title: ChIP-seq from induced pluripotent stem cell (ENCSR655HDE)

summary:
Chip-Seq on PGP1 iPSC-human (fragmentation date:2015-09-03)

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


title: ChIP-seq from neural cell (ENCSR654VRX)

status: Public on Mar 12 2017

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

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


title: ChIP-seq from HepG2 (ENCSR656JZL)

summary:
Chip-Seq on HepG2

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


title: ChIP-seq from K562 (ENCSR668LDD)


title: ChIP-seq from esophagus squamous epithelium (ENCSR652EPR)


title: ChIP-seq from HepG2 (ENCSR649FPL)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 07-22-13)

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


title: ChIP-seq from cardiac muscle cell (ENCSR652QNW)


title: ChIP-seq from Loucy (ENCSR648HLP)


title: ChIP-seq from Loucy (ENCSR657RRI)


title: ChIP-seq from MCF-7 (ENCSR639RHG)


title: ChIP-seq from K562 (ENCSR642VZY)

summary:
ChIP-Seq on K562-human

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


title: ChIP-seq from HepG2 (ENCSR633UAP)

summary:
Chip-Seq on HepG2-human (fragmentation date:2015-08-12

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


title: ChIP-seq from smooth muscle cell (ENCSR651JDA)


title: ChIP-seq from HepG2 (ENCSR639IIZ)


title: ChIP-seq from neural progenitor cell (ENCSR645BCH)


title: ChIP-seq from thyroid gland (ENCSR639NMN)


title: ChIP-seq from hepatocyte (ENCSR637RLN)


title: ChIP-seq from HepG2 (ENCSR654ORQ)


title: ChIP-seq from OCI-LY3 (ENCSR629TDG)


title: ChIP-seq from liver (ENCSR628ONI)

summary:
Chip-Seq on STL011-human (fragmentation date: 2014-09-15)

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


title: ChIP-seq from GM12878 (ENCSR626VUC)

summary:
ETV6 ChIP-seq on human GM12878

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


title: ChIP-seq from K562 (ENCSR633EIC)

summary:
Chip-Seq on K562

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


title: ChIP-seq from gastrocnemius medialis (ENCSR775IMI)


title: ChIP-seq from H9 (ENCSR625CEM)


title: ChIP-seq from liver (ENCSR621CSR)

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

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


title: ChIP-seq from vagina (ENCSR620XWM)


title: ChIP-seq from MCF-7 (ENCSR610GTD)

summary:
Reverse Crosslink Control ChIP-seq on human MCF-7 (fragmentation date 02-24-14)

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


title: ChIP-seq from DOHH2 (ENCSR623GZY)


title: ChIP-seq from HepG2 (ENCSR616WEG)


title: ChIP-seq from fibroblast of arm (ENCSR611CRY)


title: ChIP-seq from HepG2 (ENCSR633OVO)


title: ChIP-seq from HepG2 (ENCSR616OSG)


title: ChIP-seq from bipolar spindle neuron (ENCSR619IUE)

summary:
Chip-Seq on biopolar spindle neuron

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


title: ChIP-seq from esophagus muscularis mucosa (ENCSR607ARN)


title: ChIP-seq from neural progenitor cell (ENCSR603SVD)


title: ChIP-seq from K562 (ENCSR599SPN)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 11-05-13)

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


title: ChIP-seq from liver (ENCSR601OGE)

summary:
Chip-Seq on HNF4A-human

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


title: ChIP-seq from thyroid gland (ENCSR597BWL)


title: ChIP-seq from GM12878 (ENCSR596QDC)

summary:
Reverse Crosslink Control ChIP-seq on human GM12878 (fragmentation date 11-12-13)

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


title: ChIP-seq from neural cell (ENCSR608VNA)


title: ChIP-seq from HepG2 (ENCSR590CNM)

summary:
ChIP-Seq on HepG2-human

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


title: ChIP-seq from A673 (ENCSR581PUR)


title: ChIP-seq from HepG2 (ENCSR586DEH)


title: ChIP-seq from HepG2 (ENCSR589SNT)


title: ChIP-seq from endothelial cell of umbilical vein (ENCSR578QSO)


title: ChIP-seq from HepG2 (ENCSR578CXC)


title: Single-cell chromatin accessibility data from K562 cells using scATAC-seq

status: Public on May 23 2017

first: William

middle: J

last: Greenleaf

address: 279 Campus Drive West

department: Genetics

institute: Stanford University

summary: Profiles of single cell epigenomes, assayed using scATAC-seq, in K562 cells.

overall_design: scATAC-seq in K562 cells.

first: Alicia

last: Schep

first: Jason

last: Buenrostro

first: Will

first: Beijing

last: Wu


title: ChIP-seq from HepG2 (ENCSR575RRX)


title: ChIP-seq from neural progenitor cell (ENCSR591KSN)


title: ChIP-seq from K562 (ENCSR588AKU)


title: ChIP-seq from Karpas-422 (ENCSR604III)


title: ChIP-seq from neural progenitor cell (ENCSR573CWZ)


title: ChIP-seq from K562 (ENCSR571CEX)

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

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


title: ChIP-seq from HepG2 (ENCSR571PDN)


title: ChIP-seq from PC-3 (ENCSR566UMF)

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


title: ChIP-seq from MM.1S (ENCSR562SRW)


title: ChIP-seq from DND-41 (ENCSR564VIX)


title: ChIP-seq from SK-N-SH (ENCSR564IGJ)


title: ChIP-seq from fibroblast of arm (ENCSR562MOC)


title: ChIP-seq from Loucy (ENCSR566GSO)


title: ChIP-seq from HepG2 (ENCSR562POI)

summary:
Chip-Seq on HepG2

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


title: ChIP-seq from HepG2 (ENCSR560SEP)


title: ChIP-seq from neutrophil (ENCSR557RDB)


title: ChIP-seq from NCI-H929 (ENCSR562JTY)


title: ChIP-seq from NCI-H929 (ENCSR559IFS)


title: ChIP-seq from PC-9 (ENCSR555TAX)


title: ChIP-seq from HCT116 (ENCSR555LYM)


title: ChIP-seq from body of pancreas (ENCSR554RQQ)


title: ChIP-seq from Loucy (ENCSR543IKB)


title: ChIP-seq from SUDHL6 (ENCSR538KLU)


title: ChIP-seq from smooth muscle cell (ENCSR540UZV)


title: ChIP-seq from NCI-H929 (ENCSR536SZD)


title: ChIP-seq from HepG2 (ENCSR569ARC)


title: ChIP-seq from HepG2 (ENCSR531VIJ)


title: ChIP-seq from induced pluripotent stem cell (ENCSR534VHI)

summary:
Chip-Seq on PGP1 iPSC

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


title: ChIP-seq from HepG2 (ENCSR524VNV)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 06-18-14)

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


title: ChIP-seq from heart left ventricle (ENCSR526EXI)


title: ChIP-seq from neutrophil (ENCSR524RIH)


title: ChIP-seq from HepG2 (ENCSR528PSI)


title: ChIP-seq from neural cell (ENCSR531QHM)


title: ChIP-seq from A673 (ENCSR521IZK)


title: ChIP-seq from PC-9 (ENCSR521GRK)


title: ChIP-seq from liver (ENCSR521IID)

summary:
Chip-Seq on MAX-human

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


title: ChIP-seq from body of pancreas (ENCSR523JCB)


title: ChIP-seq from HepG2 (ENCSR553QMC)


title: ChIP-seq from KMS-11 (ENCSR521AIV)


title: ChIP-seq from HepG2 (ENCSR518WPL)


title: ChIP-seq from body of pancreas (ENCSR520BIM)


title: ChIP-seq from gastrocnemius medialis (ENCSR519WQH)


title: ChIP-seq from MCF-7 (ENCSR511PAE)

summary:
Reverse Crosslink ControlChIP-seq on human MCF-7 (fragmentation date 03-05-14)

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


title: ChIP-seq from neural progenitor cell (ENCSR518LDN)


title: ChIP-seq from H9 (ENCSR516KSY)


title: ChIP-seq from smooth muscle cell (ENCSR515PKY)


title: ChIP-seq from PC-9 (ENCSR513KNS)


title: ChIP-seq from gastroesophageal sphincter (ENCSR510NXV)


title: ChIP-seq from esophagus squamous epithelium (ENCSR508UPW)


title: ChIP-seq from heart left ventricle (ENCSR500ZGF)


title: ChIP-seq from GM12878 (ENCSR501DKS)

summary:
TCF7 ChIP-seq on human GM12878

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


title: ChIP-seq from hepatocyte (ENCSR507UDH)


title: ChIP-seq from HepG2 (ENCSR502GAX)


title: ChIP-seq from HepG2 (ENCSR500WXT)


title: ChIP-seq from KMS-11 (ENCSR499RMZ)


title: ChIP-seq from PC-9 (ENCSR491WAP)


title: ChIP-seq from HepG2 (ENCSR487CPI)


title: ChIP-seq from liver (ENCSR480LIS)

summary:
Chip-Seq on ATF3-human

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


title: ChIP-seq from HepG2 (ENCSR497JLX)


title: ChIP-seq from liver (ENCSR516HUP)

summary:
Chip-Seq on ZBTB33-human

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


title: ChIP-seq from ACC112 (ENCSR475NLR)


title: ChIP-seq from KMS-11 (ENCSR474VGQ)


title: ChIP-seq from bipolar spindle neuron (ENCSR472SEY)


title: ChIP-seq from Karpas-422 (ENCSR473TDG)


title: ChIP-seq from HepG2 (ENCSR455DOO)


title: ChIP-seq from induced pluripotent stem cell (ENCSR447FVP)

summary:
Chip-Seq on PGP1 iPSC-human (fragmentation date: 2015-09-03)

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


title: ChIP-seq from bipolar spindle neuron (ENCSR484PTR)


title: ChIP-seq from liver (ENCSR445QRF)


title: ChIP-seq from smooth muscle cell (ENCSR493FIV)


title: ChIP-seq from liver (ENCSR443AIH)

summary:
Chip-Seq on STL010-human (fragmentation date: 2015-01-29)

