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Series GSE153767 Query DataSets for GSE153767
Status Public on Jul 26, 2020
Title ATF4 regulates MYB to increase g-globin in response to loss of β-globin [ChIP-seq]
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Boontanrart et al model the cellular stress that occurs upon reduction in β-globin in human erythroid cells. Decrease in β-globin attenuates the eIF2aP-ATF4 pathway and results in upregulating fetal -globin. Down-regulation of ATF4 leads to decreased levels of the -globin repressor MYB through direct binding at the HBS1L-MYB intergenic region.
 
Overall design ATF4 ChIP-seq in HUDEP-2 and primary erythroid progenitors
 
Contributor(s) Boontanrart M
Citation(s) 32755585
Submission date Jul 03, 2020
Last update date Oct 26, 2020
Contact name Jacob Corn Lab
Organization name ETH Zurich
Street address Otto-Stern-Weg 7
City ZURICH
State/province zURICH
ZIP/Postal code 8093
Country Switzerland
 
Platforms (1)
GPL18573 Illumina NextSeq 500 (Homo sapiens)
Samples (13)
GSM4653919 ATF4 CHIP ATF4 KO undiff
GSM4653920 ATF4 CHIP HBBko diff
GSM4653921 ATF4 CHIP HBBko undiff
This SubSeries is part of SuperSeries:
GSE153768 ATF4 regulates MYB to increase g-globin in response to loss of β-globin
Relations
BioProject PRJNA643998
SRA SRP269944

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
GSE153767_RAW.tar 6.5 Gb (http)(custom) TAR (of BIGWIG)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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