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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
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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.
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Overall design |
ATF4 ChIP-seq in HUDEP-2 and primary erythroid progenitors
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Contributor(s) |
Boontanrart M |
Citation(s) |
32755585 |
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Submission date |
Jul 03, 2020 |
Last update date |
Oct 26, 2020 |
Contact name |
Jacob Corn Lab |
Organization name |
ETH Zurich
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Street address |
Otto-Stern-Weg 7
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City |
ZURICH |
State/province |
zURICH |
ZIP/Postal code |
8093 |
Country |
Switzerland |
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Platforms (1) |
GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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Samples (13)
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This SubSeries is part of SuperSeries: |
GSE153768 |
ATF4 regulates MYB to increase g-globin in response to loss of β-globin |
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Relations |
BioProject |
PRJNA643998 |
SRA |
SRP269944 |