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


title: ChIP-seq from HepG2 (ENCSR444LIN)


title: ChIP-seq from HepG2 (ENCSR462KYU)


title: ChIP-seq from esophagus muscularis mucosa (ENCSR474WLZ)


title: ChIP-seq from HepG2 (ENCSR445ACU)

summary:
Chip-Seq on HepG2-human

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


title: ChIP-seq from hepatocyte (ENCSR442ZOI)


title: ChIP-seq from HepG2 (ENCSR441KFW)


title: ChIP-seq from HCT116 (ENCSR474DOV)


title: ChIP-seq from KOPT-K1 (ENCSR438PYA)


title: ChIP-seq from radial glial cell (ENCSR433PUR)


title: ChIP-seq from PC-9 (ENCSR441JWF)


title: ChIP-seq from DOHH2 (ENCSR463DSJ)


title: ChIP-seq from HepG2 (ENCSR430JGJ)


title: ChIP-seq from thoracic aorta (ENCSR416CYZ)


title: ChIP-seq from NCI-H929 (ENCSR409FGC)


title: ChIP-seq from B cell (ENCSR424XBP)


title: ChIP-seq from breast epithelium (ENCSR416AUW)


title: ChIP-seq from neural progenitor cell (ENCSR449AXO)


title: ChIP-seq from SK-N-SH (ENCSR423UOT)


title: ChIP-seq from HepG2 (ENCSR407BEZ)

summary:
ZHX2 ChIP-seq on human HepG2

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


title: ChIP-seq from HepG2 (ENCSR415AEB)


title: ChIP-seq from MM.1S (ENCSR461LTR)


title: ChIP-seq from adrenal gland (ENCSR406PCK)


title: ChIP-seq from neural cell (ENCSR405NQJ)


title: ChIP-seq from MM.1S (ENCSR404LJZ)


title: ChIP-seq from PC-9 (ENCSR402SJV)


title: ChIP-seq from MM.1S (ENCSR399VPY)


title: ChIP-seq from fibroblast of arm (ENCSR397TUH)


title: ChIP-seq from HepG2 (ENCSR381PHD)

summary:
Chip-Seq on HepG2-human (fragmentation date:2014-10-14

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


title: ChIP-seq from neutrophil (ENCSR393SYU)


title: ChIP-seq from HepG2 (ENCSR396SOH)


title: ChIP-seq from neural cell (ENCSR397HSO)


title: ChIP-seq from induced pluripotent stem cell (ENCSR386RIJ)


title: ChIP-seq from bipolar spindle neuron (ENCSR375IXS)


title: ChIP-seq from fibroblast of arm (ENCSR377QMP)


title: ChIP-seq from gastrocnemius medialis (ENCSR380KNE)


title: ChIP-seq from K562 (ENCSR387SYS)

summary:
Chip-Seq on K562-human

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


title: ChIP-seq from MCF-7 (ENCSR374RZR)


title: ChIP-seq from induced pluripotent stem cell (ENCSR369NGL)


title: ChIP-seq from liver (ENCSR350ORK)

summary:
Chip-Seq on GABPA-human

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


title: ChIP-seq from K562 (ENCSR353HEP)

summary:
TARDBP ChIP-seq on human K562

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


title: ChIP-seq from HepG2 (ENCSR372JXR)


title: ChIP-seq from GM12878 (ENCSR360XQV)

summary:
Reverse Crosslink Control ChIP-seq on human GM12878 (fragmentation date 04-19-13)

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


title: ChIP-seq from MM.1S (ENCSR361FWQ)

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


title: ChIP-seq from SK-N-SH (ENCSR366QMB)


title: ChIP-seq from GM12878 (ENCSR372GIN)

summary:
ChIP-Seq on GM12878-human

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


title: ChIP-seq from HepG2 (ENCSR396QWK)

summary:
Chip-Seq on HepG2

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


title: ChIP-seq from HepG2 (ENCSR345EZN)

summary:
Chip-Seq on HepG2-human (fragmentation date:2015-07-09

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


title: ChIP-seq from coronary artery (ENCSR343ZOV)


title: ChIP-seq from liver (ENCSR382MOM)

summary:
Chip-Seq on YY1-human

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


title: ChIP-seq from liver (ENCSR345YWJ)


title: ChIP-seq from HeLa-S3 (ENCSR340WQU)


title: ChIP-seq from NCI-H929 (ENCSR339FOO)


title: ChIP-seq from PC-3 (ENCSR339ZMJ)


title: ChIP-seq from HCT116 (ENCSR333OPW)


title: ChIP-seq from OCI-LY7 (ENCSR331RGM)


title: ChIP-seq from liver (ENCSR338MMB)

summary:
Chip-Seq on NR2F2-human

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


title: ChIP-seq from K562 (ENCSR331GDC)

summary:
Chip-Seq on K562

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


title: ChIP-seq from right lobe of liver (ENCSR344TLI)


title: ChIP-seq from NCI-H929 (ENCSR327OGS)


title: ChIP-seq from GM12878 (ENCSR331HPA)

summary:
GABPA ChIP-seq on human GM12878

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


title: ChIP-seq from PC-3 (ENCSR328AHC)


title: ChIP-seq from neural cell (ENCSR308JFE)


title: ChIP-seq from Karpas-422 (ENCSR317NQG)


title: ChIP-seq from HepG2 (ENCSR327RFM)


title: ChIP-seq from HepG2 (ENCSR331ORD)


title: ChIP-seq from liver (ENCSR324RCI)

summary:
Chip-Seq on FOXA1-human

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


title: ChIP-seq from induced pluripotent stem cell (ENCSR313NJN)


title: ChIP-seq from smooth muscle cell (ENCSR301VIW)


title: ChIP-seq from SUDHL6 (ENCSR307DQT)


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability [CENPB-3'-end-KO]

city: New York

first: Xuebing

state: NY

address: 630 West 168th Street

department: Medicine/Systems Biology

institute: Columbia University

type: Expression profiling by high throughput sequencing

summary: Understanding the physiological relevance of structures in mammalian mRNAs remains elusive, especially considering the global unfolding of mRNA structures in eukaryotic organisms recently examined, as well as the decade-long observation that mRNAs generally seem no more likely than random sequences to be stably folded. Here we show that RNA secondary structures, mostly weak and close-to-random, facilitate the 3′-end processing of thousands of human mRNAs by juxtaposing poly(A) signals (PASs) and cleavage sites that are otherwise too far apart. Folding of these 3′-end structures also enhances mRNA stability. Global structure probing shows that 3′-end regions are indeed folded in cells despite substantial unfolding of PAS-upstream regions. Analyses of thousands of ectopically expressed variants prove that folding both enhances processing and increases stability. Mutagenesis of a genomic locus further implicates structure-controlled processing in regulating neighboring gene expression. These results reveal widespread roles for RNA structure in mammalian mRNA biogenesis and metabolism.

overall_design: Two samples: sequencing the variants in genomic DNA and cDNA

first: David

middle: P

last: Bartel


title: ChIP-seq from bipolar spindle neuron (ENCSR301AEA)


title: ChIP-seq from fibroblast of arm (ENCSR328AVV)


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability [DIM-2P-seq]

overall_design: Comparing mutational patterns of RNA 3' ends with and without DMS treatment


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability [Artificial-3'-end]

overall_design: Two samples: sequencing cleaved and uncleaved variants at a library of artificial poly(A) sites


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability

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

overall_design: Refer to individual Series


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability [4sU-2P-seq]

overall_design: Three samples: steady-state, nascent RNA labeled by 4sU for 30 min, and labeled for 60 min


title: Human and feline adipose-derived mesenchymal stem cells have comparable immunomodulatory functions

city: Sacramento

first: Clifford

middle: G.

last: Tepper

address: 4645 2nd Avenue, Room 2300A

department: Biochemistry and Molecular Medicine

institute: UC Davis School of Medicine

summary: Adipose-derived mesenchymal stem cells (ASCs) are a promising cell therapy to treat inflammatory and immune-mediated diseases. Development of appropriate pre-clinical animal models is critical to determine safety and attain early efficacy data for the most promising therapeutic candidates. Naturally occurring diseases in cats already serve as valuable models to inform human clinical trials in oncologic, cardiovascular and genetic diseases. The objective of this study was to complete a comprehensive side-by-side comparison of human and feline ASCs with an emphasis on their immunomodulatory capacity and transcriptome. Similar to  human ASCs, feline ASCs were highly proliferative at low passages and fit the minimal criteria of multipotent stem cells including a compatible surface protein phenotype, osteogenic capacity and normal karyotype. Like ASCs from all species, feline ASCs inhibited mitogen activated lymphocyte proliferation in vitro, with or without direct ASC-lymphocyte contact. Feline ASCs mimic human ASCs in their mediator secretion pattern including prostaglandin E2, indoleamine 2,3 dioxygenase, transforming growth factor beta and interleukin-6, all augmented by interferon gamma secretion by lymphocytes. The transcriptome of 3 unactivated feline ASC lines were  highly similar. Functional analysis of the most highly expressed genes highlighted processes including: 1) the regulation of apoptosis, 2) cell adhesion, 3) response to oxidative stress, and 4) regulation of cell differentiation. Finally, feline ASCs had a similar gene expression profile to noninduced human ASCs. These data will help inform clinical trials using cats with naturally occurring diseases as surrogate models for human clinical trials in the regenerative medicine arena.

overall_design: A total of 3 total RNA samples were analyzed in this study. The study included primary adipose-derived mesenchymal stem cell (MSC) cultures derived from 3 individual feline subjects: Gray Boy, Luna, and SPF2. The MSC cultures were cultured in standard tissue culture medium. At the desired density, total RNA was isolated and then submitted for RNA-sequencing analysis.

first: Dori

middle: L

last: Borjesson

first: Kaitlin

middle: C

last: Clark

middle: G


title: Widespread Influence of 3′-end Structures on Mammalian mRNA Processing and Stability [CENPB-3'-end-library]

overall_design: This series includes 8 samples designed to measure the efficiency of 3' end processing from a reporter library expressed in HEK293T cells and HeLa cells, in steady state or in nascent RNAs (by 4sU labeling and capture).


