132

institute: Justus-Liebig-University Giessen

summary: Histone chaperones prevent promiscuous histone interactions before chromatin assembly. They guarantee faithful deposition of canonical histones and functionally specialized histone variants into chromatin in a spatial- and temporally-restricted manner. Here, we identify the binding partners of the primate-specific and H3.3-related histone variant H3.Y using several quantitative mass spectrometry approaches, and biochemical and cell biological assays. We find the HIRA, but not the DAXX/ATRX, complex to specifically recognize H3.Y, explaining its presence in transcriptionally active euchromatic regions. Accordingly, H3.Y nucleosomes are enriched in the transcription-promoting FACT complex and depleted of repressive posttranslational histone modifications. H3.Y mutational gain-of-function analyses screens reveal an unexpected combinatorial amino acid sequence requirement for histone H3.3 interaction with DAXX but not HIRA, and for H3.3 recruitment to PML nuclear bodies. We demonstrate the importance and necessity of specific H3.3 core region and C-terminal amino acids in discriminating between distinct chaperone complexes. Further, ChIP-seq experiments reveal that in contrast to euchromatic HIRA-dependent deposition sites, human DAXX/ATRX-dependent regions of histone H3 variant incorporation are enriched in heterochromatic H3K9me3 and simple repeat sequences. These data demonstrate that H3.Y's unique amino acids allow a functional distinction between HIRA and DAXX binding and its consequent deposition into open chromatin.

overall_design: Examination of genome-wide localization of H3.3, H3.Y and mutants thereof in HeLa Kyoto cells. Respective histones were expressed with an eGFP-tag and immunoprecipitated with a GFP antibody after chromatin shearing.

first: Sandra

last: Hake

first: Lisa

last: Zink


title: microRNA expression in bovine cumulus cells and its relation to oocyte developmental competence

city: Utrecht

first: Karen

last: Uhde

address: Yalelaan 104

country: Netherlands

institute: Utrecht University

summary: microRNA sequencing to find differences in miRNA expression in bovine cumulus cells between cumulus pieces retrieved from COCs developing into a blastocyst after fertilization or remain uncleaved after fertilization

overall_design: cumulus pieces of the two different groups were analysed, if there is a difference in miRNA expression

first: Helena

last: van Tol

first: Tom

last: Stout

first: Bernard

last: Roelen


title: Well-positioned nucleosomes punctuate polycistronic Pol II transcription units and flank silent VSG gene arrays in Trypanosoma brucei

city: Bethesda

first: David

middle: Johannes

last: Clark

address: 6 Center Drive Bldg 6A Rm 2A02

department: DDB

institute: NICHD, NIH

summary: Trypanosoma brucei, a member of the Excavates supergroup, falls in an evolutionarily ancient branch of eukaryotes. We have mapped nucleosome positions in T. brucei and identified a map that differs from that of other eukaryotes in several important ways. Unlike in other eukaryotes, the RNA polymerase II initiation regions in T. brucei do not exhibit pronounced nucleosome depletion, and show little evidence for defined -1 and +1 nucleosomes. In contrast, a well-positioned nucleosome is present directly on the splice acceptor sites within the polycistronic transcription units. The RNA polyadenylation sites were depleted of nucleosomes, with a single well-positioned nucleosome present immediately downstream of the predicted sites. The regions flanking the silent Variant Surface Glycoprotein (VSG) gene arrays showed extensive arrays of well-positioned nucleosomes, which may act to repress cryptic transcription initiation. The silent VSG genes themselves exhibited a less regular nucleosomal pattern in both bloodstream and procyclic form trypanosomes. The DNA replication origins, when present within arrays of silent VSG genes, displayed a defined nucleosomal organization compared with replication origins in other chromosomal core regions. Our results indicate that some organizational features of chromatin are evolutionarily ancient, and may already have been present in the last eukaryotic common ancestor.

overall_design: MNase-seq data to identify and compare genome-wide nucleosome positions in two different life-cycle stages of T. brucei: BF (bloodstream form) and PF (procyclic form). We provide 2 biological replicate experiments for two BF isolates and two PF isolates.

first: Johannes

middle: P

last: Maree

first: Megan

last: Povelones

middle: J

first: Gloria

last: Rudenko

first: Hugh

last: Patterton


title: Genome-wide maps of chromatin state and chromatin accessibility in CD8 T cell subsets

city: Stanford

first: Howard

middle: Y

last: Chang

state: California

address: 269 Campus Drive

institute: Stanford University

summary: To understand epigenetic mechanisms underlying CD8 T cell differentiation, we performed ChIP-seq of 4 histone modifications (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and ATAC-seq to probe chromatin states and accessibility. We identified subset-specific regulatory elements (enhancers and promoters) from chromatin states and predicted key transcription factors from accessible regulatory regions using ATAC-seq.

