title: Arabidopsis AGO3 predominantly recruits 24-nucleotide small RNAs to regulate epigenetic silencing [Bisulfite-seq]

summary: AGO3 predominantly bound 24-nt sRNAs with 5’ terminal adenine. The spectrum of AGO3-associated sRNAs was different from those bound to AGO2. By contrast, approximately 30% of AGO3-bound 24-nt sRNAs overlapped with those bound to AGO4 and over 60% of AGO3-associated 24-nt sRNA enriched loci were identical to those of AGO4. In addition, expression of AGO3 driven by AGO4 native promoter partially complemented AGO4 function and rescued DNA methylation defect in ago4-1 background.

overall_design: Examination of DNA methylation using bisulfite conversion of unmethylated cytosines in three genetic backgrounds of Arabidopsis thaliana.

first: Zhonghui

last: Zhang

first: Xiuren

first: Xiu-Jie

last: Wang


title: Elucidating the molecular pathways active in chemoresistant head and neck cancer stem cells and their role in resistance

status: Public on Jun 01 2016

city: Ann Arbor

first: Sean

middle: Patrick

last: McDermott

state: MI

address: 2800 Plymouth Rd

department: Internal Medicine - Hem/Onc

country: USA

institute: University of Michigan

summary: Recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) has a poor prognosis with less than 1-year median survival. Platinum-based chemotherapy (cisplatin or carboplatin) remains the first-line treatment for HNSCC. The cancer stem cell (CSC) hypothesis postulates that tumors are maintained by a self-renewing CSC population that is also capable of differentiating into non-self renewing cell populations that constitute the bulk of the tumor. A small population of CSCs exists within HNSCC that are relatively resistant to chemotherapy and clinically predicted to mediate tumor recurrence. These CSCs are identified by high cell-surface expression of CD44 and high intracellular activity of aldehyde dehydrogenase (ALDH) and termed ALDHhighCD44high.  We investigated the molecular pathways active in ALDHhighCD44high cells, which remain poorly studied. Additionally, we performed a molecular examination of cisplatin-resistant ALDHhighCD44high cells, which has not been reported.    Two HNSCC cell lines, UM-SCC-1 and UM-SCC-22b, were utilized in this study. For microarray analysis, UM-SCC-22b cells were treated for 5 days in vitro with 2uM cisplatin and analyzed by flow cytometry, sorted and submitted for microarray analysis of ALDHhighCD44high and ALDHlowCD44low cells from untreated and cisplatin treated cells. Four separate flow cytometry experiments were performed using Affymetrix Human Gene ST 2.1 microarrays. Microarray data was analyzed using R/Bioconductor. Files were preprocessed by Robust Multiarray Average (RMA) with background substraction, quantile normalization, and median polish (oligo package). Data was fitted with robust probe level linear models to all the probesets (oligo package). Experiment and processing batch differences were accounted for using 'ComBat' within the SVA package. Differentially expressed genes were identified using univariate comparisons after fitting data to a linear model (limma package). Initial statistics were determined using an empirical Bayesian model. Multiple testing comparisons were adjusted using Benjamini and Hochberg (aka FDR). Probes with an adjusted p-value <0.05 were considered statistically significant. Unsupervised hierarchical clustering with complete linkage and Euclidean distance was performed on only statistically significant probes.

overall_design: In four separate experiments, the head and neck squamous cell carcinoma cell line UM-SCC-22b were cultured for 5 days with or without 2uM (micromolar) cisplatin in 6-well plates. Media was replaced every other day. Control and cisplatin treated cells were trypsinized, procesed, and stained for CD44 cell-surface expression and intracellular aldehyde dehydrogenase (ALDH) activity to identify cancer stem cells (ALDH+CD44+). CSCs and non-CSCs (ALDH-CD44-) were collected by flow cytometry from both groups. Total RNA was collected from each fraction (ALDH+CD44+, ALDH-CD44-), treatment (control, cisplatin), and experiment (#1-4). A total of 16 samples were analyzed. One set of 4 (experiment #4) were analyzed on a Human Gene ST 2.1 strip and the rest on a Human Gene ST 2.1 plate. Differential gene expression was determined with R/Bioconductor with Robust Multiarray Average (RMA) and fitting the data to linear models (limma). Experimental and processing batch effects were accounted for using ComBat. Four sets of univariate comparisons were made: 1) Cisplatin ALDH+CD44+ vs Control ALDH+CD44+; 2) Control ALDH+CD44+ vs Control ALDH-CD44-; 3) Cisplatin ALDH+CD44+ vs Cisplatin ALDH-CD44-; 4) Cisplatin ALDH-CD44- vs Control ALDH-CD44-. Multiple testing comparisons were adjusted using Benjamini and Hochberg (aka FDR). Probes with an adjusted p-value <0.05 were considered statistically significant.

middle: P

first: Sarah

middle: C

first: Max

middle: S

last: Wicha

first: Jacques

middle: E

last: Nor


title: Arabidopsis AGO3 predominantly recruits 24-nucleotide small RNAs to regulate epigenetic silencing [miRNA-seq]

status: Public on May 31 2016

city: Beijing

first: Xiuying

last: Liu

address: Yard 28, Science Park Road, Changping District

country: China

institute: Changping Laboratory

type: Non-coding RNA profiling by high throughput sequencing

overall_design: Examination of AGO3 and AGO2 bound small RNAs with/without salt stress.


title: Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10

city: St. Louis

first: John

middle: R.

last: Edwards

state: MO

address: 660 S. Euclid Ave, Campus Box 8220

department: Center for Pharmacogenomics

institute: Washington University School of Medicine

type: Expression profiling by high throughput sequencing

summary: The FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1) is bound to essentially all CpG-rich promoters in the mammalian genome. FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal JmjC domain with C- terminal F-box, CXXC, PHD, RING, and leucine rich repeat (LRR) domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the JmjC domain but retains the other domains. Selective deletion of Fbxl10-1 had been reported to produce a minor and variable phenotype, and most mutant animals were essentially normal. We show here that deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) resulted in a very different phenotype with craniofacial abnormalities, greatly increased lethality, and female sterility in surviving homozygous mutants. The phenotype of the Fbxl10-2 deletion was more severe in female mutants. We found that mutants that lacked both FBXL10-1 and -2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally down-regulated in mutant female as compared to male embryos. FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene.

overall_design: Expression analysis using RNA-seq was performed on WT and Fbxl10T/T male and female embryos.

first: Mathieu

last: Boulard

middle: R

first: Timothy

middle: H

last: Bestor


title: In vivo genome-wide profiling reveals a tissue-specific role for 5-formylcytosine

city: Cambridge

first: Dario

last: Beraldi

address: Robinson Way

country: United Kingdom

institute: Cambridge Research Institute

summary:
Background: Genome-wide methylation of cytosine can be modulated in the presence of TET and thymine DNA glycosylase (TDG) enzymes. TET enzymes are able to oxidise 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). TDG can excise the oxidative products 5fC and 5caC, initiating base excision repair. Furthermore, these modified bases are stable and detectable in the genome, raising the possibility that they could have epigenetic functions in their own right. To date, functional investigation of the genome-wide distribution of 5fC has been restricted to cell culture based systems, while its in vivo profile, in particular during development, remains unknown.
Results: Here we describe the first analysis of the in vivo genome-wide profile of 5fC, across a range of dissected tissues from both wild type and Tdg-deficient E11.5 mouse embryos. Changes in the formylation profile of cytosine upon depletion of TDG suggest TET/TDG-mediated active demethylation occurs preferentially at intron-exon boundaries, and reveals a major role for TDG in shaping 5fC distribution at CpG islands. Moreover, we find enhancer regions exhibit high levels of 5fC, which accumulates at tissue-specific enhancers implicating a role in embryonic development.
Conclusions: The tissue-specific distribution of 5fC can be regulated by the collective contribution of TET-mediated oxidation and excision by TDG. We show that the in vivo profile of 5fC during embryonic development resembles that of embryonic stem cells, sharing key features including enrichment of 5fC in enhancer and intragenic regions. Additionally, by investigating 5fC profiles in a tissue-specific manner from mouse embryos, we identified a targeted enrichment at active enhancers involved in tissue development.

overall_design: 5-formylcytosine has been mapped genomewide by pull-down and sequencing in mouse hindbrain, heart, carcass and liver. Each tissue was replicated in two different mice except for hindbrain which was replicated in four different mice.

first: Mario

last: Iurlaro

first: Gordon

last: McInroy

first: Heather

last: Burgess

first: Wendy

last: Dean

first: Eun-Ang

last: Raiber

first: Martin

last: Bachman

first: Shankar

last: Balasubramanian

first: Wolf

last: Reik


title: Transcriptome analysis of  E.coli at different growth conditions

city: Tianjin

first: Du

last: Wen

address: Tianjin Economic and Technological Development 13th street NO.29

institute: Tianjin University  of Science and Technology

summary: In different medium, the grow condition of the bacterium are different. Showing up the difference, the yield of purpose production are different significantly. So we decide enucleate the reasons accroding to the transcriptome analysis.