title: Profiles from dorsal raphe and amygdala of high-responder and low-responder rats

city: Birmingham

first: Joshua

last: Cohen

state: AL

department: Psychiatry

institute: University of Alabama at Brmingham

type: Non-coding RNA profiling by high throughput sequencing


title: microRNA profiles from dorsal raphe and amygdala of high-responder and low-responder rats

summary: We report 33 microRNAs are differentially expressed in the dorsal raphe and/or amygdala of rats selectively bred for high and low locomotor response to novelty (high responder and low responder rats)

overall_design: microRNA profiles were generated from 4 tissue samples per region (dorsal raphe and amygdala) and per rat strain (high responder and low responder) were

first: Anooshah

middle: E

last: Ata

first: Nateka

last: Jackson

first: Elizabeth

last: Rahn

first: Ryne

last: Ramaker

first: Sara

last: Cooper

first: Ilan

middle: A

last: Kerman

first: Sarah

middle: M

last: Clinton


title: mRNA profiles from dorsal raphe and amygdala of high-responder and low-responder rats

summary: We identified 271 transcripts as differentially regulated in the dorsal raphe and/or the amygdala of high-responder and low-responder rats

overall_design: Counts of transcripts (n=6/brain region/strain) from two brain regions (dorsal raphe and amygdala) from rat strains selectively-bred for response to novelty (high-responder/low-responder rats)


title: The Quantitative Analysis of Transcriptomes Derived From Ezh2- or Ezh1/2-Deleted Leukemia Stem Cells of Murine Acute Myloid Leukemia

status: Public on Mar 11 2017

city: Tokyo

first: Shuhei

last: Fujita

address: 5-1-1 Tsukiji, Chuo-ku

department: Division of Hematological Malignancy

country: Japan

institute: National Cancer Center

summary: We report dual genetic delstion of Ezh1/2 in murine AML model induced cell cyle progression of quiescent LSCs and cell differentiation of LSCs. To investigate the underlying mechanism by which Ezh1/2 regulate quiescent LSCs and maintein the stemness of LSCs, we performed RNA sequencing of L-GMPs derived from Ezh2- and Ezh1/2-deleted  AML mice.

overall_design: Examination and comprison of transcriptomes from c-kit+ AML cells with 4 types of genetic backgraound; Ezh1 +/+ Ezh2 flox/flox, Ezh1+/+ Ezh2 Δ/Δ, Ezh1 -/- Ezh2 flox/flox and Ezh1-/- Ezh2 Δ/Δ.

first: Issay

last: Kitabayashi


title: Neuroserpin polymers cause oxidative stress in a neuronal model of the dementia FENIB

city: Rome

first: Valerio

last: Licursi

address: via degli Apuli, 4

department: c/o Dept. Biology and Biotechnologies "C. Darwin", Sapienza University of Rome

country: Italy

institute: Institute of Molecular Biology and Pathology (IBPM), National Research Council (CNR)

summary: The serpinopathies are human pathologies caused by mutations that promote polymerisation and intracellular deposition of proteins of the serpin superfamily, leading to a poorly understood cell toxicity. The dementia familial encephalopathy with neuroserpin inclusion bodies (FENIB) is caused by polymerisation of the neuronal serpin neuroserpin (NS) within the endoplasmic reticulum (ER) of neurons. We have generated transgenic neural progenitor cell (NPC) cultures from mouse embryonic cerebral cortex, stably expressing the control protein GFP (green fluorescent protein), or human wild type, G392E or deltaNS. We have characterised these cells in the proliferative state and after differentiation to neurons. Our results show that G392E NS formed polymers that were mostly retained within the ER, while wild type NS was correctly secreted as a monomeric protein into the culture medium. DeltaNS was absent at steady state due to its rapid degradation, but it was easily detected upon proteasomal block. Looking at their intracellular distribution, wild type NS was found in partial co-localisation with ER and Golgi markers, while G392E NS was localised within the ER only. Furthermore, polymers of NS were detected by ELISA and immunofluorescence in neurons expressing the mutant but not the wild type protein. We used our model system to investigate which cellular pathways were activated by intracellular polymers of G392E NS by performing RNA sequencing of differentiated cells expressing G392E NS or the negative control protein GFP, and identified 747 genes with a significant upregulation (623) or downregulation (124) in G392E NS-expressing cells. We focused our attention on genes involved in the defence against oxidative stress that were up-regulated in cells expressing G392E NS. Inhibition of these defences by specific pharmacological reagents uncovered the damaging effects of NS polymers. Our results support a role for oxidative stress in the cellular toxicity underlying the neurodegenerative dementia FENIB.

overall_design: mRNA profiles of neural progenitor cells stably overexpressing GFP or G392E neuroserpin were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.

first: Noemi

last: Guadagno

first: Claudia

last: Moriconi

first: Emanuela

last: D'Acunto

first: Paola

last: Nisi

first: Emanuele

last: Cacci

first: Rodolfo

last: Negri

first: Antonella

last: De Jaco

first: Giuseppe

last: Lupo

first: Elena

last: Miranda


title: A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress

city: Cambridge

first: Julie

last: Ahringer

address: Tennis Court Road

department: The Gurdon Institute

country: United Kingdom

institute: University of Cambridge


title: A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress [ChIP-seq]

summary: Repetitive sequences derived from transposons make up a large fraction of eukaryotic genomes and must be silenced to protect genome integrity. Repetitive elements are often found in heterochromatin; however, the roles and interactions of heterochromatin proteins in repeat regulation are poorly understood. Here we show that a diverse set of C. elegans heterochromatin proteins act together with the piRNA and nuclear RNAi pathways to silence repetitive elements and prevent genotoxic stress in the germ line. Mutants in genes encoding HPL-2/HP1, LIN-13, LIN-61, LET-418/Mi-2, and H3K9me2 histone methyltransferase MET-2/SETDB1 also show functionally redundant sterility, increased germline apoptosis, DNA repair defects, and interactions with small RNA pathways. Remarkably, fertility of heterochromatin mutants could be partially restored by inhibiting cep-1/p53, endogenous meiotic double strand breaks, or the expression of MIRAGE1 DNA transposons. Functional redundancy among these factors and pathways underlies the importance of safeguarding the genome through multiple means.

overall_design: Wild-type young adults (YA) were prepared by growing synchronized L1s in liquid culture using standard S-basal medium with HB101 E. coli for 60 hours at 20°C. Adults were sucrose floated, washed in PBS, and flash frozen in liquid nitrogen. Extract preparation and chromatin immunoprecipitation were performed as in Kolasinska-Zwierz et al., 2009 with the following modifications: broken tissue was fixed for 10 minutes in 1.5 mM EGS, then formaldehyde added to 1% for a further 10 minutes before quenching with 0.125M glycine and washing 2X with PBS plus protease inhibitors. Pellets were washed once in FA buffer, then resuspended in 1ml FA buffer per 1 mL of ground worm powder and the extract sonicated to an average size of 250 base pairs with a Diagenode Bioruptor or Bioruptor Pico for 28 pulses of 30 seconds followed by 30 seconds pause. Following ChIP and DNA purification, libraries were prepared using the Illumina TruSeq kit. Fragments in the 250-300 base pair range were selected using Agencourt AMPure XP beads. Two biological replicate ChIPs were conducted for each factor.

first: A

middle: N

last: McMurchy

first: P

last: Stempor

first: T

last: Gaarenstroom

first: B

last: Wysolmerski

first: Y

last: Dong

first: D

last: Aussianikava

last: Appert

first: N

last: Huang

last: Kolasinska-Zwierz

last: Sapetschnig

first: E

last: Miska

first: J


title: A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress [RNA-seq]

overall_design: Synchronized, starved L1 stage worms were grown on NGM plates under one of two conditions. Condition 1: growth was at 20°C (hpl-2, let-418, lin-61, met-2 set-25, and wild-type N2) until the L4 stage and then worms were shifted to 25°C for 15-18 hours until they reached young adult stage. Condition 2: growth was at 15°C (lin-13, prg-1, nrde-2, nrde-2; let-418, and wild-type N2) until the L4 stage, and then worms were shifted to 25°C for 15-18 hours until they reached young adult stage. Worms were then washed off plates, flash frozen in liquid nitrogen, and stored at -80°C until use. RNA was extracted from frozen worms using TriPure (Roche). RNA was purified with Zymo Research RNA Clean and Concentrator-5 (Cambridge Bioscience) following DNase I digestion. Ribosomal RNA was depleted using Ribo-Zero rRNA Removal Kit (Human/Mouse/Rat) (Illumina). Libraries were prepared using the NEBNext Ultra Directional RNA Library Prep Kit for Illumina (New England Biolabs). Two biological replicates were prepared for each strain.


title: Time-course analysis of astrocyte-specific RNA-seq in two severities of spinal cord injury

status: Public on Mar 10 2017

city: Geneva

first: Celine

last: Delucinge

address: 1 rue Michel Servet

department: iGE3 Genomics Platform

country: Switzerland

institute: University of Geneva

summary: RNA-seq analysis of astrocytes following spinal cord injury demonstrated an autologous injury-induced astroglial conversion towards neuronal lineage.

overall_design: Astrocytes were purified by FACS in non-injured Aldh1l1-EGFP mice and at 2 time points following moderate and severe spinal cord lesion. Gene profiles were then compared.

first: Harun

last: Noristani

first: Florence

last: Perrin


title: Adaptive upregulation of Clumping Factor A (ClfA) by S. aureus in the obese, type 2 diabetic host mediates increased virulence

city: Rochester

first: Steven

middle: R.

last: Gill

address: 601 Elmwood Avenue

department: Microbiology & Immunology

institute: University of Rochester

summary: Determination of S. aureus adaptation to obese/T2D host in chronic orthopaedic infection

overall_design: Mice were infected with S. aureus for 14d by transtibial orthopaedic implant at 200k CFU/pin.  RNA from mouse and S. aureus were isolated from infected tibiaie

first: Christopher

middle: W

last: Farnsworth

first: Robert

last: Mooney


title: Quantitative Analysis of Wild Type and miR-203 KO transcriptomes in the rat endometrial adenocarcinoma cell line RUCA-I

city: Dresden

first: Georg

last: Kretzschmar

address: Zellescher Weg 20b

department: Zoology

country: Germany

institute: Technische Universität Dresden

summary:
Purpose: identification of mRNAs that are potential targets of miR-203 in the endometrium and endometrial carcinoma
Methods: mRNA profiles of three batches of wild-type (WT) and three independently generated miR-203 knockout (miR-203 KO) RUCA-I cells were produced by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks.
Results: Using an optimized data analysis workflow, we mapped between 30 and 50 million sequence reads per sample to the rat genome (build rn6) and identified 26751 transcripts of which 1591 are differentially expressed in WT and miR-203 KO cells (p<0.05).

overall_design: mRNA profiles of three WT batches and three independently generated miR-203 KO RUCA-I rat endometrial adenocarcinoma cell lines were produced by deep sequencing, using Illumina HiSeq2500.

first: Andreas

last: Dahl


title: Repression of interstitial cell identity in nephron progenitor cells by Pax2 establishes the nephron-interstitium lineage boundary throughout mammalian kidney development

city: Cincinnati

last: Potter

state: OH

address: 3333 Burnet Ave.