overall_design: Examination of 4 different histone modifications and open chromatin in 4 cell types.

first: Bingfei

last: Yu

first: Ananda

last: Goldrath


title: Gene expression profile of  high amylolytic enzyme producing mutant strain of Aspergillus luchuensis obtained by ion beam mutagenesis

city: Kagoshima

first: Taiki

last: Futagami

address: Korimoto 1-21-24

department: Department of Agriculture

country: Japan

institute: Kagoshima University

summary: Aspergillus luchuensis is a kuro (black) koji mold that have been used as starch degrader for awamori and shochu making industries in Japan. In this study, we investigated the effect of ion beam irradiation on the A. luchuensis RIB2601 and successfully obtained a high starch degrading mutant strain U1. Strain U1 showed reduced growth rate, whereas showed higher α-amylase, glucoamylase, and α-glucosidase activities per mycelial growth than those of wild type strain both in the agar plate and rice koji. In addition, strain U1 showed higher N-acetylglucosamine content in the cell wall and showed higher sensitivity to calcofluor white, indicating deficient cell wall integrity. Interestingly, the analysis of secreted protein showed higher expression of acid labile α-amylase (AmyA) and glucoamylase (GlaA) in strain U1 although the real-time-RT-PCR analysis indicated that the transcriptional levels of the amyA and glaA genes are not changed significantly. These results suggested that the high amylolytic activity of strain U1 is attributed to the high AmyA and GlaA expression level, but it is not through transcriptional regulation of the amyA and glaA genes. Furthermore, the RNA-seq analysis indicated that strain U1 shows transcriptional change of at least 604 genes related to oxidation-reduction, transport, and glucosamine-containing compound metabolic processes, which may be involved in the deficient cell wall integrity of strain U1.

overall_design: mRNA profiles of Aspergillus luchuensis wild type and its mutant strain U1 were investigated by Illumina HiSeq2000.

first: Kazuki

last: Mori


title: DNA breaks and chromatin structural changes enhance the transcription of Autoimmune Regulator target genes

city: Tartu

first: Pärt

last: Peterson

address: Ravila 19

department: Department of Biomedicine

country: Estonia

institute: University of Tartu


title: Exploration of the Chicken Adipose Tissue

city: Newark

first: Carl

last: Schmidt

state: DE

address: 601 Sincock Ln

institute: University of Delaware

summary: Adipose tissue is essential for lipid storage and thus, energy regulation and maintenance.  Many organs in the body utilize lipids as their primary energy source, such as the heart.  In addition, when glucose supplies are insufficient adipose tissue is broken down and fats are utilized systemically as a primary energy source.  This is regulated by the endocrine system primarily through the regulation of glucagon and insulin.  Adipose tissue is also involved with the immune system particularly in eliciting an inflammatory response through cytokine signaling and the release of interleukins.  Chickens have two major fat pads:  an abdominal fat pad and a cardiac fat pad.  The abdominal fat pad is located on the ventral side, above the GI tract.  The cardiac fat pad is situated on the atria of the heart and surrounds the aorta.  These fat pads are different in coloration and size which leads to the hypothesis that these fat pads have different functions.  The objectives of the project are to (a) identify genes that are unique to each type of adipose tissue when compared to the rest of the body, through the collection of other tissues and (b) to identify genes that are differentially expressed in each type of adipose tissue in comparison to each other to better understand the functioning of these fat pads in the chicken and the pathways that they are involved in at the transcriptomic level.

overall_design: Male Ross 708 broiler chickens were raised from day of hatch to day 42, typical market age, on the University of Delaware farm. Birds were placed into a house. The house was kept at 23 hours of light and 1 hour of dark and birds were placed on litter and given feed (meeting all NRC requirements) and water with ad libitum access.  The house was kept at 35 degrees celsius for the first week and the temperature was decreased 5 degrees celsius each week until 25 degrees celsius. The house was maintained at 25 degrees celsius for the remainder of the study. Necropsies were performed at several points throughout the trial (days 21, 22, 26, 32, and 42).