overall_design: Transcriptome analysis of  E.coli at middle and late periods of logarithmic growth


title: The Nrd1-like protein Seb1 coordinates co-transcriptional 3’ end processing and polyadenylation site decision

city: Newark

first: Bin

last: Tian

state: NEW JERSEY

address: 205 South Orange Ave., CC-F1230

department: Department of Microbiology, Biochemistry and Molecular Genetics

institute: Rutgers University

summary: Seb1 promotes co-transcriptional 3’ end processing events that influence polyadenylation site decision

overall_design: knockdown experiments of Seb1 in Pombe

first: Xiaochuan

first: Mainul

last: Hoque

first: Jean-François

last: Lemay

first: François

last: Bachand


title: Extra-coding RNAs regulate neuronal DNA methylation and long-term memory formation [MBD-seq]

city: Birmingham

first: Jeremy

middle: Jason

last: Day

state: AL

address: 1825 University Blvd

department: Neurobiology

institute: UAB

type: Methylation profiling by high throughput sequencing

summary: This dataset contains whole-genome MBD (methylbinding domain) sequencing results from cortical neuronal cultures and serves as the basis for characterization of DNA methylation profiles from neuronal systems.

overall_design: This experiment contains three sequencing datasets from 2 biological samples. Two datasets originate from samples that underwent MBD-capture prior to whole-genome sequencing. A third dataset contains non-MBD-captured genomic DNA as a control.

first: Katherine

last: Savell

first: Nancy

last: Gallus

first: Esther

last: Song

first: Rhiana

last: Simon

first: Mary

middle: K

last: Osborn

first: Jordan

last: Brown

first: John

middle: J

last: O'Malley

first: J

middle: D

last: Sweatt


title: Affinity and Dose of TCR Engagement Yield Proportional Enhancer and Gene Activity in CD4+ T Cells

city: La Jolla

first: Karmel

last: Allison

state: CA

address: 9500 Gilman Dr

department: Cellur and Molecular Medicine

institute: University of California, San Diego

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Affinity and dose of T cell receptor (TCR) interaction with antigens govern the magnitude of CD4+ T cell responses, but questions remain regarding the quantitative translation of TCR engagement into downstream signals. We find that while the response of CD4+ T cells to antigenic stimulation is bimodal, activated cells exhibit analog responses proportional to signal strength. Gene expression output reflects TCR signal strength, providing a signature of T cell activation. Expression changes rely on a pre-established enhancer landscape and quantitative acetylation at AP-1 binding sites. Finally, we show that graded expression of activation genes depends on ERK pathway activation, suggesting that an ERK-AP-1 axis translates TCR signal strength into proportional activation of enhancers and genes essential for T cell function.

overall_design: CD4+ T cells from transgenic AND mice were sequenced under the conditions indicated. Replicates are included for each type of data (RNA-Seq, ChIP-Seq), and are numbered accordingly. The No Peptide condition serves as the untreated control for the peptide-treated samples, and inputs are provided for ChIP-Sequencing samples.

middle: A

first: Christopher

last: Glass


title: Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [ChIP-seq]

status: Public on May 30 2016

city: New Haven

first: Marina

last: Picciotto

state: CT

address: 301 Cedar Street Congess place/YPI 4th floor

department: Psychiatry

institute: Yale University

summary: Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2l, a component of a histone methyltransferase complex. We therefore examined genome-wide changes in H3MeK4 tri-methylation, a mark induced by the Ash2l complex associated with increased gene transcription. A significant number of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3MeK4 trimethylation. Knockdown of Ash2l or Mef2c abolishes nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuates nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimics nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a novel target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior.

overall_design: Cortical Histone 3 Lysine 4 tri-methylation profiles of 3 month old C57BL6/J mice were generated by deep sequencing, in triplicate or quadruplicate, using Illumina GAII

first: Yonwoo

last: Jung

first: Zhifeng

last: Zhou

first: Qiaoping

last: Yuan

first: David

last: Goldman


title: Next Generation Sequencing Facilitates Quantitative Analysis of peritoneal macrophages Transcriptomes of Dnmt3a macrophage conditional knockout mouse

city: shang hai

first: Qian

last: Zhang

address: xiangyin road 800

institute: Second military medical university

summary:
Purpose:The purpose of this study is to measure the gene expression profile in Dnmt3a conditional knockout macrophages.
Methods:Dnmt3a conditional knockout macrophages mRNA profiles were generated by deep sequencing,using Illumina.
Results: We mapped about 20 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation during Dnmt3a conditional knockout in macrophages.

overall_design: Dnmt3a conditional knockout mRNA profiles were generated by deep sequencing

first: Cao

middle: X

last: Tao

first: li

last: Xia


title: Extra-coding RNAs regulate neuronal DNA methylation and long-term memory formation [RNA-seq]

first: Jeremy

last: Day

summary: This dataset contains whole-genome RNA sequencing results from cortical neuronal cultures and serves as the basis for characterization of extra-coding RNA species from neuronal systems.

overall_design: This experiment contains six biological samples, each of which underwent PolyA+ and PolyA- RNA-seq. Samples were either unstimulated (i.e., treated with media alone; samples V1 and V2), stimulated with 25mM potassium chloride for 1hr (K1, K2) or inactivated with tetrodotoxin for 1hr (T1, T2). Datasets were obtained using RNA-seq from PolyA+ fractions or PolyA- fractions of RNA. PolyA- fractions are denoted "ec". Thus, 12 samples are listed here due to the difference in RNA library preparation.

first: Katherine

last: Savell

first: Nancy

last: Gallus


title: Requirement for flap endonuclease 1 (FEN1) to maintain genomic stability and transcriptional gene silencing in Arabidopsis

status: Public on May 28 2016

first: Jinkui

last: Cheng

address: No.2 Yuanmingyuan West Road

institute: China Agricultural University

summary: As a central component during Okazaki fragment maturation, flap endonuclease 1 (FEN1) removes the 5’ flap and maintains genomic stability. Here, FEN1 was cloned as a suppressor of transcriptional gene silencing (TGS) from a forward genetic screen. FEN1 is abundant in the root and shoot apical meristems and FEN1-GFP shows a nucleolus-localized signal in tobacco cells. Arabidopsis fen1-1 mutant is hypersensitive to MMS and shows reduced telomere length. Interestingly, genome-wide ChIP-seq and RNA-seq results demonstrate that FEN1 mutation leads to a decrease in the H3K27me3 level and an increase in the expression of a subset of genes marked with H3K27me3. Overall, these results uncover a role for FEN1 in mediating TGS besides maintaining genome stability in Arabidopsis.

overall_design: To characterized the role of FEN1 in epigenetic silencing, we examine histone modification and RNA expression changes by whole-genome RNA sequencing; H3K27me3-, H3K4me3-, H3K9me2-, H3-ChIP-seq in A. thaliana transgenic wild type (TWT) and fen1 mutant

first: Jixiang

first: Shaojun

last: Xie

first: Jian-Kang

last: Zhu

first: Zhizhong

last: Gong


title: Impaired DNA damage metabolism promotes autoimmunity in TREX1 deficiency

city: Dresden

first: Min Ae

last: Lee-Kirsch

address: Fetscherstr. 74

department: Klinik für Kinder- und Jugendmedizin

country: Germany

institute: Universitätsklinikum Carl Gustav Carus an der Technischen Universität Dresden

summary: Constitutive low level DNA damage is linked to innate immune activation. Hierarchical clustering of over 9000 transcripts revealed remarkably similar profiles in a patient with lupus erythematosus and a patient with AGS with up-regulation of genes involved in DNA damage signaling, p53-inducible genes, senescence-associated genes as well as  up-regulation of interferon-stimulated genes. Transcriptional profiling of fibroblasts exposed to oxidative stress showed a marked up-regulation of genes involved in DNA replication/repair and replication licensing in TREX1-deficient cells compared to wild type cells suggesting massive replication stress.

overall_design: Comparison of transcriptional profiles of unstressed patient fibroblasts with wild type cells as well as fibroblasts exposed to oxidative stress

first: Christine

last: Wolf

first: Nicole

last: Berndt

first: Alexander

last: Rapp

first: Manuela

last: Dobrick-Mattheuer

first: Stefanie

last: Kretschmer

first: Claudia

last: Krug

first: Thomas

last: Kurth

first: Dagmar

last: Wieczorek

first: Dimitra

last: Alexopoulou

first: Andreas

last: Dahl

first: M

last: Cardoso

last: Günther

first: Min


title: Extra-coding RNAs regulate neuronal DNA methylation dynamics

first: Jeremy

last: Day

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

overall_design: Refer to individual Series


title: MiRNA signatures in cell cycle sorted cells [HeLa_H295R_miRNA_seq]

city: Budapest

first: Vince

middle: Kornél

last: Grolmusz

address: Szentkirályi 46.