department: Developmental Biology

institute: Children's hospital Medical Center

summary: The kidney contains the functional units, the nephrons, surrounded by the renal interstitium. Previously, we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal interstitial progenitor cells form at the onset of kidney development, descendant cells from these populations contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, indicating a lineage boundary between the nephron and renal interstitial compartments. Currently, it is unclear how lineages are regulated during kidney organogenesis. We demonstrate that nephron progenitor cells lacking Pax2 activity failed to differentiate into nephron cells, but can switch fates into renal interstitium cell types. These data suggest that Pax2 function maintains nephron progenitor cells by repressing transdifferentiation into renal interstitial cell states. Thus, the lineage boundary between the nephron and renal interstitial compartments is maintained by the Pax2 activity in nephron progenitor cells during kidney organogenesis.

overall_design: We carried out single cell RNA-seq on mouse embryonic kidneys. Looking at wild type capping mesenchyme and wild type stromal cells, as well as Pax2 mutant capping mesenchyme cells.

first: Natalie

last: Naiman

first: Kaoru

last: Fujioka

first: Mari

last: Fujino

first: M

middle: T

last: Valerius

first: S

middle: S

first: Andrew

last: McMahon

first: Akio

last: Kobayashi


title: Transcriptome analysis of the epidermis of the purple quail-like (q-lp) mutant of silkworm, Bombyx mori

city: Zhenjiang

first: Pingyang

last: Wang

state: Jiangsu province

address: Nanxu street

department: School of Biotechnology

country: China

institute: Jiangsu University of Science and Technology

summary: A new purple quail-like (q-lp) mutant found from the plain silkworm strain 932VR has pigment dots on the epidermis similar to the pigment mutant quail (q). In addition, q-lp mutant larvae are inactive, consume little and grow slowly, with a high death rate and other developmental abnormalities. Pigmentation of the silkworm epidermis consists of melanin, ommochrome and pteridine. Silkworm development is regulated by ecdysone and juvenile hormone. In this study, we performed RNA-Seq on the epidermis of the q-lp mutant in the 4th instar during molting, with 932VR serving as the control. The results showed 515 differentially expressed genes, of which 234 were upregulated and 281 downregulated in q-lp. BLASTGO analysis indicated that the downregulated genes mainly encode protein-binding proteins, membrane components, oxidation/reduction enzymes, and proteolytic enzymes, whereas the upregulated genes largely encode cuticle structural constituents, membrane components, transport related proteins, and protein-inding proteins. Quantitative reverse transcription PCR was used to verify the accuracy of the RNA-Seq data, focusing on key genes for biosynthesis of the three pigments and chitin as well as genes encoding cuticular proteins and several related nuclear receptors, which are thought to play key roles in the q-lp mutant. We drew three conclusions based on the results: 1) melanin, ommochrome and pteridine pigments are all increased in the q-lp mutant; 2) more cuticle proteins are expressed in q-lp than in 932VR, and the number of upregulated cuticular genes is significantly greater than downregulated genes; 3) the downstream pathway regulated by ecdysone is blocked in the q-lp mutant. Our research findings lay the foundation for further research on the developmental changes responsible for the q-lp mutant.

overall_design: To analyze the differentially expressed genes related to pigmentation and development between the wildtype silkworm strain 932VR and q-lp mutant, the epidermises in 4th instar of 932VR and q-lp are used for RNA-Seq.

first: Qiaoling

last: Zhao


title: 3D organization of chicken genome demonstrates evolutionary conservation of topologically associated domains and highlights unique architecture of erythrocytes’ chromatin [Hi-C]

city: Novisibirsk

first: Veniamin

last: Fishman

address: Prospekt Lavrentyeva 10

country: Russia

institute: Institute of Cytology and Genetics The Siberian Branch of the Russian Academy of Sciences

summary: We present the first Hi-C map of non-mammalian vertebrate, Gallus gallus (domestic chicken). We show the presence of TADs in chicken embryonic fibroblast genome, distributed in accordance with gene density, transcriptional activity, and CTCF binding sites localization. In contrast to mammals, where all examined cell types display relatively similar chromatin architecture profile, in mature and immature chicken erythrocytes we identify unique chromatin spatial organization strongly differed from fibroblasts. Comparing mammalian and chicken genome architectures, we provide evidence highlighting evolutionary role of spatial organization and their significance in genome activity and regulation.

overall_design: HiC-Seq examination of chromatin contact profiles for 3 cell types.

first: Nariman

last: Battulin

first: Miroslav

last: Nuriddinov

first: Antonina

last: Maslova

first: Anna

last: Zlotina

first: Anton

last: Strunov

first: Darya

last: Chervyakova

first: Alexey

last: Korablev

first: Oleg

last: Serov

first: Alla

last: Krasikova


title: Analysis of genome-wide occupancy of menin in T47D and MCF-10A cells

city: Boston

first: Xintao

last: Qiu

state: MA

address: 440 brookline ave

institute: Dana Faber Cancer Institute

summary: We performed ChIP-seq using antibodies directed at menin in T47D and MCF-10A cells in order to assess the genome-wide presence of menin in these cells.

overall_design: T47D cells were synchronized in phenol red-free medium containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). MCF-10A cells were cultured in DMEM. Menin ChIP-seq was performed.

first: Koen

last: Dreijerink

first: Prakash

last: Rao


title: Next generation sequencing of RNA expression on total splenic B cells  from NOD mice fed variable diets

city: Clayton

first: Kirill

last: Tsyganov

state: Victoria

address: Wellington Road

department: Monash Bioinformatics Platform

country: Australia

institute: Monash University

summary:
Purpose: The goals of this study is to examine if  feeding NOD mice with diets supplemented with SCFAs causes altered gene expression in Splenic B cells
Methods: B cell RNA profiles from NOD.LT mice fed fed different diets, a non-purified diet (n=4), a high amylose diet (n=4), a high amylose diet supplemented with acetate (n=4) or a high amylose diet supplemented with butyrate (n=4) were generated by deep sequencing, in triplicate, by Illumina 100 - base HT mode the sequence reads that passed quality filters were summarized into gene models using featureCounts from the Rsubread package, and differential gene expression for the various contrasts between dietary treatments was identified using the EdgeR analysis in R
Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the mouse genome (build GRCm38) and identified 16,257 transcripts present in B cells from NOD.LT mice fed different diet.
Conclusions: Our study investigates how differing diets alter the expression of important genes in B cells, allowing us to further understand the role diets can play in modulating T1D development.

overall_design: B cell mRNA profiles of 15 week NOD.LT mice fed either NP (N=4), HAMS (N=4), HAMSA (N=4) or HAMSB (N=4) were generated by deep sequencing, in triplicate, using ?.

first: Eliana

last: Marino

first: Keiran

middle: H

last: McLeod

first: Trevor

last: Wilson

first: Stuart

last: Archer

first: David

last: Powell


title: ChIP-seq from induced pluripotent stem cell (ENCSR293NAJ)

status: Public on Mar 09 2017

first: ENCODE

last: DCC

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


title: ChIP-seq from HepG2 (ENCSR290UXF)

summary:
Chip-Seq on HepG2-human (fragmentation date:Thu Jan 15 2015 00:00:00 GMT-0600 (CST)

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


title: ChIP-seq from B cell (ENCSR290YLQ)


title: Sub-population RNAseq characterization of cell types produced over time in an in vitro model of human inhibitory interneuron differentiation.

city: Seattle

first: Allen

last: Institute

state: WA

address: 615 Westlake Ave N

institute: The Allen Institute for Brain Science

summary: Diverse cell types are produced from dorsal and ventral regions of the developing neural tube. In this study we describe a system for generating human inhibitory interneurons by ventralizing human embryonic stem cells in vitro and characterizing the gene expression of the cell types produced over time. We engineered a DCX-Citrine/Y hESC line to sort and characterize progenitor and neuron transcriptomics separately at both the subpopulation and single cell level. The cells generated in vitro were compared to similar populations present in human fetal brain samples by mapping gene expression data from human fetal cells onto the principal component analysis (PCA) space of in vitro-derived populations. Weighted gene co-expression network analysis (WGCNA) was used to determine the discreet cell types present at D24, D54, D100 and D125 of culture, and describe the gene expression changes that occur in progenitor and neuron populations over time. Immature lateral ganglionic eminence and medial ganglionic eminence cells are present at early timepoints, along with MGE-like and dorsal pallium-like neuronal progenitors. At later timepoints we observe the emergence of SST-expressing interneurons, as well as oligodendrocyte and astrocyte progenitors. We also identified genes that were upregulated in somatostatin-expressing interneurons as they mature.

overall_design: The transcriptomes of 1732 ventralized single cells were profiled by SmartSeq2 at different timepoints throughout a 125-day differentiation protocol that converted H1 human embryonic stem cells to a variety of ventrally-derived cell types.

first: Jennie

last: Close

first: Zizhen

last: Yao

first: Boaz

last: Levi

first: Jeremy

last: Milller

first: Trygve

last: Bakken

first: Vilas

last: Menon

first: Jonathan

last: Ting

first: Abigail

last: Wall

first: Anne-Rachel

last: Krostag

first: Elliot

middle: R

last: Thomsen

first: Angel

last: Nelson

first: John

middle: K

last: Mich

first: Rebecca

middle: D

last: Hodge

first: Soraya

middle: I

last: Shehata

first: Ian

last: Glass

first: Susan

last: Bort

first: Nadiya

middle: V

last: Shapovalova

first: Olivia

last: Fong

first: Kiet

last: Ngo

first: Joshua

last: Grimley

last: Phillips

first: Carol

last: Thompson

first: Sharad

last: Ramanathan

first: Ed

last: Lein


title: ChIP-seq from mid-neurogenesis radial glial cells (ENCSR287XMW)

first: ENCODE

last: DCC

institute: ENCODE DCC


title: ChIP-seq from Loucy (ENCSR429QYS)


title: ChIP-seq from hepatocyte (ENCSR289TGF)


title: ChIP-seq from K562 (ENCSR286PCG)

summary:
ZBED1 ChIP-seq on human K562

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


title: ChIP-seq from SK-N-MC (ENCSR287VPM)

summary:
ChIP-seq against H3K4me3 using SK-N-MC cell line which was previously described as a neuroepithelioma (ATCC HTB-10). However recent evidence reveals it is Ewing's Sarcoma (www.ncbi.nlm.nih.gov/pubmed/15548687, www.ncbi.nlm.nih.gov/biosample/3151999, www.ncbi.nlm.nih.gov/pubmed/25453903).