first: Blair

last: Schneider


title: High activity of a broad panel of housekeeping and tissue-specific cis-regulatory elements depends on a subset of ETS proteins

city: Rozzano

first: Alberto

last: Termanini

state: MI

address: Via Manzoni, 113

country: Italy

institute: Istituto Clinico Humanitas

summary: The genomic repertoire of enhancers and promoters that control the transcriptional output of terminally differentiated cells includes cell type-specific and housekeeping elements. Whether the constitutive activity of these two groups of cis-regulatory elements relies on entirely distinct or instead shared regulators is unknown. By dissecting the cis-regulatory repertoire of macrophages, we found that the ELF subfamily of ETS proteins selectively bound within 60 bp from the transcription start sites of highly active housekeeping genes. ELFs also bound constitutively active, but not poised macrophage-specific enhancers and promoters. The role of ELFs in promoting constitutive transcription is suggested by multiple evidences: ELF sites enabled transcriptional activation by endogenous and minimal synthetic promoters; ELF recruitment was stabilized by the transcriptional machinery, and ELF proteins mediated recruitment of transcriptional and chromatin regulators to core promoters. These data indicate that a distinct subfamily of ETS proteins imparts high transcriptional activity to a broad range of housekeeping and tissue-specific cis-regulatory elements, which is consistent with the role of an ETS family ancestor in core promoter regulation in a lower eukaryote.

overall_design: Chromatin immuno-precipitations of transcription factors Fli1, Elf1, Elf4, GABP-α, H3 lysine 4 trimethylated, H3 lysine 4 monomethylated, PU.1, H3 lysine 27 and RNA polymerase II followed by multiparallel sequencing, performed in bone marrow-derived macrophages from wild type (WT) mice. Cells were treated with alpha amanitin for 5 hours or left unstimulated.

first: Alessia

last: Curina

first: Serena

last: Ghisletti

first: Elena

last: Prosperini

first: Gioacchino

last: Natoli


overall_design:
Nascent RNA sequencing of primary bone marrow-derived macrophages (BMDM)

This series contains a re-analysis of GSM1880858 from GSE73021. The file MacroTFs_171-genes.fpkm_tracking.gz contains the FPKM values for this sample.


title: DNA breaks and chromatin structural changes enhance the transcription of Autoimmune Regulator target genes [FAIRE-Seq]

summary: The Autoimmune Regulator (AIRE) protein is the key factor in thymic negative selection of autoreactive T-cells by promoting the ectopic expression of tissue-specific genes in thymic medullary epithelium. Mutations in AIRE cause a monogenic autoimmune disease called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). AIRE has been shown to promote DNA breaks via its interaction with topoisomerase 2 (TOP2). In this study, we investigated topoisomerase-induced DNA breaks and chromatin structural alterations in conjunction with AIRE-dependent gene expression. Using RNA-seq, we found that the inhibition of TOP2 religation activity by etoposide in AIRE-expressing cells had a synergistic effect on genes with low expression levels. AIRE-mediated transcription was not only enhanced by TOP2 inhibition but also by topoisomerase 1 (TOP1) inhibitor camptothecin. The transcriptional activation was associated with structural rearrangements in chromatin, notably the accumulation of γH2AX and the exchange of histone H1 with HMGB1 at AIRE target gene promoters. In addition, we found the transcriptional upregulation to co-occur with the chromatin structural changes within the genomic cluster of carcino-embryonic antigen-like cellular adhesion molecule (CEACAM) genes. Overall, our results suggest that the presence of AIRE can trigger molecular events leading to an altered chromatin landscape and the enhanced transcription of low-expressed genes.

overall_design: FAIRE-seq of 8 AIRE-Tet cell line samples belonging to 4 experimental conditions, each in duplicate

first: Mario

last: Saare

first: Lili

last: Milani


title: Reconstituting development of pancreatic intraepithelial neoplasia from primary human pancreas duct cells

first: Jonghyeob

last: Lee

address: 279 Campus Drive, Beckman Center B300

institute: Stanford University School of Medicine

summary: Development of systems that reconstitute hallmark features of human pancreatic intraepithelial neoplasia (PanINs), the precursor to pancreatic ductal adenocarcinoma, could generate new strategies for early diagnosis and intervention. However, human cell-based PanIN models with defined mutations are unavailable. Here, we report that genetic modification of primary human pancreatic cells leads to development of lesions resembling native human PanINs. Primary human pancreas duct cells harbouring oncogenic KRAS and induced mutations in CDKN2A, SMAD4 and TP53 expand in vitro as epithelial spheres. After pancreatic transplantation, mutant clones form lesions histologically similar to native PanINs, including prominent stromal responses. Gene expression profiling reveals molecular similarities of mutant clones with native PanINs, and identifies potential PanIN biomarker candidates including Neuromedin U, a circulating peptide hormone. Prospective reconstitution of human PanIN development from primary cells provides experimental opportunities to investigate pancreas cancer development, progression and early-stage detection.

overall_design: We performed RNAseq analysis using KCT, KCST, KECST clones along with donor-matched control ductal sphere cells (S1-CTRL, S1 KCSTclone3, S1 KECSTclone3, S1 KCSTclone4, S1 KECSTclone4, S2 KCTclone3, S2 KCSTclone8, S2 KECSTclone8).