country: Hungary

institute: Semmelweis University

summary: For the further examination of cell cycle dependent miRNA expression profile, DNA content based fluorescence activated cell sorting (cell cycle sort) was performed on human transformed cancer cell lines. Phase-dependent miRNA expression profiling was performed on G1, S and G2 phases. Results were validated by quantitative real-time PCR.

overall_design: Phase-dependent miRNA expression profiling was performed on sorted human cancer (cervical - HeLa, adrenocortical - NCI-H295R) cells). G1, S and G2 phases were successfully sorted and analyzed.

first: Attila

last: Patocs


title: The mutual effect of Staphylococcus epidermidis and Staphylococcus aureus in dual species biofilms as revealed by RNA-Seq

status: Public on May 27 2016

city: Ghent

first: Ilse

last: Vandecandelaere

address: Ottergemsesteenweg 460

department: Pharmaceutical Sciences

country: Belgium

institute: Ghent University

summary: We examined the differential gene expression of Staphylococcus epidermidis and Staphylococcus epidermidis in dual species biofilms. Therefore, we performed RNA-Seq on single and dual species biofilms and we compared the gene expression levels in dual species biofilms to those in single species biofilms.

sample_organism:
Staphylococcus aureus
Staphylococcus epidermidis

overall_design: RNA was extracted from single and dual species biofilms of S. epidermidis ET-024 and S. aureus Mu50, converted to cDNA and RNA-Seq was performed. Three biological replicates were included.

first: Filip

last: Van Nieuwerburgh

first: Dieter

last: Deforce

first: Tom

last: Coenye


title: An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior

first: Marina

last: Picciotto


title: Protospacer integration into plasmid DNA by Cas1–Cas2

city: Berkeley

first: James

last: Nunez

address: 731 Stanley Hall

institute: University of California, Berkeley

summary: We report the integration site specificity of Cas1–Cas2 into target plasmid DNA encoding a CRISPR locus. The goal of this study is to determine the effect of IHF on target site selection of Cas1–Cas2.

overall_design: Methods: After DNA integration reactions, the target plasmid products were fragmented, end-repaired, adapter ligated, PCR amplified and analyzed by Illumina sequencing. Protospacer-containing reads were selected by Cutadapt and mapped to the plasmid with Bowtie

last: Nuñez

first: Lawrence

last: Bai

first: Lucas

middle: B

last: Harrington

first: Tracey

middle: L

last: Hinder

first: Jennifer

last: Doudna


title: Transcriptomic profile of several temperate extrachromosomal actinobacteriophages during various stages of growth

city: Pittsburgh

first: Travis

last: Mavrich

state: Pennsylvania

address: 4249 Fifth Avenue

department: Biological Sciences

institute: University of Pittsburgh

summary: Several temperate actinobacteriophages have been identified that lack integration machinery and instead have genes with predicted partitioning functions. The goal of this sequencing project was to measure transcription levels of these extrachromosomal phages during different stages of their lifecycle, including lysogeny, early infection (30 minutes), and late infection (2 hours 30 minutes), in order to study which genes contribute to extrachromosomal stability.

overall_design: Total RNA was isolated from cultures grown in log phase, depleted of rRNA and prepared for sequencing using a strand-specific library kit during lysogeny, early infection (30 minutes), and late infection (2 hours 30 minutes) of phages Alma, EagleEye, Pioneer, and RedRock. A total of seven different RNA samples were prepared.

first: Graham

middle: F

last: Hatfull

first: Rebekah

middle: M

last: Dedrick

middle: N

first: Daniel

last: Russell


title: Transcriptome and translatome landscape of Streptomyces coelicolor M145

city: Daejeon

first: Yujin

last: Jeong

address: 291 Daehak-ro

country: South Korea

institute: KAIST

summary: We have integrated nucleotide resolution genome-scale measurements of the transcriptome and translatome of the Streptomyces coelicolor A3(2), the model antibiotic-producing actinomycete. Our systematic study determined 3,473 transcription start sites, leading to discovery of a high proportion (~21%) of leaderless mRNAs and 230 non-coding RNAs; this enabled deduction of promoter architecture on a genome-scale. Ribosome profiling analysis revealed that the translation efficiency was negatively correlated for secondary metabolic genes. These results provide novel fundamental insights into translational regulation of secondary metabolism that enables rational synthetic biology approaches to awaken such ‘silent’ secondary metabolic pathways.

overall_design: Profiles of primary transcripts, whole transcripts, and ribosome protected fragments (RPFs) of  Streptomyces coelicolor were generated by deep sequencing using Illumina Miseq.

first: Ji-Nu

last: Kim

first: Min

first: Giselda

last: Bucca

first: Suhyung

last: Cho

first: Yeo

last: Yoon

first: Byung-Gee

first: Sun

first: Jung-Hye

last: Roe

first: Colin

middle: P

last: Smith

first: Byung-Kwan


title: Characterizing the monocyte H3K4me3 landscape throughout development

city: Iowa City

middle: Rachelle

last: Bermick

state: IA

address: 431 Newton Road, 505 EMRB

department: Pediatrics

institute: University of Iowa

summary: Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) was then performed to establish the H3K4me3 landscape in neonatal and adult CD14+ monocytes. As development progressed from neonate to adult, monocytes gained the activating mark H3K4me3. The decreased H3K4me3 abundance at immunologically important neonatal monocyte gene promoters correlated with reduced gene expression, providing evidence that neonatal immune cells exist in an epigenetic state that is distinctly different from adults, and that this state contributes to neonatal specific immune responses.

overall_design: Examination of H3K4me3 in CD14+ monocytes in 4 experimental groups, each in triplicate: under 30 weeks gestation preterm neonate, 30-36 weeks gestation preterm neonate, over 37 weeks term neonate, adult


title: eIF4B preferentially stimulates translation of long mRNAs with structured 5’UTRs and low closed-loop potential but weak dependence on eIF4G

city: Bethesda

first: Alan

middle: G

last: Hinnebusch

state: MD

address: 6 CENTER DR Room 230, MSC 0609

institute: NICHD

summary: DEAD-box RNA helicases eIF4A and Ded1 promote translation by resolving mRNA secondary structures that impede preinitiation complex (PIC) attachment to mRNA or scanning. eIF4B is a cofactor for eIF4A but might also function independently of eIF4A. Ribosome profiling of mutants lacking eIF4B or with impaired eIF4A or Ded1 activity revealed that eliminating eIF4B reduces the relative translational efficiencies of many more genes than does inactivation of eIF4A, despite comparable reductions in bulk translation, and few genes display unusually strong requirements for both factors. However, either eliminating eIF4B or inactivating eIF4A preferentially impacts mRNAs with longer, more structured 5’UTRs. These findings reveal an eIF4A-independent role for eIF4B in addition to its function as eIF4A cofactor in promoting PIC attachment or scanning on structured mRNAs. eIF4B, eIF4A, and Ded1 mutations also preferentially impair translation of longer mRNAs in a fashion mitigated by the ability to form closed-loop mRNPs via eIF4F-Pab1 association, suggesting cooperation between closed-loop assembly and eIF4B/helicase functions. Remarkably, depleting eIF4G, the scaffold subunit of eIF4F, preferentially impacts short mRNAs with strong closed-loop potential and unstructured 5’UTRs, exactly the opposite features associated with hyperdependence on the eIF4B/helicases. We propose that short, highly efficient mRNAs preferentially depend on the stimulatory effects of eIF4G-dependent closed-loop assembly.

overall_design: We compared the effects of mutations in eIF4B on global translational efficiencies (TEs) in yeast by ribosome footprint profiling. The study includes 16 samples, comprised of 8 mRNA-Seq samples and 8 ribosome footprint profiling samples, derived from biological replicates of tif3Δ mutant strain, and the corresponding TIF3 wild-type strain . These strains were analyzed following a temperature shift at 37°C or 15°C.

first: Neelam

last: Sen

first: Fujun

last: Zhou

first: Michael

last: Harris

first: Nicholas

middle: T

last: Ingolia


title: Effects of Drought and Flooding on Herbivore-Triggered Transcriptomic Response in Solanum dulcamara

city: Nijmegen

first: Duy

last: Nguyen

address: Heyendaalseweg 135

department: Molecular Plant Physiology

country: Netherlands

institute: Radboud University

summary: We use Solanum dulcamara subjected to drought or flooding and damaged by Spodoptera exigua to analyze such interactions at multiple levels. Drought and herbivory caused comparable effects on S. dulcamara physiological response, which was reflected by a considerable overlap in S. dulcamara transcriptomic profiles. This included many defense responses and genes involved in biosynthesis of secondary metabolites that were induced by drought and herbivory but repressed by flooding. Furthermore, combination of drought and herbivory additively induced a part of these herbivore-induced responses suggesting that drought-stressed plants were more resistant. Our study provides concrete evidence of how abiotic stresses differentially affect the plant complex hormonal interactions to fine-tune plant responses to insects.

overall_design: Plants were under 3 water treatments (control, drought and flooding) for 5 days before subjected to 2 insect treatments (with 48-h herbivory by Spodoptera exigua (BAW) or without it (no)). 3 biological replicates per treatment combination, 18 in total.