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


title: ChIP-seq from right lobe of liver (ENCSR276SJT)


title: ChIP-seq from DOHH2 (ENCSR279JHU)


title: Single cell RNAseq characterization of cell types produced over time in an in vitro model of human inhibitory interneuron differentiation.

first: Allen

last: Institute

first: Jennie

last: Close

first: Zizhen

last: Yao

first: Boaz

middle: P

last: Levi

first: Jeremy

last: Milller

first: Trygve

last: Bakken

first: Vilas

last: Menon

first: Jonathan

last: Ting

first: Abigail

last: Wall

last: Krostag

middle: L


title: Comprehensive and quantitative mapping of RNA-protein interactions across a transcribed eukaryotic genome

first: Richard

last: She

state: Massachusetts

address: 455 Main St Rm 639, Whitehead Institute

institute: Whitehead Institute

summary:
Purpose: High-throughput sequencing has transformed modern biology, but its repertoire is currently confined to reading DNA molecules. Here, we report hardware and software adaptations that allow the very methods that enabled the genomic sequencing revolution to be applied to fluorescence-based biochemical assays, on a massive scale.
Methods: Using commonly available hardware, we built a customizable, open-source platform that leverages the inherent throughput of Illumina technology for direct biophysical measurements. We used the platform to quantitatively measure the binding affinity of the prototypical RBP Vts1 for every transcript in the S. cerevisiae genome.
Results: Our transcribed genome array (TGA) assayed both rare and abundant transcripts with equivalent proficiency, revealing hundreds of low-abundance targets missed by previous approaches. These targets regulated diverse biological processes including nutrient sensing and the DNA damage response, and implicated Vts1 in the ‘birth’ of new genes. TGA provided single nucleotide resolution for each binding site and delineated a highly specific sequence and structure motif for Vts1 binding.
Conclusions: Our technology establishes a flexible new platform for high-throughput biochemistry that can be easily extended to any nucleic acid template (e.g. the human exome), used to study diverse types of biochemical interaction (e.g. RNA-guided nucleases), and adapted to even higher- throughput systems (e.g. HiSeq). Our application of TGA to Vts1 i) doubled the number of known Vts1 targets, identifying key regulators of cell cycle and the DNA damage response ii) provided a marked improvement in the specificity of the protein’s binding motif, iii) generated structural insight into its ability to discriminate among targets, and iv) suggested that Vts1 may have a role in regulating the transcripts of evolutionarily nascent genes. The breadth of new findings stemming from analysis of an already exceptionally well-studied RBP suggests that TGA technology will be similarly enabling for other RBPs and establishes a new paradigm for quantitative, ultra high-throughput biochemistry.

overall_design: A yeast genome sequenced on a MiSeq flow cell with an RNA polymerase promoter and stall sequence attached as adaptors.

first: Daniel

last: Jarosz


title: Characterization of cell types produced over time in an in vitro model of human inhibitory interneuron differentiation.

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

overall_design: Refer to individual Series


title: ChIP-seq from cardiac muscle cell (ENCSR276OLB)

address: 300 Pasteur Dr


title: Genome-wide changes in FOXA1 binding after MEN1 silencing in MCF-7  cells

first: Xintao

last: Qiu

summary: We performed ChIP-seq using FOXA1 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at menin-bound loci FOXA1 binding is disrupted by MEN1 silencing.

overall_design: Comparison of genome-wide FOXA1 binding after ShMEN1 induction vs ShCtrl

first: Koen

last: Dreijerink

first: Prakash

last: Rao


title: ChIP-seq from PC-3 (ENCSR275NCH)


title: ChIP-seq from K562 (ENCSR272JAT)

summary:
CBX5 ChIP-seq on human K562

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


title: identification by RNA-Seq of PhoP and polymyxin B resistant regulons in Photorhabdus luminescens TT01.

city: Montpellier

first: Sophie

last: Gaudriault

address: case courrier 54, Place Eugène Bataillon

country: France

institute: Université Montpellier 2 - Institut National de la Recherche Agronomique

summary: A phoP mutant of the entomopathogenic bacterium P. luminescens is attenuated in virulence in insects and susceptible   to antimicrobial peptides such as Polymyxin B.  The first goal of this study is to compare transcriptomes of the phoP mutant and wild type strain to identify the PhoP regulon.   (i) We first compared both strains grown in LB medium.  (ii) As we know that low Mg conditions induce expression of PhoP-dependent genes, we also compared transcriptomes   of the phoP and wild-type strain after growth in M9 low Mg and in M9 High Mg.    To decipher the polymyxin B regulon, comparisons of transcriptomes of the  wild type strain grown in LB medium with or without addition of polymyxin B   were also performed

sample_organism: Photorhabdus laumondii subsp. laumondii TTO1

overall_design: Two biological replicates of total RNA from exponential cultures (OD= 0.3) of :  WT strain grown in LB,   phoP mutant grown in LB,   WT strain grown in LB plus polymyxin B,   WT strain grown in M9 Low Mg,   phoP mutant grown in M9 Low Mg   Deep sequencing, performed using Illumina HiSeq 2000

first: Anne

last: Lanois

first: Alain

last: Givaudan

first: Annabelle

last: Mouammine

first: Julien

last: Brillard

first: Maurine

last: Bonabaud

first: Emeric

last: Dubois

first: Stéphane

last: Cruveiller

first: David

last: Roche


title: ChIP-seq from cardiac muscle cell (ENCSR269ULZ)

city: Stanford

first: ENCODE

last: DCC


title: ChIP-seq from mid-neurogenesis radial glial cells (ENCSR290EHP)


title: ChIP-seq from thoracic aorta (ENCSR266XMB)


title: ChIP-seq from K562 (ENCSR264VDP)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 06-19-14)

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


title: ChIP-seq from HepG2 (ENCSR269TNX)

summary:
Chip-Seq on HepG2

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


title: ChIP-seq from Loucy (ENCSR267UCE)


title: ChIP-seq from neural progenitor cell (ENCSR274OIJ)


title: ChIP-seq from neutrophil (ENCSR267YXV)


title: ChIP-seq from radial glial cell (ENCSR279HKO)


title: ChIP-seq from induced pluripotent stem cell (ENCSR264RJX)

summary:
Chip-Seq on PGP1 iPSC

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


title: ChIP-seq from KOPT-K1 (ENCSR255BOF)


title: ChIP-seq from vagina (ENCSR258UUX)


title: ChIP-seq from neural progenitor cell (ENCSR256KTR)


title: ChIP-seq from breast epithelium (ENCSR247XFQ)


title: ChIP-seq from GM12878 (ENCSR251OVJ)

summary:
Chip-Seq on GM12878

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


title: ChIP-seq from induced pluripotent stem cell (ENCSR249YGG)


title: ChIP-seq from thyroid gland (ENCSR266EYO)


title: ChIP-seq from MM.1S (ENCSR264HOB)


title: ChIP-seq from GM12878 (ENCSR237VSG)

summary:
Reverse Crosslink Control ChIP-seq on human GM12878 (fragmentation date 08-23-13)

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


title: ChIP-seq from HepG2 (ENCSR237LVA)

summary:
Chip-Seq on HepG2-human (fragmentation date:2014-06-18)

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


title: ChIP-seq from bipolar spindle neuron (ENCSR247PYK)


title: ChIP-seq from liver (ENCSR230ZWH)

summary:
Chip-Seq on RAD21-human

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


title: ChIP-seq from HepG2 (ENCSR226ULX)

summary:
Chip-Seq on HepG2-human (fragmentation date:2015-01-27

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


title: ChIP-seq from HepG2 (ENCSR240FKS)

summary:
Reverse Crosslink Control ChIP-seq on human HepG2 (fragmentation date 01-30-13)

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


title: ChIP-seq from HepG2 (ENCSR226QQM)


title: ChIP-seq from K562 (ENCSR221GAN)

summary:
ChIP-Seq on K562-human

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


title: ChIP-seq from induced pluripotent stem cell (ENCSR236YPE)

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


title: ChIP-seq from HepG2 (ENCSR260UJI)


title: ChIP-seq from MCF-7 (ENCSR204BLL)

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

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


title: ChIP-seq from thyroid gland (ENCSR225VCV)


title: ChIP-seq from liver (ENCSR205FOW)

summary:
Chip-Seq on ATF3-human

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


title: ChIP-seq from HCT116 (ENCSR227XNT)


title: ChIP-seq from HepG2 (ENCSR201GGK)


title: ChIP-seq from HepG2 (ENCSR253OON)


title: ChIP-seq from thyroid gland (ENCSR203KCB)


title: ChIP-seq from GM12878 (ENCSR199WXF)

summary:
ChIP-Seq on GM12878-human

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


title: ChIP-seq from OCI-LY7 (ENCSR199KHR)


title: ChIP-seq from HepG2 (ENCSR346XJA)

summary:
Chip-Seq on HepG2-human (fragmentation date:2015-07-21

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


title: ChIP-seq from HepG2 (ENCSR239QGH)

summary:
Chip-Seq on HepG2-human (fragmentation date:2016-06-05

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


title: ChIP-seq from smooth muscle cell (ENCSR210ZPC)


title: ChIP-seq from PC-3 (ENCSR197QXT)


title: ChIP-seq from MCF-7 (ENCSR197XDQ)


title: ChIP-seq from A673 (ENCSR196CXJ)


title: ChIP-seq from Loucy (ENCSR186EAD)


title: ChIP-seq from smooth muscle cell (ENCSR189XIE)


title: ChIP-seq from HepG2 (ENCSR184SVO)


title: ChIP-seq from gastroesophageal sphincter (ENCSR178MWD)


title: ChIP-seq from Loucy (ENCSR183CQK)


title: ChIP-seq from HCT116 (ENCSR179BUC)


title: ChIP-seq from PC-9 (ENCSR180AAB)


title: ChIP-seq from bipolar spindle neuron (ENCSR170WVI)

summary:
Chip-Seq on biopolar spindle neuron-human (fragmentation date:Tue Sep 29 2015 00:00:00 GMT-0500 (CDT)

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


title: ChIP-seq from thyroid gland (ENCSR164POT)


title: ChIP-seq from bipolar spindle neuron (ENCSR175OYG)


title: ChIP-seq from HepG2 (ENCSR173CTF)


title: ChIP-seq from liver (ENCSR168SMX)

summary:
Chip-Seq on NR2F2-human

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


title: ChIP-seq from Loucy (ENCSR165LOF)


title: ChIP-seq from B cell (ENCSR162DGX)


title: ChIP-seq from gastrocnemius medialis (ENCSR206STN)


title: ChIP-seq from HCT116 (ENCSR161MXP)


title: ChIP-seq from thoracic aorta (ENCSR158PLZ)


title: ChIP-seq from Karpas-422 (ENCSR159CDJ)


title: ChIP-seq from gastrocnemius medialis (ENCSR161HZJ)


title: ChIP-seq from liver (ENCSR196HGZ)

summary:
Chip-Seq on JUND-human

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


title: ChIP-seq from HepG2 (ENCSR156CWW)

summary:
Chip-Seq on HepG2

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


title: ChIP-seq from induced pluripotent stem cell (ENCSR154HDX)


title: ChIP-seq from adrenal gland (ENCSR177QFY)


title: ChIP-seq from PC-9 (ENCSR152YYY)


title: ChIP-seq from K562 (ENCSR159OCC)

summary:
Chip-Seq on K562

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


title: ChIP-seq from MCF-7 (ENCSR155VDK)

summary:
ChIP-Seq on MCF7-human

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


title: ChIP-seq from GM12878 (ENCSR142REC)


title: ChIP-seq from smooth muscle cell (ENCSR143RMH)


title: ChIP-seq from HepG2 (ENCSR142IGM)


title: ChIP-seq from SK-N-MC (ENCSR143HBU)

summary:
ChIP-seq against H3K27me3 using SK-N-MC cell line which was previously described as a neuroepithelioma (ATCC HTB-10). However recent evidence reveals it is Ewing's Sarcoma (www.ncbi.nlm.nih.gov/pubmed/15548687, www.ncbi.nlm.nih.gov/biosample/3151999, www.ncbi.nlm.nih.gov/pubmed/25453903).