first: Seung

last: Kim


title: The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells [RNA-Seq]

first: Hamish

last: King

address: 4 Newark St

department: Blizard Institute

institute: Queen Mary University of London

summary: Pioneer transcription factors are able to recognise and bind their motif sequences in inaccessible or closed chromatin, and their ability to achieve this is required to establish new regulatory elements and transcriptional networks during development and cellular reprogramming. An essential feature of this pioneering activity is the transition from inaccessible chromatin to a nucleosome-depleted and accessible chromatin state typical of normal regulatory elements, and this is believed to facilitate further transcription factor binding events. However, the mechanisms by which many pioneer transcription factors achieve this remarkable feat remain elusive. Here we reveal that the pluripotency-associated pioneer factor OCT4 binds inaccessible chromatin to shape the chromatin accessibility, transcription factor co-binding and regulatory potential of thousands of distal regulatory elements in mouse embryonic stem cells, demonstrating that its pioneering activity is a feature of normal pluripotency, and not just reprogramming. The accessible chromatin formed at OCT4 binding sites relies on the chromatin remodelling factor BRG1, which is recruited to these sites by OCT4. The occupancy of BRG1 is then required to support OCT4/SOX2 co-binding and normal expression of the pluripotency-associated transcriptome, and this reliance on BRG1 reflects OCT4 binding dynamics during cellular reprograming and early mouse development. Together these observations reveal a distinct requirement for the chromatin remodelling factor BRG1 in shaping the pioneering activity of OCT4 and regulating the pluripotency network in embryonic stem cells.

overall_design: ZHBTC4 and Brg1fl/fl mouse embryonic stem cells were used to ablate OCT4 and BRG1 expression respectively, followed by ATAC-seq, ChIP-seq or RNA-seq to examine their contribution towards chromatin accessibility, transcription factor occupancy, and gene expression.

first: Robert

last: Klose


title: The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells


title: A Bach2-Cebp gene regulatory network for the commitment of multipotent hematopoietic progenitors [ChIP-seq]

city: Sendai

first: Mitsuyo

last: Matsumoto

address: 2-1 Seiryo-machi Aoba-ku

department: Biochemistry

institute: Tohoku university school of medicine

summary: The commitment of hematopoietic stem cells and multipotent progenitors (MPPs) can be tuned to reprogram their differentiation capacity to be biased toward myeloid cells in response to an infection. Bach2, which inhibits myeloid differentiation in common lymphoid progenitors, repressed a cohort of genes of myeloid function (myeloid genes) and activated those for lymphoid function (lymphoid genes) in MPPs. In addition, Bach2 repressed both Cebpb and its target Csf1, encoding C/EBPβ and macrophage colony-stimulating factor (M-CSF), respectively, whereas C/EBPβ repressed Bach2 and activated the M-CSF receptor gene Csf1r. Bach2 and C/EBPβ bound to overlapping regulatory regions of their myeloid target genes, suggesting the presence of a gene regulatory network (GRN) with mutual repression and antagonistic, feed-forward regulation of myeloid genes. Lipopolysaccharide reduced the expression of Bach2, resulting in enhanced myeloid differentiation. Bach2 tunes the commitment of multipotent progenitors to myeloid and lymphoid lineages under both normal and infectious conditions.

overall_design: Sarch of Bach2 target genes in progenitor cells

first: Akihiko

last: Muto

first: Ari

last: Itoh-Nakadai

first: Ryo

last: Funayama

first: Keiko

last: Nakayama

first: Kazuhiko

last: Igarashi


title: The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells [ChIP-Seq]


first: Alberto

last: Termanini

overall_design:
Chromatin immuno-precipitations of transcription factors Fli1, Elf1, Elf4, GABP-α, H3 lysine 4 trimethylated, H3 lysine 4 monomethylated, PU.1, H3 lysine 27 and RNA polymerase II followed by multiparallel sequencing, performed in bone marrow-derived macrophages from wild type (WT) mice. Cells were treated with alpha amanitin for 5 hours or left unstimulated.

This study includes re-analysis of the following samples from GSE38377: GSM940891, GSM940902, GSM940904, GSM940913, and GSM940924.  The .bed files with called peaks for these samples are available on the series record.