first: Nunzio

last: D'Agostino

first: Nicole

last: van Dam

first: Celestina

last: Mariani

first: Ivo

last: Rieu


title: Topoisomerase 1 Regulates Gene Expression in Neurons through Cleavage Complex-Dependent and -Independent Mechanisms

city: Chapel Hill

first: Mark

last: Zylka

state: NC

address: 5109D Neuroscience Research Building

institute: University of North Carolina - Chapel Hill

summary: Topoisomerase 1 (TOP1) inhibitors, including camptothecin and topotecan, covalently trap TOP1 on DNA, creating cleavage complexes (cc’s) that must be resolved before gene transcription and DNA replication can proceed. We previously found that topotecan reduces the expression of long (>100 kb) genes and unsilences the paternal allele of Ube3a in neurons. Here, we sought to evaluate overlap between TOP1cc-dependent and -independent gene regulation in neurons. To do this, we utilized Top1 conditional knockout mice, Top1 knockdown, the CRISPR-Cas9 system to delete Top1, TOP1 catalytic inhibitors that do not generate TOP1cc’s, and a TOP1 mutation (T718A) that stabilizes TOP1cc’s. We found that topotecan treatment significantly alters the expression of many more genes, including long neuronal genes, immediate early genes, and paternal Ube3a, when compared to Top1 deletion. Our data show that topotecan has a stronger effect on neuronal transcription than Top1 deletion, and identifies TOP1cc-dependent and -independent contributions to gene expression.

overall_design: Cortical neurons from WT and Top1 conditional knockout mice, both topotecan-treated and vehicle controls, were processed in triplicate.

first: Jeremy

last: Simon

first: Angela

last: Mabb


title: dbl-1/TGF-β and daf-12/NHR signaling mediate cell-nonautonomous effects of daf-16/FOXO on starvation-induced developmental arrest

city: Durham

middle: Scott

last: Maxwell

address: 4314 FFSC

department: Biology

institute: Duke University

summary: Post-embryonic development of the nematode C. elegans is governed by nutrient availability. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor daf-16/FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that daf-16/FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by daf-16/FOXO during L1 arrest. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR steroid hormone signaling pathway, were up-regulated during L1 arrest in a daf-16/FOXO mutant. Using genetic epistasis analysis, we show that dbl-1/TGF-β and daf-12/NHR steroid hormone signaling pathways are required for the daf-16/FOXO arrest-defective phenotype, suggesting that daf-16/FOXO represses dbl-1/TGF-β and daf-36. The dbl-1/TGF-β and daf-12/NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved daf-16/FOXO mutants. Though the dbl-1/TGF-β and daf-12/NHR pathways are epistatic to daf-16/FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of daf-16/FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype, and revealing that inappropriate development during starvation does not cause the early demise of daf-16/FOXO mutants. Overall, this study shows that daf-16/FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.

overall_design: Two biological replicates of arrested L1 daf-16(mgDf50) larvae. Compare to arrested N2 larvae from GEO accession GSE33023 (Accessions GSM818545, GSM818548, and GSM818552). We used the previously processed data in the analysis of the current study.

middle: S

first: L

middle: R

last: Baugh


title: Patient-derived xenograft platform for metastatic melanoma: RNA sequencing of 4 melanoma PDX samples

city: Amsterdam

first: Oscar

last: Krijgsman

state: Outside the US or Canada

address: Plesmanlaan 121

department: Molecular Oncology and Immunology

institute: Netherlands Cancer Institute

summary: The therapeutic landscape of melanoma is rapidly changing. While targeted inhibitors yield significant responses, their clinical benefit is often limited by the early onset of drug resistance. This motivates the pursuit to establish more durable clinical responses, by developing combinatorial therapies. But while potential new combinatorial targets steadily increase in numbers, they cannot possibly all be tested in patients. Similarly, while genetically engineered mouse melanoma models have great merit, they do not capture the enormous genetic diversity and heterogeneity typical in human melanoma. Furthermore, whereas in vitro studies have many advantages, they lack the presence of micro-environmental factors, which can have a profound impact on tumor progression and therapy response. This prompted us to develop an in vivo model for human melanoma that allows for studying the dynamics of tumor progression and drug response, with concurrent evaluation and optimization of new treatment regimens. Here, we present a collection of patient-derived xenografts (PDX), derived from BRAFV600E, NRASQ61 or BRAFWT/NRASWT melanoma metastases. The BRAFV600E PDX melanomas were acquired both prior to treatment with the BRAF inhibitor vemurafenib and after resistance had occurred, including six matched pairs. We find that PDX resemble their human donors’ melanomas regarding biomarkers, chromosomal aberrations, RNA expression profiles, mutational spectrum and targeted drug resistance patterns. Mutations, previously identified to cause resistance to BRAF inhibitors, are captured in PDX derived from resistant melanomThis melanoma PDX platform represents a comprehensive public resource to study both fundamental and translational aspects of melanoma progression and treatment in a physiologically relevant setting.

overall_design: RNA sequencing of 4 melanoma PDX samples to validate the effects of a structural variant on BRAF mRNA in BRAF inhibitor resistant melanoma.

first: Kristel

last: Kemper

first: Daniel

last: Peeper


title: TRIM24 occupancy and TRIM24-dependent gene expression in prostate cancer cells

city: Boston

first: Anna

middle: C

last: Groner

state: MA

address: 450 Brookline Ave

department: Medical Oncology

institute: Dana-Farber Cancer Institute


title: Patient-derived xenograft platform for metastatic melanoma: a model for studying resistance to targeted therapy.

overall_design: Melanoma samples pre and post Vemurafenib treatment from patient and matching patient derived xenografts (PDX)


title: Myb-regulated transcriptome in pancreatic cancer

city: Mobile

first: Ajay

last: Singh

state: Alabama

address: 1660 Springhill Ave

department: Oncologic Sciences

institute: University of South Alabama Mitchell Cancer Institute

summary: To understand the global view of Myb-regulated genes and pathways in pancreatic cancer.

overall_design: Determination of differential gene expression between MYB-overexpression and -silenced pancreatic cancer cells.


title: shRNA RNA-seq from HepG2 (ENCSR998RZI)

status: Public on May 26 2016

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
shRNA knockdown against TAF15 in HepG2 cells followed by RNA-seq. (TAF15-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR997FOT)

summary:
shRNA knockdown against SUB1 in HepG2 cells followed by RNA-seq. (SUB1 BGHLV14)

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: The RNA-binding profile of Acinus, a peripheral component of the Exon junction complex, reveals its role in splicing regulation

city: Edinburgh

first: Julie

last: Rodor

address: Western General Hospital

department: MRC Human Genetics Unit

institute: University of Edinburgh

summary: Acinus (Apoptotic Chromatin Condensation Inducer in the Nucleus) is an RNA-binding protein (RBP) originally identified for its role in apoptosis. It was later found to be an auxiliary component of the Exon Junction Complex (EJC), which is deposited at exon junctions as a consequence of pre-mRNA splicing. To uncover the cellular functions of Acinus and investigate its role in splicing, we mapped its endogenous RNA targets using individual-nucleotide resolution UV-crosslinking and immunoprecipitation (iCLIP). We observed that Acinus binds to pre-mRNAs, associating specifically to a subset of suboptimal introns, but also to spliced mRNAs. We also confirmed the presence of Acinus as a peripheral factor of the EJC. RNA-seq was used to investigate changes in gene expression and alternative splicing following siRNA-mediated depletion of Acinus in HeLa cells. This analysis revealed that Acinus is preferentially required for the inclusion of specific alternative cassette exons and also controls the faithful splicing of a subset of introns. Moreover, a large number of splicing changes can be related to Acinus binding, suggesting a direct role of Acinus in exon and intron definition. In particular, Acinus regulates the splicing of DFFA/ICAD transcript, a major regulator of DNA fragmentation. Globally, the genome-wide identification of RNA targets of Acinus revealed its role in splicing regulation as well as its involvement in other cellular pathways, including cell cycle progression. Altogether, this study uncovers new cellular functions of an RBP transiently associated with the EJC

overall_design:
We performed iCLIP in triplicates in HeLa cells transfected with a T7-Acinus S* (common part of Acinus L, S and S’) or a control empty vector (pCG). Peaks present in protein coding gene regions were detected using Pyicoclip (Althammer et al, 2011) after pooling the reads from the replicates.
We carried out the iCLIP-seq of endogenous Acinus-L and Acinus-S/S’ in duplicates as well as a control iCLIP after IP with rabbit IgG in HeLa cells.
We performed RNA-Seq on polyA+ RNA isolated from HeLa cells following siRNA knockdown of all three Acinus isoforms. Knockdown was performed in triplicate using an Acinus siRNA together with three independent control experiments using a non-targeting siRNA.