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


title: ChIP-seq from SK-N-SH (ENCSR125IJY)


title: ChIP-seq from K562 (ENCSR129NAJ)

summary:
Reverse crosslink control Chip-Seq on K562 human (fragmentation date 06-20-14)

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


title: ChIP-seq from Peyer's patch (ENCSR124GAS)


title: ChIP-seq from SK-N-MC (ENCSR152QRE)

summary:
ChIP-seq against H3K4me1 using SK-N-MC cell line which was previously described as a neuroepithelioma (ATCC HTB-10). However recent evidence reveals it is Ewing's Sarcoma (www.ncbi.nlm.nih.gov/pubmed/15548687, www.ncbi.nlm.nih.gov/pubmed/25453903, www.ncbi.nlm.nih.gov/biosample/3151999).

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


title: ChIP-seq from coronary artery (ENCSR122GIL)


title: ChIP-seq from radial glial cell (ENCSR136NUH)


title: ChIP-seq from SK-N-SH (ENCSR121INC)


title: ChIP-seq from neural cell (ENCSR124VOE)


title: ChIP-seq from HepG2 (ENCSR115PIK)


title: ChIP-seq from HepG2 (ENCSR130VQL)


title: ChIP-seq from HepG2 (ENCSR125DAD)


title: ChIP-seq from smooth muscle cell (ENCSR130IMV)


title: ChIP-seq from SUDHL6 (ENCSR114GLZ)


title: ChIP-seq from bipolar spindle neuron (ENCSR138PGW)


title: ChIP-seq from mid-neurogenesis radial glial cells (ENCSR113LFZ)


title: ChIP-seq from MM.1S (ENCSR120LGC)


title: ChIP-seq from hepatocyte (ENCSR107PGG)


title: ChIP-seq from HepG2 (ENCSR117CHD)


title: ChIP-seq from neural progenitor cell (ENCSR139PIA)


title: ChIP-seq from SK-N-MC (ENCSR111QAW)

summary:
ChIP-seq against H3K9ac using SK-N-MC cell line which was previously described as a neuroepithelioma (ATCC HTB-10). However recent evidence reveals it is Ewing's Sarcoma (www.ncbi.nlm.nih.gov/pubmed/15548687, www.ncbi.nlm.nih.gov/pubmed/25453903, www.ncbi.nlm.nih.gov/biosample/3151999).

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


title: ChIP-seq from HepG2 (ENCSR108TYQ)


title: ChIP-seq from gastrocnemius medialis (ENCSR105YNJ)


title: ChIP-seq from radial glial cell (ENCSR104BSN)


title: ChIP-seq from K562 (ENCSR102KIN)


title: ChIP-seq from HepG2 (ENCSR103SZL)

summary:
ChIP-Seq on HepG2-human

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


title: ChIP-seq from neural progenitor cell (ENCSR105NMJ)

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


title: ChIP-seq from MM.1S (ENCSR094VCE)


title: ChIP-seq from OCI-LY1 (ENCSR076JBA)


title: ChIP-seq from body of pancreas (ENCSR099LGH)


title: ChIP-seq from HepG2 (ENCSR072GJV)


title: ChIP-seq from SK-N-SH (ENCSR074TRC)


title: ChIP-seq from HepG2 (ENCSR071YVR)


title: ChIP-seq from HCT116 (ENCSR091QXP)


title: ChIP-seq from Karpas-422 (ENCSR058SHN)


title: ChIP-seq from K562 (ENCSR077DKV)

summary:
CREM ChIP-seq on human K562

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


title: ChIP-seq from HCT116 (ENCSR093SHE)


title: ChIP-seq from HepG2 (ENCSR092OVN)


title: ChIP-seq from NCI-H929 (ENCSR082NQB)


title: ChIP-seq from ACC112 (ENCSR059MVB)


title: ChIP-seq from K562 (ENCSR076YPO)

summary:
ChIP-Seq on K562-human

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


title: ChIP-seq from MM.1S (ENCSR086YIH)


title: ChIP-seq from smooth muscle cell (ENCSR090QTV)


title: ChIP-seq from HepG2 (ENCSR055XHN)


title: ChIP-seq from MCF-7 (ENCSR057MWG)


title: ChIP-seq from neutrophil (ENCSR058FCG)


title: ChIP-seq from MCF-7 (ENCSR056UBA)


title: ChIP-seq from GM12878 (ENCSR057BWO)


title: ChIP-seq from HepG2 (ENCSR087NSR)


title: ChIP-seq from GM12878 (ENCSR207PFI)

summary:
Chip-Seq on GM12878

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


title: ChIP-seq from hepatocyte (ENCSR220XCD)


title: ChIP-seq from HepG2 (ENCSR054FKH)


title: ChIP-seq from HepG2 (ENCSR031ING)


title: ChIP-seq from liver (ENCSR038GMB)

summary:
Chip-Seq on GABPA-human

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


title: ChIP-seq from neural cell (ENCSR045HLL)


title: ChIP-seq from Loucy (ENCSR036KFJ)


title: ChIP-seq from hepatocyte (ENCSR034BEQ)


title: ChIP-seq from liver (ENCSR019XRC)

summary:
Chip-Seq on STL011-human (fragmentation date: 2015-12-09)

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


title: ChIP-seq from PC-9 (ENCSR011GWK)


title: ChIP-seq from GM12878 (ENCSR016UEH)

summary:
TARDBP ChIP-seq on human GM12878

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


title: ChIP-seq from HepG2 (ENCSR009KLQ)


title: ChIP-seq from HepG2 (ENCSR019NPF)


title: ChIP-seq from adrenal gland (ENCSR053PIY)


title: ChIP-seq from bipolar spindle neuron (ENCSR001KCX)


title: ChIP-seq from thoracic aorta (ENCSR015GFK)


title: ChIP-seq from SUDHL6 (ENCSR018LUP)


title: ChIP-seq from gastrocnemius medialis (ENCSR001UFN)


title: ChIP-seq from NCI-H929 (ENCSR011CSR)


title: ChIP-seq from liver (ENCSR016BMM)

summary:
Chip-Seq on TAF1-human

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


title: ChIP-seq from GM12878 (ENCSR000BVP)

summary:
Control ChIP-seq protocol v042211.1 on human GM12878

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


title: ChIP-seq from K562 (ENCSR000FCA)

summary:
Reverse Crosslink Control ChIP-seq on human K562 (fragmentation date 07-22-13)

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


title: ChIP-seq from cardiac muscle cell (ENCSR000NPF)


title: ChIP-seq from B cell (ENCSR000AUW)

summary:
ChIP-seq on human CD20+ Control

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


title: ChIP-seq from K562 (ENCSR000FCB)

summary:
MITF ChIP-seq on human K562

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


title: ChIP-seq from K562 (ENCSR000FCE)

summary:
ETV6 ChIP-seq on human K562

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


title: ChIP-seq from K562 (ENCSR000FCC)

summary:
NFE2 ChIP-seq on human K562

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


title: ChIP-seq from DND-41 (ENCSR000ASA)

summary:
ChIP-seq on human Dnd41 Control

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


title: ChIP-seq from H1-hESC (ENCSR000AMI)

summary:
Control ChIP-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: ChIP-seq from HeLa-S3 (ENCSR000AOB)

summary:
Control ChIP-seq on human HeLa-S3

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


title: ChIP-seq from endothelial cell of umbilical vein (ENCSR000ALG)

summary:
Control ChIP-seq on human endothelial cell of umbilical vein

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


title: ChIP-seq from K562 (ENCSR000AKY)

summary:
Control ChIP-seq on human K562

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


title: ChIP-seq from K562 (ENCSR000FCD)

summary:
SMAD5 ChIP-seq on human K562

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


title: Simultaneous mapping of active DNA demethylation and sister chromatid exchange in single cells

first: Xiaoji

last: Wu

address: 149G Warren Alpert Building, 200 Longwood Avenue

department: PCMM

institute: Boston Children's Hospital

type: Methylation profiling by high throughput sequencing

summary: MAB-seq and BS-seq were performed for mouse embryonic stem cells, zygotic paternal pronuclei and 2-cell and 4-cell stage embryos.

overall_design: Regular MAB-seq and BS-seq were performed using purified genomic DNA. Low-input MAB-seq and BS-seq were performed using around 100 diploid cells. Single-cell MAB-seq was performed using single cells from mouth pipetting.

first: Azusa

last: Inoue

first: Tsukasa

last: Suzuki

first: Yi

last: Zhang


title: Functional Analysis of Regional Gene Expression in Zebrafish Craniofacial Development

city: Los Angeles

first: Gage

middle: DeKoeyer

last: Crump

state: California

address: 1425 San Pablo St, BCC403

department: Broad CIRM Center for Regenerative Medicine and Stem Cell Research

institute: University of Southern California

summary: Patterning of the facial skeleton involves the precise deployment of thousands of genes in distinct regions of the pharyngeal arches. Despite their significance for craniofacial development, how genetic programs drive this regionalization remains poorly understood. Here we use combinatorial labeling of zebrafish cranial neural crest-derived cells (CNCCs) to define global gene expression along the dorsoventral axis of the developing arches. Intersection of region-specific transcriptomes with expression changes in response to signaling perturbations demonstrates complex roles for Endothelin1 (Edn1) signaling in the intermediate joint-forming region yet a surprisingly minor role in ventral-most regions. Analysis of co-variance across multiple sequencing experiments further reveals clusters of co-regulated genes, with in situ hybridization confirming the expression of novel genes with domain-specific expression. We then performed mutational analysis of a number of these genes, which uncovered antagonistic functions of two Edn1 targets, follistatin a (fsta) and emx2, in regulating cartilaginous joints in the hyoid arch. Our unbiased discovery and functional analysis of genes with regional expression in arch CNCCs reveals complex regulation by Edn1 and points to novel candidates for craniofacial disorders.