The input sample used for all samples for which peak calling was performed, including the re-analyzed samples, is GSM2344452. No peak calling was done for RNAPolII ChIP samples. BigWig files with genome-wide IP signal are available for the RNAPolII ChIP samples.


title: DNA breaks and chromatin structural changes enhance the transcription of Autoimmune Regulator target genes [RNA-Seq]

first: Pärt

last: Peterson

overall_design: RNA-seq of 8 AIRE-Tet cell line samples belonging to 4 experimental conditions, each in duplicate

first: Julia

last: Maslovskaja


title: The pioneer factor OCT4 requires the chromatin remodeller BRG1 to support gene regulatory element function in mouse embryonic stem cells [ATAC-Seq]


title: ChIP-seq from K562 (ENCSR996HUG)

status: Public on Mar 12 2017

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 11-13-13)

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 MCF-7 (ENCSR999WHE)

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 liver (ENCSR994YLZ)

summary:
Chip-Seq on YY1-human

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: Molecular phenotyping of antisense oligonucleotides (ASOs) in immortalized proximal tubule epithelial cells (PTEC-TERT1)

city: Basel

first: Jitao David

last: Zhang

address: Grenzacherstrasse 124

department: Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel

country: Switzerland

institute: F. Hoffmann-La Roche

summary: Molecular phenotyping quantifies expression of pathway reproter genes by next-generation sequencing of pre-defined amplicons. We applied the technology to quantify pathway-level impact of ASOs to PTECs in the presence and absence of exogeneous EGF.

overall_design: Five ASOs, each in three concentrations, and vehicle controls were added to the cell culture of PTEC-TERT1 cells either in the presence or in the absence of exogeneous EGF. Molecular phenotyping was performed 6 hours later. Three biological replicates were performed for each condition

first: Jitao

first: Annie

last: Moisan

first: Regine

last: Gerard

first: Erich

last: Kueng


title: ChIP-seq from OCI-LY3 (ENCSR996GHD)


title: ChIP-seq from cardiac muscle cell (ENCSR994NPK)


title: ChIP-seq from DOHH2 (ENCSR992YSL)


title: ChIP-seq from HepG2 (ENCSR988ZSI)

summary:
Chip-Seq on HepG2

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 HepG2 (ENCSR988LZG)


title: ChIP-seq from A673 (ENCSR988EGR)


title: ChIP-seq from thoracic aorta (ENCSR988DFT)


title: ChIP-seq from MCF-7 (ENCSR985MIB)


title: ChIP-seq from right lobe of liver (ENCSR981UJA)


title: ChIP-seq from SK-N-SH (ENCSR978CNH)


title: ChIP-seq from bipolar spindle neuron (ENCSR983CSB)


title: ChIP-seq from K562 (ENCSR962APM)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 02-26-14)

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 HepG2 (ENCSR993LMB)


title: ChIP-seq from KMS-11 (ENCSR976JHS)


title: ChIP-seq from gastrocnemius medialis (ENCSR972ETR)


title: ChIP-seq from DOHH2 (ENCSR966HBM)


title: ChIP-seq from H9 (ENCSR967HXD)


title: ChIP-seq from SK-N-SH (ENCSR975GZA)


title: ChIP-seq from keratinocyte (ENCSR970FPM)


title: ChIP-seq from HepG2 (ENCSR966PJY)


title: ChIP-seq from OCI-LY3 (ENCSR957CQH)


title: ChIP-seq from OCI-LY1 (ENCSR960ZMM)


title: ChIP-seq from KMS-11 (ENCSR955IXZ)


title: ChIP-seq from PC-3 (ENCSR946QFD)


title: ChIP-seq from HepG2 (ENCSR945JOR)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 04-29-13)

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 K562 (ENCSR948QLZ)

summary:
ChIP-Seq on K562-human

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 thyroid gland (ENCSR975NOU)


title: ChIP-seq from HepG2 (ENCSR959OMS)


title: ChIP-seq from PC-3 (ENCSR943LZX)


title: ChIP-seq from liver (ENCSR931XLP)

summary:
Chip-Seq on STL011-human (fragmentation date: 2015-01-29)

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 HepG2 (ENCSR961WLZ)


title: ChIP-seq from HepG2 (ENCSR938ETG)


title: Atrophin (Atro) ChIP-seq data from Drosophila S2 cells

city: Stockholm

first: Mattias

last: Mannervik

address: Arrheniuslaboratories E3

department: Molecular Biosciences, the Wenner-Gren Institute

country: Sweden

institute: Stockholm University

summary: We performed ChIP-seq with Drospohila Atrophin (also known as Grunge) antibody using S2 cell chromatin. Atro ChIP-seq peaks are most frequent in promoters and introns of highly expressed, paused genes in S2 cells, including several components of developmental signaling pathways. The Atro peaks overlap significantly with GAGA factor (Trithorax-like, Trl).