first: Qun

last: Pan

first: Benjamin

middle: J

last: Blencowe

first: Eduardo

last: Eyras

first: Javier

last: Cáceres


title: Fluorescence activated cell sorting followed by small RNA sequencing reveals stable microRNA expression during cell cycle progression

first: Vince

last: Grolmusz


title: Evolutionary origin and functional divergence of stem cell homeobox genes in eutherian mammals

city: Oxford

first: Thomas

last: Dunwell

address: South Parks Road

department: Zoology

institute: University of Oxford

summary: We individually examined the ability of human ARGFX, DPRX, LEUTX, and TPRX1 to regulate gene expression by ectopically expressing these proteins in fibroblasts.

overall_design: Each gene along with an empty control vector were transfected individually to drive ectopic expression in human dermal fibroblasts, in triplicate.

first: Ignacio

last: Maeso

first: Peter

middle: W

last: Holland


title: shRNA RNA-seq from HepG2 (ENCSR995ZGJ)

summary:
shRNA knockdown against SMNDC1 in HepG2 cells followed by RNA-seq. (SMNDC1 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR961YAG)

summary:
shRNA knockdown against EIF4A3 in K562 cells followed by RNA-seq. (EIF4A3-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR957EEG)

summary:
shRNA knockdown against EIF4A3 in HepG2 cells followed by RNA-seq. (EIF4A3-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR952RRH)

summary:
shRNA knockdown against IGF2BP2 in K562 cells followed by RNA-seq. (IGF2BP2-LV11)

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: shRNA RNA-seq from K562 (ENCSR961WVL)

summary:
shRNA knockdown against DDX21 in K562 cells followed by RNA-seq. (DDX21-LV11)

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: shRNA RNA-seq from K562 (ENCSR947OIM)

summary:
shRNA knockdown against RBM22 in K562 cells followed by RNA-seq. (RBM22-LV11)

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: Whole organism lineage tracing by combinatorial and cumulative genome editing

city: Seattle

first: Jay

last: Shendure

state: Wa

address: 6528 19th Avenue NE

department: Genome Sciences

institute: University of Washington

type: Genome variation profiling by high throughput sequencing

summary: Multicellular systems develop from single cells through a lineage, but current lineage tracing approaches scale poorly to whole organisms. Here we use genome editing to progressively introduce and accumulate diverse mutations in a DNA barcode over multiple rounds of cell division. The barcode, an array of CRISPR/Cas9 target sites, records lineage relationships in the patterns of mutations shared between cells. In cell culture and zebrafish, we show that rates and patterns of editing are tunable, and that thousands of lineage-informative barcode alleles can be generated. By sampling hundreds of thousands of cells from individual zebrafish, we find that most cells in adult zebrafish organs derive from relatively few embryonic progenitors. Genome editing of synthetic target arrays for lineage tracing (GESTALT) will help generate large-scale maps of cell lineage in multicellular systems.

sample_organism:
Danio rerio
Homo sapiens

platform_organism:
Danio rerio
Homo sapiens

overall_design: The GESTALT lineage tracing barcode was introduced into human cell culture (HEK293T) or the Danio rerio model organism. Mutations in this barcode, introduced by the CRISPR/Cas9 system, persist through cell divisions, and provide a means to trace the shared lineage of cells.  These compact barcodes were read out by sequencing either the RNA or DNA of specific cell populations. Specifics of the protocol can found in the accompanying citation.The GESTALT lineage tracing barcode was introduced into human cell culture (HEK293T) or the Danio rerio model organism. Mutations in this barcode, introduced by the CRISPR/Cas9 system, persist through cell divisions, and provide a means to trace the shared lineage of cells.  These compact barcodes were read out by sequencing either the RNA or DNA of specific cell populations. Specifics of the protocol can found in the accompanying citation.

first: Aaron

last: McKenna

first: Gregory

last: Findlay

first: James

middle: A

last: Gagnon

first: Marshall

last: Horwitz

first: Alexander

last: Schier


title: shRNA RNA-seq from HepG2 (ENCSR939ZRA)

summary:
shRNA knockdown against RDBP in HepG2 cells followed by RNA-seq. (RDBP-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR916WOI)

summary:
shRNA knockdown against TRA2A in K562 cells followed by RNA-seq. (TRA2A-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR914WQV)

summary:
shRNA knockdown against CSTF2T in HepG2 cells followed by RNA-seq. (CSTF2T BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR913CAE)

summary:
Control shRNA against no target in K562 cells followed by RNA-seq. (Nontarget-LV08)

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: shRNA RNA-seq from K562 (ENCSR895BTE)

summary:
shRNA knockdown against CPSF6 in K562 cells followed by RNA-seq. (CPSF6-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR906WTM)

summary:
shRNA knockdown against RTF1 in HepG2 cells followed by RNA-seq. (RTF1 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR904CJQ)

summary:
shRNA knockdown against U2AF2 in K562 cells followed by RNA-seq. (U2AF2-LV08)

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: shRNA RNA-seq from K562 (ENCSR904BCZ)

summary:
shRNA knockdown against RAVER1 in K562 cells followed by RNA-seq. (RAVER1-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR850CKU)

summary:
shRNA knockdown against KHSRP in HepG2 cells followed by RNA-seq. (KHSRP-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR849STR)

summary:
shRNA knockdown against MAGOH in K562 cells followed by RNA-seq. (MAGOH-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR861ENA)

summary:
shRNA knockdown against EIF2S1 in HepG2 cells followed by RNA-seq. (EIF2S1-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR853ZJS)

summary:
shRNA knockdown against HNRNPK in HepG2 cells followed by RNA-seq. (HNRNPK-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR906RHU)

summary:
shRNA knockdown against SRSF5 in K562 cells followed by RNA-seq. (SRSF5-41-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR778AJO)

summary:
shRNA knockdown against EIF3G in HepG2 cells followed by RNA-seq. (EIF3G BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR792XFP)

summary:
shRNA knockdown against MATR3 in K562 cells followed by RNA-seq. (MATR3-06-LV11)

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: shRNA RNA-seq from K562 (ENCSR792CBM)

summary:
shRNA knockdown against G3BP1 in K562 cells followed by RNA-seq. (G3BP1-LV11)

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: shRNA RNA-seq from K562 (ENCSR780YFF)

summary:
shRNA knockdown against FXR1 in K562 cells followed by RNA-seq. (FXR1-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR746EKS)

summary:
shRNA knockdown against MAGOH in HepG2 cells followed by RNA-seq. (MAGOH-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR945UYL)

summary:
shRNA knockdown against G3BP2 in HepG2 cells followed by RNA-seq. (G3BP2-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR840QFR)

summary:
shRNA knockdown against DAZAP1 in HepG2 cells followed by RNA-seq. (DAZAP1 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR708GKW)

summary:
shRNA knockdown against IGF2BP1 in HepG2 cells followed by RNA-seq. (IGF2BP1 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR774BXV)

summary:
shRNA knockdown against EIF4B in K562 cells followed by RNA-seq. (EIF4B-LV08)

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: shRNA RNA-seq from K562 (ENCSR648QFY)

summary:
shRNA knockdown against PCBP2 in K562 cells followed by RNA-seq. (PCBP2-LV11)

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: shRNA RNA-seq from K562 (ENCSR694LKY)

summary:
shRNA knockdown against TIA1 in K562 cells followed by RNA-seq. (TIA1-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR637JLM)

summary:
shRNA knockdown against DDX3X in HepG2 cells followed by RNA-seq. (DDX3X-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR927JXU)

summary:
shRNA knockdown against FUS in HepG2 cells followed by RNA-seq. (FUS BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR732IYM)

summary:
shRNA knockdown against XRCC5 in HepG2 cells followed by RNA-seq. (XRCC5 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR627NVU)

summary:
shRNA knockdown against RBM15 in K562 cells followed by RNA-seq. (RBM15-LV08)

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: WGBS from H1-hESC (ENCSR617FKV)

summary:
HAIB Whole Genome Bisulfite Sequencing H1-hESC

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: shRNA RNA-seq from HepG2 (ENCSR603TCV)

summary:
Control shRNA against no target in HepG2 cells followed by RNA-seq. (NT-BGHLV12-93-94)

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: shRNA RNA-seq from HepG2 (ENCSR610AEI)

summary:
shRNA knockdown against RBM25 in HepG2 cells followed by RNA-seq. (RBM25-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR611ZAL)

summary:
shRNA knockdown against TAF15 in K562 cells followed by RNA-seq. (TAF15-LV08)