overall_design: mRNA profiles of 3 distinct populations of zebrafish pharyngeal arch cells isolated using FACS from 36 hpf wild type (WT) zebrafish. fli1a:GFP+;sox10:DsRed- and fli1a:GFP-;sox10:DsRed+ populations were also isolated at the same time and sequenced as controls (3 replicate each). Additionally there are mRNA profiles of zebrafish pharyngeal arches (all domains combined) isolated by FACS from 36 hpf zebrafish with the following genotypes: edn1-/- (2 replicates), jag1b-/-, jag1b+/+ (control), hsp70I:Gal4; UAS:Edn1, hsp70I:Gal4; UAS:Nicd, and hsp70I:Gal4 (control).

first: Amjad

last: Askary

first: Pengfei

last: Xu

first: Lindsey

last: Barske

first: Maxwell

last: Bay

first: Paul

last: Bump

first: Bartosz

last: Balczerski

first: Michael

last: Bonaguidi

middle: J


title: β-Actin-dependent global chromatin organization and gene expression programs control cellular identity.

city: Abu Dhabi

first: Piergiorgio

last: Percipalle

state: Abu Dhabi

address: Saadiyat Campus, Abu Dhabi

department: Biology Department, Science Division

country: United Arab Emirates

institute: New York University Abu Dhabi

summary:
Purpose: The goals of this study are to use NGS to perform transcriptome profiling (RNA-seq) to find the difference of the gene expression programs among Wild Type (Wt), Actb+/- (Hetero) and Actb-/- (KNO) Mouse Embryonic Fibroblasts
Methods: Total RNA was extracted from 70% confluent cells using TRI Reagent according to the manufacturer protocol (Sigma-Aldrich). Quality of total RNA was evaluated at SciLIfe lab (Stockholm, Sweden) using Qubit and Bioanalyzer respectively, samples which pass the QC were used for library construction according to the SciLife lab guideline using TruSeq Stranded mRNA Library Prep Kit (Illumina). Deep sequencing was performed at Science for Life Laboratory, the National Genomics Infrastructure, NGI, Karolinska Institute, Stockholm. Data was processed through the standard RNAseq analysis pipeline at NYUAD. Read aligmnet was performed using tophat2 v2.1.0 against Mus musculus GRCm38.p4 genome version. Cufflinks v2.2.1 was used to derive expression (FPKM) values. Cuffdiff was used to identify differential gene expression.
Results: Using an optimized data analysis workflow, we identified genes differentially expressed between Wild Type and Actb+/-, WT and Actb-/-, Actb+/- and Actb-/- Mouse Embryonic Fibroblasts. Selected differentially expressed genes were confirmed by qRT-PCR. Gene ontology analysis further identified biological processes, cellular components and molecular functions that were overrepresented in the differentially expressed genes.
Conclusions: Our study shows that there are gene programs differentially regulated among Wild Type, Actb+/- and Actb-/- Mouse Embryonic Fibroblasts

overall_design: mRNA profiles of Wild Type (Wt), Actb+/- (Hetero) and Actb-/- (KNO) Mouse Embryonic Fibroblasts were generated by deep sequencing, in four biological replicates. One of Actb-/- sequencing sample that failed to pass initial QC analysis was excluded from differential gene expression analysis.

first: Bader

last: Almuzzaini

first: Xin

last: Xie

first: Nizar

last: Drou


title: Conserved forkhead dimerization motif controls DNA replication timing and spatial organization of chromosomes in S. cerevisiae

first: Andrew

middle: Zachary

last: Ostrow

address: 1050 Childs Way

department: Biological Sciences

type: Genome binding/occupancy profiling by genome tiling array

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


title: Presence of NAD+-capped RNA in human cells: function and removal by the DXO deNADing Protein

city: Piscataway

first: Ronald

middle: P.

last: Hart

state: NJ

address: 604 Allison Rd Rm B430

department: Cell Biology & Neuroscience

institute: Rutgers University

summary: Eukaryotic mRNAs generally possess an N7 methyl guanosine cap at their 5? end to promote their translation and stability. Here we demonstrate mammalian mRNAs can carry a 5'-end nicotinamide adenine dinucleotide (NAD+) cap. We further demonstrate fungal and mammalian noncanonical DXO family of decapping enzymes can efficiently remove NAD+ caps from mRNAs in vitro and cocrystal structures of DXO with 3´ phosphate NAD+ illuminates the molecular mechanism for the “deNADing” reaction.  An NAD+ cap promotes mRNA decay in wild type mammalian cells and confers mRNA stability in the absence of DXO.  Importantly, mammalian cells possess a capping mechanism that NAD+ caps a subset of intronic small nucleolar RNAs that are selectively enriched in DXO deficient cells.  Our data establish NAD+ as a bona fide mammalian RNA cap and identifies the DXO proteins as potent deNADing enzymes that modulate the levels of NAD+-capped RNAs in cells.

overall_design: Two replicates of HEK293T cell RNA were prepared and sequenced using standard methods.  Three replicates each of HEK293T (Wt) and HEK293T-DXO-KO (DXO-KO) cell RNA were prepared and enriched by NAD-Capture for sequencing library preparation and seqeuencing.

first: Xinfu

last: Jiao

first: Megerditch

last: Kiledjian


title: Brain Xanthophyll Content and Exploratory Gene Expression Analysis: Subspecies Differences in Rhesus Macaque

first: Emily

last: Mohn

address: 711 Washington Street

department: Jean Mayer USDA Human Nutrition Research Center on Aging

institute: Tufts University

summary:
Objective: The dietary xanthophylls, lutein and zeaxanthin, accumulate in primate brain and may be beneficial for cognition. Brain xanthophyll content varies greatly among individuals and genetic factors are likely to be significant contributors. Subspecies of rhesus macaques originating from different geographic locations differ genetically, but the effect of origin on gene expression and carotenoid status has not been determined. The study objective was to determine whether xanthophyll status and expression of carotenoid-related genes, as well as genes with known variants between subspecies, differ between the brains of adult rhesus monkeys of Indian and Chinese origin.
Methods: Next generation RNA sequencing was used to determine differentially expressed carotenoid-related genes and genes with known variants among rhesus monkey subspecies in the prefrontal cortex, cerebellum, and striatum of Indian-origin monkeys (n=3) versus Chinese-origin monkeys (n=3). Serum and brain xanthophylls were determined using HPLC. FastQC was performed on raw sequenced reads to determine the quality of each read. Reads were mapped to the Rhesus Macaque reference genome and differences in gene expression (FPKM) were determined using TopHat and Cuffdiff, respectively. Findings from RNAseq were validated using RT-PCR.
Results: Indian-origin monkeys had higher xanthophyll levels in brain tissue compared to Chinese-origin monkeys despite consuming similar amounts of dietary carotenoids. In a region-specific manner, 4 genes related to carotenoid and fatty acid metabolism (BCO2, RPE65, ELOVL4, FADS2) and 4 genes involved in the immune response (CD4, CD74, CXCL12 LTBR) were differentially expressed between Indian- and Chinese-origin monkeys. Expression of all four genes involved in carotenoid and fatty acid metabolism were correlated with brain xanthophyll concentration in a region-specific manner.
Conclusions: These results indicate that origin is related to differences in both gene expression and xanthophyll content in the brain. Findings from this study may have important implications regarding genetic diversity, lutein status, and cognition in primates.

overall_design: Sequenced reads were generated for rhesus monkeys of Indian origin (n=3) and Chinese origin (n=3) for 3 different brain regions (prefrontal cortex, cerebellum, and striatum) using single-end 50 base pair sequencing on the HiSeq Illumina 2500

first: John

last: Erdman Jr

first: Martha

last: Neuringer

first: Matthew

last: Kuchan

first: Elizabeth

last: Johnson


title: Super-enhancer-mediated RNA processing revealed by integrative microRNA network analysis [SmallRNA-seq]

city: Nagoya

first: Hiroshi

middle: I.

last: Suzuki

address: 65 Tsurumai-cho, Showa-ku

department: DIvision of Molecular Oncology, Graduate School of Medicine

institute: Nagoya University

summary: Super-enhancers are an emerging sub-class of regulatory regions controlling cell identity and disease genes. However, their biological function and impact on miRNA networks are unclear. Here we report that super-enhancers drive the biogenesis of master miRNAs crucial for cell identity by enhancing both transcription and Drosha/DGCR8-mediated primary miRNA processing. Super-enhancers, together with broad H3K4me3 domains, shape a tissue-specific and evolutionarily conserved atlas of miRNA expression and function. CRISPR/Cas9 genomics revealed that super-enhancer constituents act cooperatively and facilitate Drosha/DGCR8 recruitment and pri-miRNA processing to boost cell-specific miRNA production. BET-bromodomain inhibitor JQ1 preferentially inhibited super-enhancer-directed cotranscriptional pri-miRNA processing. Furthermore, super-enhancers are characterized by pervasive interaction with DGCR8/Drosha and DGCR8/Drosha-regulated mRNA stability control, suggesting unique RNA regulation at super-enhancers. Finally, super-enhancers mark multiple miRNAs associated with cancer hallmark traits. This study presents a principle underlying miRNA biology in health and disease and a unrecognized higher-order property of super-enhancers in RNA processing beyond transcription.

overall_design: Small RNA sequencing (SmallRNA-seq) in Dicer knockout mESCs with/without JQ1.

first: Richard

middle: A

last: Young

first: Phillip

last: Sharp


title: ChIP-seq from keratinocyte (ENCSR000ALS)

first: ENCODE

last: DCC

summary:
Control ChIP-seq on human NHEK

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


title: Super-enhancer-mediated RNA processing revealed by integrative microRNA network analysis [X-ChIP-seq]

overall_design: X-ChIP-seq of DGCR8 and Drosha in mESCs with/without JQ1.