overall_design: ChIP-seq in Drosophila S2 cells with an antibody (4H6) raised against the peptide SRQSPLHPVP in the C-terminus of Drospohila Atro

first: Ann

last: Boija

first: Per

last: Stenberg


title: ChIP-seq from thoracic aorta (ENCSR939RLS)


title: ChIP-seq from induced pluripotent stem cell (ENCSR932ZMX)

summary:
Chip-Seq on PGP1 iPSC

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 MCF-7 (ENCSR940MHE)

summary:
ChIP-Seq on MCF7-human

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 neural cell (ENCSR958ZMM)


title: ChIP-seq from gastrocnemius medialis (ENCSR948YYZ)


title: ChIP-seq from HepG2 (ENCSR954KIC)


title: ChIP-seq from HepG2 (ENCSR925QAW)


title: ChIP-seq from MCF-7 (ENCSR924PBF)

summary:
Chip-Seq on MCF7-human (fragmentation date:2015-03-26

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-9 (ENCSR945KBK)


title: ChIP-seq from HepG2 (ENCSR925BFV)


title: ChIP-seq from liver (ENCSR917QNE)

summary:
Chip-Seq on RAD21-human

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 mid-neurogenesis radial glial cells (ENCSR922CAT)


title: ChIP-seq from PC-9 (ENCSR913MGR)


title: ChIP-seq from thoracic aorta (ENCSR909VUB)


title: ChIP-seq from thoracic aorta (ENCSR930HLX)


title: ChIP-seq from gastrocnemius medialis (ENCSR922OXX)


title: ChIP-seq from liver (ENCSR904IXG)


title: ChIP-seq from gastrocnemius medialis (ENCSR897RRA)


title: ChIP-seq from thyroid gland (ENCSR906YES)


title: ChIP-seq from bipolar spindle neuron (ENCSR905TYC)


title: ChIP-seq from GM12878 (ENCSR890ZMI)

summary:
Reverse Crosslink Control ChIP-seq on human GM12878 (fragmentation date 02-19-14)

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 fibroblast of arm (ENCSR900AQX)


title: ChIP-seq from Loucy (ENCSR900HAP)


title: ChIP-seq from neuroepithelial stem cell (ENCSR890NXD)


title: ChIP-seq from induced pluripotent stem cell (ENCSR908FQA)


title: ChIP-seq from ACC112 (ENCSR897FOZ)


title: ChIP-seq from SK-N-MC (ENCSR899XXQ)

summary:
Control ChIP-seq 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 bipolar spindle neuron (ENCSR889GGV)

summary:
Chip-Seq on biopolar spindle neuron

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 GM12878 (ENCSR897MMC)

summary:
Chip-Seq on GM12878

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 HepG2 (ENCSR909GJR)


title: ChIP-seq from KMS-11 (ENCSR900DFO)

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 body of pancreas (ENCSR888RBQ)


title: ChIP-seq from HepG2 (ENCSR903ELW)


title: ChIP-seq from Loucy (ENCSR884QDT)


title: ChIP-seq from hepatocyte (ENCSR883XRM)


title: ChIP-seq from SK-N-SH (ENCSR878HPJ)


title: ChIP-seq from Peyer's patch (ENCSR878KIY)


title: ChIP-seq from KOPT-K1 (ENCSR879WTY)


title: ChIP-seq from PC-3 (ENCSR881TWJ)


title: ChIP-seq from MCF-7 (ENCSR876UYH)

summary:
Chip-Seq on MCF7

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 K562 (ENCSR896JFO)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 04-08-13)

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 (ENCSR876DCP)


title: ChIP-seq from OCI-LY1 (ENCSR874HSH)


title: ChIP-seq from HepG2 (ENCSR882VRP)

summary:
Chip-Seq on HepG2-human (fragmentation date:2015-02-14

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 gastroesophageal sphincter (ENCSR872WVR)


title: ChIP-seq from neural cell (ENCSR873EIA)


title: ChIP-seq from MCF-7 (ENCSR875KOJ)


title: ChIP-seq from H9 (ENCSR870IUC)


title: ChIP-seq from cardiac muscle cell (ENCSR867SJE)


title: ChIP-seq from MM.1S (ENCSR872PRJ)


title: ChIP-seq from cardiac muscle cell (ENCSR864LRY)


title: ChIP-seq from K562 (ENCSR863KUB)


title: ChIP-seq from liver (ENCSR849OTN)

summary:
Chip-Seq on STL010-human (fragmentation date: 2015-12-09)

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 (ENCSR859FGW)


title: ChIP-seq from hepatocyte (ENCSR850ODD)


title: ChIP-seq from SUDHL6 (ENCSR869HJR)


title: ChIP-seq from Karpas-422 (ENCSR870IGD)


title: ChIP-seq from HepG2 (ENCSR853ADA)

summary:
Chip-Seq on HepG2

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 bipolar spindle neuron (ENCSR849YFO)


title: ChIP-seq from OCI-LY7 (ENCSR850QKN)


title: ChIP-seq from adrenal gland (ENCSR857XRG)


title: ChIP-seq from HepG2 (ENCSR855LCA)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 12-15-13)