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: shRNA RNA-seq from K562 (ENCSR629EWX)

summary:
shRNA knockdown against IGF2BP1 in K562 cells followed by RNA-seq. (IGF2BP1-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR597XHH)

summary:
shRNA knockdown against SRSF9 in HepG2 cells followed by RNA-seq. (SRSF9-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR622MCX)

summary:
shRNA knockdown against U2AF2 in HepG2 cells followed by RNA-seq. (U2AF2 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR576GOW)

summary:
shRNA knockdown against RAVER1 in HepG2 cells followed by RNA-seq. (RAVER1 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR577XBW)

summary:
shRNA knockdown against FXR2 in K562 cells followed by RNA-seq. (FXR2-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR716WZH)

summary:
shRNA knockdown against FASTKD2 in HepG2 cells followed by RNA-seq. (FASTKD2 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR597IYB)

summary:
shRNA knockdown against EXOSC9 in HepG2 cells followed by RNA-seq. (EXOSC9 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR572AMC)

summary:
shRNA knockdown against RECQL in HepG2 cells followed by RNA-seq. (RECQL-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR561CBC)

summary:
shRNA knockdown against KHSRP in K562 cells followed by RNA-seq. (KHSRP-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR635FRH)

summary:
shRNA knockdown against PCBP1 in HepG2 cells followed by RNA-seq. (PCBP1-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR545AIK)

summary:
shRNA knockdown against PCBP1 in K562 cells followed by RNA-seq. (PCBP1-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR529QEZ)

summary:
shRNA knockdown against PRPF6 in HepG2 cells followed by RNA-seq. (PRPF6 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR529JNJ)

summary:
shRNA knockdown against HNRNPK in K562 cells followed by RNA-seq. (HNRNPK-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR533HXS)

summary:
shRNA knockdown against EIF2C1 in HepG2 cells followed by RNA-seq. (EIF2C1 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR546MBH)

summary:
shRNA knockdown against EIF2S1 in K562 cells followed by RNA-seq. (EIF2S1-LV08)

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: shRNA RNA-seq from K562 (ENCSR560AYQ)

summary:
shRNA knockdown against RBM34 in K562 cells followed by RNA-seq. (RBM34-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR500WHE)

summary:
shRNA knockdown against XRCC6 in HepG2 cells followed by RNA-seq. (XRCC BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR492UFS)

summary:
shRNA knockdown against MATR3 in HepG2 cells followed by RNA-seq. (MATR3 17-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR491FOC)

summary:
Control shRNA against no target in HepG2 cells followed by RNA-seq. (NT BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR485ZTC)

summary:
shRNA knockdown against DDX21 in HepG2 cells followed by RNA-seq. (DDX21 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR527IVX)

summary:
shRNA knockdown against PTBP1 in K562 cells followed by RNA-seq. (PTBP1-LV11)

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: shRNA RNA-seq from K562 (ENCSR464ADT)

summary:
shRNA knockdown against SRSF7 in K562 cells followed by RNA-seq. (SRSF7-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR455VZH)

summary:
shRNA knockdown against PABPC4 in HepG2 cells followed by RNA-seq. (PABPC4-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR424YSV)

summary:
shRNA knockdown against AATF in HepG2 cells followed by RNA-seq. (AATF BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR410UHJ)

summary:
shRNA knockdown against RPS10 in HepG2 cells followed by RNA-seq. (RPS10 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR373KOF)

summary:
shRNA knockdown against FUBP3 in K562 cells followed by RNA-seq. (FUBP3-LV08)

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: microRNA-seq from H1-hESC (ENCSR430YFL)

summary:
miRNA-seq on human H1-hESC

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: shRNA RNA-seq from K562 (ENCSR344XID)

summary:
Control shRNA against no target in K562 cells followed by RNA-seq. (nontarget-LV08)

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: shRNA RNA-seq from K562 (ENCSR338CON)

summary:
shRNA knockdown against AKAP1 in K562 cells followed by RNA-seq. (AKAP1-LV08)

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: shRNA RNA-seq from K562 (ENCSR361LBE)

summary:
shRNA knockdown against NCBP2 in K562 cells followed by RNA-seq. (NCBP2-LV08)

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: shRNA RNA-seq from K562 (ENCSR342EDG)

summary:
shRNA knockdown against U2AF1 in K562 cells followed by RNA-seq. (U2AF1-LV08)

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: WGBS from skeletal muscle myoblast (ENCSR328TBS)

summary:
HAIB Whole Genome Bisulfite Sequencing HSMM

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: shRNA RNA-seq from HepG2 (ENCSR313CHR)

summary:
shRNA knockdown against EIF4B in HepG2 cells followed by RNA-seq. (EIF4B-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR310VND)

summary:
shRNA knockdown against RECQL in K562 cells followed by RNA-seq. (RECQL-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR330YOU)

summary:
shRNA knockdown against QKI in HepG2 cells followed by RNA-seq. (QKI-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR300IEW)

summary:
shRNA knockdown against DDX24 in HepG2 cells followed by RNA-seq. (DDX24 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR253DCB)

summary:
shRNA knockdown against ASCC1 in K562 cells followed by RNA-seq. (ASCC1-LV08)

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: shRNA RNA-seq from K562 (ENCSR831YGP)

summary:
shRNA knockdown against EWSR1 in K562 cells followed by RNA-seq. (EWSR1-LV08)

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: shRNA RNA-seq from K562 (ENCSR256PLH)

summary:
shRNA knockdown against QKI in K562 cells followed by RNA-seq. (QKI-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR295XKC)

summary:
shRNA knockdown against GTF2F1 in HepG2 cells followed by RNA-seq. (GTF2F1 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR478FJK)

summary:
shRNA knockdown against IGF2BP2 in HepG2 cells followed by RNA-seq. (IGF2BP2-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR302JQA)

summary:
shRNA knockdown against IGF2BP3 in K562 cells followed by RNA-seq. (IGF2BP3-LV11)

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: shRNA RNA-seq from K562 (ENCSR246SOU)

summary:
shRNA knockdown against G3BP2 in K562 cells followed by RNA-seq. (G3BP2-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR230ORC)

summary:
shRNA knockdown against CIRBP in HepG2 cells followed by RNA-seq. (CIRBP-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR237YZT)

summary:
Control shRNA against no target in HepG2 cells followed by RNA-seq. (NT-BGHLV12-01-02)

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: shRNA RNA-seq from HepG2 (ENCSR193FFA)

summary:
shRNA knockdown against ASCC1 in HepG2 cells followed by RNA-seq. (ASCC1-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR149DMY)

summary:
shRNA knockdown against RBM25 in K562 cells followed by RNA-seq. (RBM25-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR398LZW)

summary:
shRNA knockdown against SND1 in HepG2 cells followed by RNA-seq. (SND1 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR148MQK)

summary:
shRNA knockdown against SF3B4 in HepG2 cells followed by RNA-seq. (SF3B4-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR185JGT)

summary:
shRNA knockdown against SLTM in HepG2 cells followed by RNA-seq. (SLTM BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR134JRE)

summary:
shRNA knockdown against TARDBP in K562 cells followed by RNA-seq. (TARDBP-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR147ZBD)

summary:
shRNA knockdown against DDX6 in HepG2 cells followed by RNA-seq. (DDX6-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR129RWD)

summary:
Control shRNA against no target in K562 cells followed by RNA-seq. (Nontarget-LV11)

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: shRNA RNA-seq from K562 (ENCSR113HRG)

summary:
shRNA knockdown against SRSF9 in K562 cells followed by RNA-seq. (SRSF9-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR094KBY)

summary:
shRNA knockdown against SRSF1 in HepG2 cells followed by RNA-seq. (SRSF1-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR318HAT)

summary:
shRNA knockdown against RBM34 in HepG2 cells followed by RNA-seq. (RBM34 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR081QQH)

summary:
shRNA knockdown against ZRANB2 in HepG2 cells followed by RNA-seq. (ZRANB2 BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR074UZM)

summary:
shRNA knockdown against G3BP1 in HepG2 cells followed by RNA-seq. (G3BP1-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR079IPT)

summary:
shRNA knockdown against TBRG4 in K562 cells followed by RNA-seq. (TBRG4-LV08)

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: shRNA RNA-seq from K562 (ENCSR119QWQ)

summary:
shRNA knockdown against DDX6 in K562 cells followed by RNA-seq. (DDX6-LV08)

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: shRNA RNA-seq from HepG2 (ENCSR064DXG)

summary:
shRNA knockdown against PTBP1 in HepG2 cells followed by RNA-seq. (PTBP1-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR057GCF)

summary:
shRNA knockdown against TIA1 in HepG2 cells followed by RNA-seq. (TIA1-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR066VOO)

summary:
shRNA knockdown against SRSF1 in K562 cells followed by RNA-seq. (SRSF1-LV11)

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: shRNA RNA-seq from K562 (ENCSR056QEW)

summary:
shRNA knockdown against CIRBP in K562 cells followed by RNA-seq. (CIRBP-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR030ARO)

summary:
shRNA knockdown against NCBP2 in HepG2 cells followed by RNA-seq. (NCBP2-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR030GZQ)

summary:
shRNA knockdown against TRA2A in HepG2 cells followed by RNA-seq. (TRA2A BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR017PRS)

summary:
shRNA knockdown against SRSF7 in HepG2 cells followed by RNA-seq. (SRSF7-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR010ZMZ)

summary:
shRNA knockdown against HLTF in HepG2 cells followed by RNA-seq. (HLTF BGHLV14)