title: Super-enhancer-mediated RNA processing revealed by integrative microRNA network analysis [ChrRNA-seq]

overall_design: Chromatin-associated RNA sequencing (ChrRNA-seq) in wild type mESCs with/without JQ1 and DGCR8 knockout mESCs.


title: Super-enhancer-mediated RNA processing revealed by integrative microRNA network analysis

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

Super-enhancers are an emerging sub-class of regulatory regions controlling cell identity and disease genes. However, their biological function and impact on miRNA networks are unclear. Here we report that super-enhancers drive the biogenesis of master miRNAs crucial for cell identity by enhancing both transcription and Drosha/DGCR8-mediated primary miRNA processing. Super-enhancers, together with broad H3K4me3 domains, shape a tissue-specific and evolutionarily conserved atlas of miRNA expression and function. CRISPR/Cas9 genomics revealed that super-enhancer constituents act cooperatively and facilitate Drosha/DGCR8 recruitment and pri-miRNA processing to boost cell-specific miRNA production. BET-bromodomain inhibitor JQ1 preferentially inhibited super-enhancer-directed cotranscriptional pri-miRNA processing. Furthermore, super-enhancers are characterized by pervasive interaction with DGCR8/Drosha and DGCR8/Drosha-regulated mRNA stability control, suggesting unique RNA regulation at super-enhancers. Finally, super-enhancers mark multiple miRNAs associated with cancer hallmark traits. This study presents a principle underlying miRNA biology in health and disease and a unrecognized higher-order property of super-enhancers in RNA processing beyond transcription.


title: Identification of unannotated small genes in Salmonella

city: Chicago

first: Hyunwoo

last: Lee

state: IL

address: 900 S. Ashland Ave., MBRB #3020

department: Center for Biomolecular Sciences

institute: University of Illinois at Chicago

summary: Bacterial genomes serve as a blueprint in all aspects of biological research, and therefore accurate annotation is of paramount importance. However, increasing evidence suggests annotated bacterial genomes have missed many, if not all, small genes encoding proteins ≤60 amino acids. To uncover unannotated small genes in Salmonella enterica, we used a genomic technique ‘ribosome profiling’ that provides a snapshot of all mRNAs being translated (translatome). For comprehensive identification of the small genes, we obtained Salmonella translatomes in four different growth conditions including Luria-Bertani medium, MOPS rich defined medium, N-minimal medium with low Mg2+ (10 μM), and N-minimal medium at pH 5.7, respectively. Ribosome profiling data were analysed in combination with in silico predicted putative open reading frames and transcriptome profiles. As a result, we uncovered 127 previously unannotated genes, the majority of which were small genes encoding proteins ≤50 amino acids. We validated expression by western blot of the identified unannotated small genes, the smallest of which is 7-amino acid long. Because some unannotated small genes identified in this study are only expressed in the infection-relevant low Mg2+ conditions, they are likely involved in cellular processes required for Salmonella virulence. Our findings suggest that currently sequenced bacterial genomes are likely under-annotated with regard to small genes and need to be revised.

sample_organism: Salmonella enterica subsp. enterica serovar Typhimurium str. 14028S

overall_design: Ribosome profiling and RNA-seq were performed on Salmonella enterica 14028s cells grown in four different growth conditions.

first: Jonghwan

last: Baek

first: Jiyoung

first: Kihoon

last: Yoon


title: Messenger RNA expression after silencing or inhibition of MEN1in MCF-7 breast cancer cells

first: Koen

last: Dreijerink

address: 450 Brookline Avenue

department: Medical Oncology

institute: Dana-Farber Cancer Institute

summary: We performed RNA-seq in MCF-7 cells after silencing of MEN1 using small hairpin RNA's directed at the MEN1 mRNA or chemical inhibition of the MEN1 gene product, menin. We demonstrate that a selected group of transcripts is affected by reduced menin function.

overall_design: Comparison of mRNA levels using RNA-seq in mCF-7 cells after silencing of MEN1 using small hairpin RNA's directed at the MEN1 mRNA or chemical inhibition of menin.

middle: M

first: Anna

middle: C

last: Groner

first: Prakash

last: Rao


title: Genome-wide changes in H3K4me3 after MEN1 silencing in MCF-7  cells

summary: We performed ChIP-seq using H3K4me3 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at a selected group of loci H3K4me3 is affected by MEN1 silencing.

overall_design: Comparison of genome-wide H3K4me3 binding after ShMEN1 induction vs ShCtrl, in duplicate.


title: Analysis of genome-wide occupancy of menin, MLL1 and MLL2 in MCF-7 cells

summary: We performed ChIP-seq using antibodies directed at menin, MLL1 and MLL2 in MCF-7 cells in order to assess the genome-wide presence of these proteins in MCF-7 cells.

overall_design: MCF-7 cells were synchronized in phenol red-free medium containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Cells were treated with 10 nM estradiol (E2) or vehicle for 45 minutes. Menin, MLL1 and MLL2 ChIP-seq was performed after vehicle treatment. In addition, the menin cistrome was defined 45 min after treatment with E2.


title: Genome-wide transcriptional profiling in relation to seed storage compounds in tetralocular Brassica rapa

city: Muan

first: Yong-Hwa

address: 199 Muanro

country: South Korea

institute: Bioenergy Crop Research Institute, National Institute of Crop Science, Rural Development Administration

summary: Purpose: To elucidate the physiological and molecular mechanisms underlying seed development, we conducted a genome-wide transcriptional profiling of developing seeds of ‘Sarsyun’ at four different time points (21, 28, 35, and 42 DAF). 34,423 contigs from four different developing seeds (21, 28, 35, and 42 DAF) were analyzed for transcript abundance and changes to the timing of transcript abundance in relation to the accumulation of seed storage products. Most genes involved in seed photosynthesis and carbohydrate metabolism were highly expressed at 21 or 28 DAF and were subsequently downregulated. Expression of genes coding for oleosins and fatty acid synthesis and elongation markedly increased at 28 DAF through 35 DAF, respectively, remaining high thereafter. Expression of major storage protein genes increased at 28 or 35 DAF. Overall, our results showed that dynamic changes to transcript abundance of most genes in relation to seed storage products occurred between 28 and 35 DAF.

overall_design: Two independent gene expression analyses (2 replications, total 8 samples, 3 comparisons; 28 DAF vs. 21 DAF , 35 DAF vs. 21 DAF , 42 DAF vs. 21 DAF)

first: Yong

first: Won

last: Park


title: Transcriptome-wide identification of transcripts regulated by MBNL3 in hepatocellular carcinoma cells

status: Public on Mar 08 2017

city: Shanghai

first: Ji-hang

last: Yuan

address: 800 Xiangyin Road

department: Department of Medical  Genetics

institute: Naval medical university

summary: Understanding the roles of splicing factors and splicing events during human tumorigenesis would open new avenues for targeted therapeutics. Here we identify an oncofetal splicing factor MBNL3, which indicates poor prognosis, and promotes hepatocellular carcinoma (HCC) tumorigenesis. Genetic MBNL3 inhibition almost completely abolishes HCC tumorigenesis. Transcriptomic analysis revealed that MBNL3 induces PXN antisense transcript 1 exon 4 inclusion. The transcript lacking exon 4 binds to coding sequences of PXN mRNA, causes dissociation of translation elongation factors from PXN mRNA, thereby inhibiting PXN mRNA translation. Whereas the transcript containing exon 4 preferentially binds to 3' untranslated region of PXN mRNA, protects PXN mRNA from microRNA-24-AGO2 complex-induced degradation, thereby increasing PXN expression. Through inducing exon 4 inclusion, MBNL3 upregulates PXN expression, which mediates the pro-tumorigenic roles of MBNL3. Collectively, these data demonstrate detailed mechanistic links between oncofetal splicing factor, splicing event, and tumorigenesis, and establish splicing factors and splicing events would be potential therapeutic targets.

overall_design: To identify transcripts regulated by MBNL3, we performed RNA sequencing using RNA retrieved from MBNL3 stably depleted and control SMMC-7721 cells.

first: Shu-han

last: Sun


title: Differential DNA methylation at conserved non-genic elements and transgenerational inheritance following developmental exposure to mono(2-ethylhexyl) phthalate and 5-azacytidine in zebrafish

city: Olso

first: Jorke

last: Kamstra

address: Ullevålsveien 72

department: Basic Sciences and Aquatic Medicine

country: Norway

institute: Norwegian University of Life Sciences

summary:
Background
Exposure to environmental stressors during development may lead to latent and transgenerational adverse health effects. To understand the role of DNA methylation in these effects, we used zebrafish as a vertebrate model to investigate heritable changes in DNA methylation following chemical induced stress during early development. We exposed zebrafish embryos to non-embryotoxic concentrations of the biologically active phthalate metabolite mono-(2-ethylhexyl) phthalate (MEHP, 30 µM), and the DNA methyltransferase 1 inhibitor 5-azacytidine (5AC, 10 µM). Direct, latent and transgenerational effects on DNA methylation were assessed using global, genome wide and locus specific DNA methylation analyses.

Results
Following direct exposure in zebrafish embryos from 0 to 6 days post fertilization (dpf), genome wide analysis revealed a multitude of differentially methylated regions, strongly enriched at conserved non-genic elements for both compounds. Pathways involved in adipogenesis were enriched with the putative obesogenic compound MEHP. Exposure to 5AC resulted in enrichment of pathways involved in embryonic development, and transgenerational effects on larval body length. Locus specific methylation analysis of 10 differentially methylated sites revealed six of these loci differentially methylated in sperm sampled from adult zebrafish exposed during development to 5AC, and in first and second generation larvae. With MEHP consistent changes were found at 2 specific loci in first and second generation larvae.

Conclusions
Our results suggest a functional role for DNA methylation on cis-regulatory conserved elements following developmental exposure to compounds. Effects on these regions are potentially transferred to subsequent generations.

overall_design:
15 RRBS samples, 5 Controls, 5 MEHP and 5 5AC exposed samples
94 BisPCR2 samples, F0 6 dpf samples (6x control, 6x MEHP and 6x 5AC 10 µM and 6x 5AC 25 µM), F0 15 dpf samples (5x Control, 5x MEHP, 5x 5AC), Control DNA (0, 25, 50, 75 and 100% methylated), Technical duplicate analysis (6 dpf F0 5AC1 and 5AC), F0 sperm (6x Control, 6x MEHP and 6x 5AC), F1 6dpf (5x control, 5x MEHP and 5x 5AC), F2 6dpf (5x control, 5x MEHP and 5x 5AC)

first: Liana

last: Bastos Sales

first: Peter

last: Aleström

first: Juliette

last: Legler