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 GM12878 (ENCSR860UHK)


title: ChIP-seq from HepG2 (ENCSR849DFF)


title: ChIP-seq from KMS-11 (ENCSR847UJW)


title: ChIP-seq from liver (ENCSR847DIT)

summary:
Chip-Seq on MAX-human

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 neuroepithelial stem cell (ENCSR842NGQ)


title: ChIP-seq from HepG2 (ENCSR848YWD)


title: ChIP-seq from bipolar spindle neuron (ENCSR839SFJ)


title: ChIP-seq from GM12878 (ENCSR839XZU)

summary:
CREM ChIP-seq on human GM12878

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 MCF-7 (ENCSR838ZOW)

summary:
Chip-Seq on MCF7-human (fragmentation date:2014-10-03

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 Loucy (ENCSR837SUQ)


title: ChIP-seq from ACC112 (ENCSR836XKP)


title: ChIP-seq from liver (ENCSR837GTK)

summary:
Chip-Seq on JUND-human

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 (ENCSR828HXJ)


title: ChIP-seq from KMS-11 (ENCSR835YBD)


title: ChIP-seq from SK-N-MC (ENCSR835MMN)

summary:
ChIP-seq against H3K27ac 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 K562 (ENCSR824WND)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 12-13-12)

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 (ENCSR827NKO)


title: ChIP-seq from bipolar spindle neuron (ENCSR821IAK)


title: ChIP-seq from HepG2 (ENCSR826YMT)


title: ChIP-seq from neutrophil (ENCSR826VJY)


title: ChIP-seq from HepG2 (ENCSR823ADL)


title: ChIP-seq from PC-3 (ENCSR826UTD)


title: ChIP-seq from PC-3 (ENCSR849APH)


title: ChIP-seq from bipolar spindle neuron (ENCSR821GUG)


title: ChIP-seq from B cell (ENCSR805DRF)

summary:
ChIP-seq on human CD20+ Control

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 neural cell (ENCSR816JBG)


title: ChIP-seq from KMS-11 (ENCSR806XIU)


title: ChIP-seq from HepG2 (ENCSR819WZE)


title: ChIP-seq from neuroepithelial stem cell (ENCSR803UDX)


title: ChIP-seq from K562 (ENCSR830KKO)


title: ChIP-seq from K562 (ENCSR837EYC)

summary:
ChIP-Seq on K562-human

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 B cell (ENCSR799SLA)


title: ChIP-seq from gastrocnemius medialis (ENCSR801IPH)


title: ChIP-seq from SUDHL6 (ENCSR804MDH)


title: ChIP-seq from SK-N-SH (ENCSR791INM)


title: ChIP-seq from H1-hESC (ENCSR814XPE)


title: ChIP-seq from HepG2 (ENCSR808FFI)


title: ChIP-seq from HepG2 (ENCSR800QIT)


title: ChIP-seq from KMS-11 (ENCSR790QWJ)


title: ChIP-seq from GM12878 (ENCSR785WMC)

summary:
Chip-Seq on GM12878-human (fragmentation date:2014-10-13)

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 (ENCSR788EQL)


title: ChIP-seq from OCI-LY1 (ENCSR790EDQ)


title: ChIP-seq from K562 (ENCSR795IYP)


title: ChIP-seq from induced pluripotent stem cell (ENCSR773IYZ)


title: ChIP-seq from thyroid gland (ENCSR777VQP)


title: ChIP-seq from OCI-LY3 (ENCSR779KYW)


title: ChIP-seq from smooth muscle cell (ENCSR783AXV)


title: ChIP-seq from SUDHL6 (ENCSR771QCM)


title: ChIP-seq from ACC112 (ENCSR778VGY)


title: ChIP-seq from liver (ENCSR769JUI)

summary:
Chip-Seq on STL010-human (fragmentation date: 2014-09-15)

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 HepG2 (ENCSR798IJO)


title: ChIP-seq from PC-9 (ENCSR769FOC)