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: shRNA RNA-seq from HepG2 (ENCSR016IDR)

summary:
shRNA knockdown against AKAP1 in HepG2 cells followed by RNA-seq. (AKAP1-BGHLV12)

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: shRNA RNA-seq from HepG2 (ENCSR003EKR)

summary:
Control shRNA against no target in HepG2 cells followed by RNA-seq. (NT BGHLV14 1)

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: shRNA RNA-seq from HepG2 (ENCSR009PPI)

summary:
shRNA knockdown against FXR1 in HepG2 cells followed by RNA-seq. (FXR1-BGHLV12)

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: shRNA RNA-seq from K562 (ENCSR201WFU)

summary:
shRNA knockdown against RDBP in K562 cells followed by RNA-seq. (RDBP-LV11)

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: shRNA RNA-seq from HepG2 (ENCSR028ITN)

summary:
shRNA knockdown against PCBP2 in HepG2 cells followed by RNA-seq. (PCBP2 BGHLV14)

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: shRNA RNA-seq from K562 (ENCSR000KYM)

summary:
shRNA knockdown against DDX3X in K562 cells followed by RNA-seq. (DDX3X-LV08)

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: shRNA RNA-seq from K562 (ENCSR047EEG)

summary:
shRNA knockdown against PABPC4 in K562 cells followed by RNA-seq. (PABPC4-LV08)

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: Transcriptome-wide mRNA alterations in Streptozotocin induced Type I diabetic mouse heart

city: Galveston

first: Muge

last: Kuyumcu-Martinez

state: TX

address: 301 University Blvd

department: Biochemistry and Molecular Biology

institute: University of Texas Medical Branch

summary: We sequenced mRNA from Left Ventricles of Streptozotocin induced Type I diabetic mouse hearts or mock treated controls at 4 weeks post-treatment in order to assess alternative splicing changes.

overall_design: Heart mRNA profiles of Control and Diabetic (STZ:T1D) mice were generated by deep sequencing using Illumina HiSeq 1000.

first: Gene

last: Yeo


title: Active and inactive enhancers co-operate to exert localized and long-range control of gene regulation [ChIP-seq]

city: New York

first: Jane

last: Skok

state: NY

address: 550 First Ave, Smillow 307

institute: NYU

summary: We report that in developing B cells individual enhancers of Igk make up super-enhancer cluster where contacts between its components rely on all constituents. Reduction of interaction frequency in enhancer knock-out cells is associated with deminished transcriptional output of enhancers and Igk locus. Moreover, we find that Igk enhancer MiEk has an effect on levels of CBFb enrichment on Tcrb enhancer, Eb afffecting Tcrb recombination and T cell development.

overall_design: Examination of expression, chromatin accessibility, histone modifications and nuclear organization in developing wild-type and Igk and Tcrb enhancer deficient B and T lymphocytes.

first: Valentina

last: Snetkova


title: shRNA RNA-seq from K562 (ENCSR081XRA)

first: ENCODE

last: DCC

summary:
shRNA knockdown against SF3B4 in K562 cells followed by RNA-seq. (SF3B4-LV08)

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: Active and inactive enhancers co-operate to exert localized and long-range control of gene regulation

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

overall_design: Refer to individual Series


title: Active and inactive enhancers co-operate to exert localized and long-range control of gene regulation [ATAC-seq]


title: shRNA RNA-seq from K562 (ENCSR067LLB)

summary:
shRNA knockdown against DDX24 in K562 cells followed by RNA-seq. (DDX24-LV08)

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: Active and inactive enhancers co-operate to exert localized and long-range control of gene regulation [4C-seq]


title: Expression profiling of MCF-7 cells with 10nM treatment of TCDD

city: Huntington

last: Denvir

state: WV

address: One John Marshall Drive

department: Biochemistry and Microbiology

institute: Marshall University School of Medicine

summary: The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that is regulated by environmental toxicants that function as AHR agonists such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD).  L-Type Amino Acid Transporter 1 (LAT1) is a leucine uptake transporter that is overexpressed in cancer.  The regulation of LAT1 by AHR in MCF-7 and MDA-MB-231 breast cancer cells (BCCs) was investigated in this report.  Ingenuity pathway analysis (IPA) revealed a significant association between TCDD-regulated genes (TRGs) and molecular transport.  Overlapping the TCDD-RNA-Seq dataset in this report with a published TCDD-ChIP-seq dataset identified that LAT1 was a direct TCDD/AHR gene target.  Short interfering RNA (siRNA)-directed knockdown of AHR confirmed that TCDD-stimulated increases in LAT1 mRNA and protein required AHR.  TCDD-stimulated increases in LAT1 mRNA was also inhibited by the AHR antagonist CH-223191.  Upregulation of LAT1 by TCDD coincided with increases in leucine uptake by MCF-7 cells in response to TCDD.  Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) assays revealed increases in AHR, AHR nuclear translocator (ARNT) and p300 binding and histone H3 acetylation at an AHR binding site in the LAT1 gene in response to TCDD.  In MDA-MB-231 cells, which exhibit high levels of endogenous AHR activity, the levels of endogenous LAT1 mRNA and protein were reduced in response to knockdown of AHR with AHR-siRNA.  The regulation of LAT1 by AHR stimulated MDA-MB-231 proliferation.  Collectively, these findings have provided a deeper mechanistic understanding of extrinsic and intrinsic regulation of LAT1 by AHR.

overall_design: Expression profiling of four replicates of MCF-7 cells treated with 10nM TCDD were compared to expression profiles of four control replicates of MCF-7 cells treated with DMSO by RNA-Seq

first: Travis

last: Salisbury

first: Justin

middle: K

last: Tomblin

first: Subha

last: Arthur

first: Donald

last: Primerano

first: Ateeq

last: Chaudhry

first: Jun

last: Fan


title: Evx1 is required to regulate appropriate anterior-posterior patterning during murine gastrulation

city: Brisbane

first: Charles

middle: Cameron

last: Bell

state: Queensland

address: 37 Kent Street

country: Australia

institute: Mater Research

summary: We generated loss of function mESC clones by CRISPR-Cas9 to test the function of Evx1 during gastrulation. Evx1Δfs Clone 14 mESCs were differentiated to D4 in serum and compared to unedited mESCs

overall_design: Three side by side differentiations (replicates) were performed and sequenced for both the Evx1Δfs Clone 14 mESCs and the WT mESCs. Each side by side differentiation was set up on a different day.

first: Graham

last: Magor

first: Marcel

middle: E

last: Dinger

first: Andrew

last: Perkins


title: Molecular mechanisms of global DNA demethylation to naïve pluripotency in ESC

city: Cambridge

first: Felix

last: Krueger

address: Granta Park

department: Bioinformatics

institute: Altos Labs

summary: Global demethylation is part of a conserved program of epigenetic reprogramming to naïve pluripotency. The transition from primed hypermethylated embryonic stem cells (ESCs) to naïve hypomethylated ones (serum-to-2i) is a valuable model system for epigenetic reprogramming. We present a mathematical model, which accurately predicts global DNA demethylation kinetics. Experimentally we show that the main drivers of global demethylation are neither active mechanisms (Aicda, Tdg, Tet1-3) nor the reduction of de novo methylation. UHRF1 protein, the essential targeting factor for DNMT1, is reduced upon transit to 2i and so is recruitment of the maintenance methylation machinery to replication foci. Concurrently there is global loss of H3K9me2, which is needed for chromatin binding of UHRF1. These mechanisms synergistically enforce global DNA hypomethylation in a replication-coupled fashion. Our observations establish the molecular mechanism for global demethylation in naïve ESCs, which has key parallels with those operating in primordial germ cells and early embryos.

overall_design: mRNA-seq, RRBS-seq and ChIPSeq of different time-points during serum to 2i conversion of mouse ESCs

first: Ferdinand

last: von Meyenn

first: Mario

last: Iurlaro

first: Edoardo

last: Petrini

first: Wolf

last: Reik


title: Evx1as does not have a function independent of Evx1 during gastrulation

summary: We generated loss of function mESC clones by CRISPR-Cas9 to test whether Evx1as has a function beyond that of Evx1. Evx1/Evx1asΔ2.6kb (Del#3) mESCs were differentiated to D4 in serum and compared directly to Evx1Δfs mESCs

overall_design: Three side by side differentiations (replicates) were performed and sequenced for both the Del3 (Evx1/Evx1asΔ2.6kb) mESCs and the Evx1Δfs Clone 14 mESCs. Each side by side differentiation was set up on a different day.


