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Series GSE84858 Query DataSets for GSE84858
Status Public on Aug 22, 2017
Title The Molecular Mechanism for EZH2 Function in DSS-induced Colitis
Organism Mus musculus
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Here we employed the genetically engineered mice models (GEM) to uncover the role of gut epithelial EZH2 in the pathogenesis of colitis. To dissect the underlying mechanism, Chip-Seq analysis is used for mechanistic study.
From the result we find EZH2 mainly targeted in the TSS region. As we have known TNF-alpha pathway can be regulated by EZH2, we try and find TRAF2/5 may be the key point for EZH2 to regulated TNF-alpha pathway. At the same time Bad, BAX, PUMA.etc which promote cell apoptosis can be find in the result, which means EZH2 may inhibit apoptosis of IEC in colitis by targenting these genes.
 
Overall design Wild-type mice were treated with 2% DSS for 3 days and IECs were isolated by EDTA isolation buffer, and each sample contains pooled IECs from 5 mice. Flash frozen cells were then sent to Active Motif, Inc. for chromatin extraction and followed by immunoprecipitation using anti-EZH2 antibody (Active Motif, cat # 39901).
 
Contributor(s) Liu Y, Qin J
Citation(s) 28439030
Submission date Jul 26, 2016
Last update date May 15, 2019
Contact name Yongfeng Liu
E-mail(s) lyf3433@163.com
Organization name The Institute of Health Sciences, SIBS, CAS / SJTUSM
Street address 320 Yueyang Road, Shanghai, 200025 P.R. China
City shanghai
ZIP/Postal code 200025
Country China
 
Platforms (1)
GPL19057 Illumina NextSeq 500 (Mus musculus)
Samples (2)
GSM2252604 EZH2 ChIPSeq
GSM2252605 input DNA
Relations
BioProject PRJNA335383
SRA SRP079911

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE84858_RAW.tar 237.1 Mb (http)(custom) TAR (of BW)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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