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 HepG2 (ENCSR765MKZ)


title: ChIP-seq from HCT116 (ENCSR794ULT)


title: ChIP-seq from PC-3 (ENCSR764KFK)


title: ChIP-seq from Loucy (ENCSR760ZVL)


title: ChIP-seq from MCF-7 (ENCSR761DLU)


title: ChIP-seq from K562 (ENCSR760UVO)

summary:
Chip-Seq on K562

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 (ENCSR760EGQ)


title: ChIP-seq from HepG2 (ENCSR759BDG)


title: ChIP-seq from adrenal gland (ENCSR754WVA)


title: ChIP-seq from hepatocyte (ENCSR758GMX)


title: ChIP-seq from HepG2 (ENCSR757EKM)


title: ChIP-seq from K562 (ENCSR757IIU)

summary:
Chip-Seq on K562-human

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 MM.1S (ENCSR758OEC)


title: ChIP-seq from H9 (ENCSR754VAJ)


title: ChIP-seq from A673 (ENCSR747BYL)


title: ChIP-seq from HepG2 (ENCSR745VSQ)


title: ChIP-seq from induced pluripotent stem cell (ENCSR740FYN)


title: ChIP-seq from OCI-LY7 (ENCSR747ZDF)


title: ChIP-seq from thyroid gland (ENCSR748LUA)


title: ChIP-seq from smooth muscle cell (ENCSR729MRJ)


title: ChIP-seq from MCF-7 (ENCSR752UOD)


title: ChIP-seq from gastrocnemius medialis (ENCSR736ALU)


title: ChIP-seq from induced pluripotent stem cell (ENCSR729ENO)


title: ChIP-seq from neural progenitor cell (ENCSR720ZAX)


title: ChIP-seq from KMS-11 (ENCSR720GSE)


title: ChIP-seq from K562 (ENCSR737LTZ)


title: ChIP-seq from HepG2 (ENCSR770AOR)


title: ChIP-seq from KOPT-K1 (ENCSR719FEJ)


title: ChIP-seq from HepG2 (ENCSR716SYG)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 02-19-14)

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-9 (ENCSR726LZG)


title: ChIP-seq from HepG2 (ENCSR714YZG)


title: ChIP-seq from H9 (ENCSR716ZJH)


title: ChIP-seq from liver (ENCSR735KEY)

summary:
Chip-Seq on FOXA1-human

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 GM12878 (ENCSR713ONE)

summary:
Reverse Crosslink Control ChIP-seq on human GM12878 (fragmentation date 11-12-12)

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 HepG2 (ENCSR711HPO)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 04-19-13)

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 A673 (ENCSR714TJD)


title: ChIP-seq from HepG2 (ENCSR712FAM)

summary:
Chip-Seq on HepG2

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 neural cell (ENCSR714KGG)


title: ChIP-seq from K562 (ENCSR707QWA)


title: ChIP-seq from OCI-LY3 (ENCSR701ZDB)


title: ChIP-seq from MCF-7 (ENCSR703TNG)

summary:
Chip-Seq on MCF7

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-9 (ENCSR705SZP)


title: ChIP-seq from MM.1S (ENCSR698CKZ)


title: ChIP-seq from HepG2 (ENCSR704IGU)


title: ChIP-seq from gastrocnemius medialis (ENCSR697RIW)


title: ChIP-seq from vagina (ENCSR718BTD)


title: ChIP-seq from HepG2 (ENCSR715UCI)


title: ChIP-seq from mid-neurogenesis radial glial cells (ENCSR691BNO)


title: ChIP-seq from radial glial cell (ENCSR689ICI)


title: ChIP-seq from bipolar spindle neuron (ENCSR683ORH)


title: ChIP-seq from MM.1S (ENCSR684BMS)


title: ChIP-seq from hepatocyte (ENCSR689QUB)


title: ChIP-seq from body of pancreas (ENCSR689SFJ)


title: ChIP-seq from SK-N-MC (ENCSR679CHH)

summary:
ChIP-seq against H3K9me3 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 OCI-LY1 (ENCSR678AFU)


title: ChIP-seq from neuroepithelial stem cell (ENCSR688ZOS)


title: ChIP-seq from induced pluripotent stem cell (ENCSR700VCN)


title: ChIP-seq from neural progenitor cell (ENCSR677XPJ)


title: ChIP-seq from NCI-H929 (ENCSR692HIO)


title: ChIP-seq from hepatocyte (ENCSR695HYL)


title: ChIP-seq from HepG2 (ENCSR662EOU)


title: ChIP-seq from HepG2 (ENCSR669LCD)


title: ChIP-seq from HepG2 (ENCSR670YPQ)


title: ChIP-seq from smooth muscle cell (ENCSR672HBY)


title: ChIP-seq from HepG2 (ENCSR666QNP)


title: ChIP-seq from SK-N-SH (ENCSR657OGA)


title: ChIP-seq from SK-N-SH (ENCSR661BMA)


title: ChIP-seq from HCT116 (ENCSR661KMA)


title: ChIP-seq from induced pluripotent stem cell (ENCSR657DYL)


title: ChIP-seq from neural progenitor cell (ENCSR661MUS)