title: Nova HITS-CLIP and RNA-Seq in mouse cortex

first: Yuhki

last: Saito

address: 1230 York avenue

institute: The Rockefeller University


title: Transcription Profiles of Regulatory T Cells in Follicular Lymphoma Lymph Nodes, Normal Lymph Nodes and Reactive Lymph Nodes

city: Birmingham

first: Alexander

last: Rosenberg

address: 1720 2nd Avenue South, Suite 276/11

institute: University of Alabama at Birmingham

summary: We have previously shown that Tregs infiltrating follicular lymphoma lymph nodes (FLN) are quantitatively and qualitatively different than those infiltrating normal and reactive nodes (NLN, RLN, respectively). To gain insight into how such Treg populations differ, we performed RNA sequence (RNAseq) analyses on flow sorted Tregs from all three sources. We identify several molecules that could contribute to the observed increased suppressive capacity of FLN tregs, including upregulation of CTLA-4, IL-10, and GITR, all confirmed by protein expression. In addition, we identify, and confirm functionally, a novel mechanism by which Tregs target to and accumulate within a human tumor microenvironment, through the down regulation of S1PR1, SELL (L-selectin) and CCR7, potentially resulting in greater lymph node retention. In addition we identify and confirm functionally the upregulation of CXCR5, CXCL13 and IL-16 demonstrating the unique ability of the follicular derived Tregs to localize and accumulate within not only the malignant lymph node, but also localize and accumulate within the malignant B cell follicle itself. Such findings offer significant new insights into how FLN Tregs may contribute to the biology of follicular lymphoma and identify several novel therapeutic targets.

overall_design: Cross sectional comparison of transcription profiles of human regulatory T cells from normal lymph nodes (n=10), follicular lymphoma lymph nodes (n=12) and reactive lymph nodes (n=5).

first: Hristina

last: Nedelkovska

middle: F

first: Shannon

last: Hilchey

first: Ollivier

last: Hyrien

first: W

last: Burack

first: Sally

last: Quataert

first: Christina

last: Baker

first: Mitra

last: Azadniv

first: Stephen

middle: L

last: Welle

last: Ansell

first: Minsoo

last: Kim

first: Steven

middle: H

last: Bernstein


title: RNAseq in E18.5 wild-type, Nova2-KO, and Nova1-KO mouse cortex and mid- and hind-brain

summary: We sequenced mRNA from E18.5 mouse cortex (3 wild-type vs 3 Nova2-/- and 3 wild-type vs 3 Nova1-/-) and from E18.5 mouse mid- and hind-brain (3 wild-type vs 3 Nova1-/-) to compare gene expression level and alternative splicing events between wild-type and Nova mutant mice.

overall_design: Mouse cortex or mid- and hind-brain mRNA profiles of embryonic 18.5 day wild type (WT), Nova2-/-, and Nova1-/- mice were generated by deep sequencing using Illumina Hiseq2500.

first: Robert

middle: B

last: Darnell


title: RNA-Seq identifies differential gene expression associated with risk-genotype for Rhodococcus equi pneumonia in horses

status: Public on May 25 2016

city: College Station

first: Cole

middle: M

last: McQueeen

address: 4467 VMRB

institute: Texas A&M University

summary: Rhodococcus equi is an intracellular bacterium that affects young foals and immuno-compromised individuals causing severe pneumonia.  Currently, the genetic mechanisms which confer susceptibility and or resistance to R. equi are not fully understood.  Previously, using a SNP-based genome-wide association study, we identified a region on equine chromosome 26 associated with clinical pneumonia.  To better characterize this region and understand the relationship of the SNPs associated with disease, we performed RNA-Seq on 12 horses representing the 3 allelic states of the SNP identified.  Differential expression analyses identified differentially expressed genes in the innate immune response pathway when comparing homozygous A allele horses with the AB and BB horses.  Isoform analyses of the RNA-Seq data predicted multiple transcripts with evidence of differential expression to exist at the TRPM2 locus.  This finding is consistent with previously demonstrated work in human cell lines in which isoform specific expression of TRPM2 was critical to cell viability.  This work demonstrates that SNPs in TRPM2 are associated with differences in gene expression, suggesting that modulation of expression of this innate immune gene contributes to susceptibility to R. equi pneumonia.

overall_design: Analysis of RNA expression derived from 3 genotypes

last: McQueen

first: Canaan

last: Whitfield-Cargile

first: Kranti

last: Konganti

first: Glenn

middle: P

last: Blodgett

first: Scott

middle: V

last: Dindot

first: Noah

middle: D

last: Cohen


title: Patient-derived xenograft platform for metastatic melanoma

first: Oscar

last: Krijgsman


title: The role of Set7 in differentiation of embryonic stem cells to smooth muscle cells

city: Melbourne

first: Mark

last: Ziemann

state: VIC

address: 85 Commercial Rd

department: Bioinformatics Working Group

institute: Burnet Institute

summary: We performed transcriptome profiling of mouse embryonic stem cells, Stem cell antigen1 (Sca1) cells, and Sca1 cells with shRNA knock-down of Set7.

overall_design: 4 sample groups, each with 2 replicates. (1) untreated embryonic stem cells, (2) untreated Sca1 cells, (3) Sca1 cells with Set7 shRNA knock-down, (4) Sca1 cells with non targeting control plasmid

first: Natasha

last: Tuano

first: Jun

last: Okabe

first: Assam

last: El-Osta

last: Cooper


title: Transcriptome of RA-responsive and RA-resistant breast cancer cell lines

city: Illkirch Cedex

first: Cecile

last: Rochette-Egly

address: 1 rue Laurent Fries

department: functional genomics and cancer

country: France

institute: IGBMC

summary: Retinoic acid (RA), the main active vitamin A metabolite, controls multiple biological processes such as cell proliferation and differentiation through genomic programs and kinase cascades activation. Several breast cancer cells respond to the antiproliferative effects of RA, but others are RA-resistant. In several cases resistance has been correlated to the amplification of the erb-b2 receptor tyrosine kinase 2 (ERBB2) gene, but the overall signaling and transcriptional pathways that are altered in such cells have not been elucidated. Here we compared two human breast cancer cell lines, the MCF7 cell line, which responds to the antiproliferative action of RA and the BT474 cell line, which is RA-resistant subsequent to ERBB2 amplification in a large-scale analysis of the phosphoproteins and in a genome-wide analysis of the RA-regulated genes. Using high-resolution nano-LC-LTQ-Orbitrap mass spectrometry associated to phosphopeptide enrichment, we found that several proteins involved in signaling and in transcription, are differentially phosphorylated after RA addition. The paradigm of these proteins is the RA receptor α (RARα), which was phosphorylated in MCF7 cells but not in BT474 cells. The panel of the RA-regulated genes was also different. Overall our results indicate that ERBB2 amplification interferes with the ability of RA to activate kinases with consequences on the phosphorylation of several proteins involved in transcription and thus on gene expression.

overall_design: Two human breast cancer cell lines were compared for their repertoire of genes regulated by retinoic acid (RA): the RA sensitive MCF7 cell line and the RA resistant B7474 cell line

first: Marilyn

last: Carrier


title: Regulation of normal B cell differentiation and malignant B cell survival by OCT2 (ChIP-Seq)

city: Bethesda

first: Louis

middle: M.

last: Staudt

address: 9000 Rockville Pike, Bldg 10, Rm 4N114

department: Lymphoid Malignancies Branch

institute: National Cancer Institute

summary: The requirement for the B cell transcription factor OCT2 (encoded by Pou2f2) in germinal center B cells has proved controversial. Here, we report that germinal center B cells are formed normally after depletion of OCT2 in a conditional knockout mouse but that their proliferation is reduced and in vivo differentiation to antibody-secreting plasma cells is blocked. This led us to examine the role of OCT2 in germinal center derived lymphomas. ShRNA knockdown showed that almost all DLBCL cell lines are addicted to the expression of OCT2 and its co-activator OCA-B. Genome-wide chromatin Immunoprecipitation analysis and gene expression profiling revealed the broad transcriptional program regulated by OCT2 that includes the expression of STAT3, IL10, ELL2, XBP1, MYC, TERT and ADA. Importantly, genetic alteration of OCT2 is not a requirement for cellular addiction in DLBCL. However, we detected amplifications of the POU2F2 locus in DLBCL tumor biopsies as well as a recurrent mutation of threonine 223 in the DNA binding domain of OCT2. This neomorphic mutation subtly alters the DNA binding preference of OCT2 leading to the transactivation of novel target genes including HIF1a and FCRL3. Finally, by introducing mutations designed to disrupt the OCT2-OCA-B interface we reveal a requirement for this protein-protein interface that might ultimately be exploited therapeutically. Our findings, combined with the predominantly B cell restricted expression of OCT2 and the absence of systemic phenotype in our knockout mice, suggest that an OCT2-targeted therapeutic strategy would be efficacious in both major subtypes of DLBCL whilst avoiding systemic toxicity.

overall_design: To identify gene targets of OCT2 and OCA-B, we performed genome-wide chromatin immunoprecipitation analysis (ChIP-Seq) in the HBL1 ABC DLBCL line (n=6). To test whether the T223A mutant isoform alters OCT2 DNA binding, we designed "Biotag" constructs that express either wild type or T223A OCT2 fused to a peptide sequence that can be biotinylated by the bacterial enzyme BirA. We engineered the DLBCL cell line BJAB to express BirA, transduced the cells with the OCT2 Biotag constructs, and performed ChIP-seq (n=3) using streptavidin to purify chromatin bound to these OCT2 isoforms.