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| Content Provider | PubMed Central |
|---|---|
| Author | Bhattacharya, Shoumo Michels, Catherine L. Leung, Man-kit Arany, Zoltàn P. Kung, Andrew L. Livingston, David M. |
| Copyright Year | 1999 |
| Abstract | Recruitment of p300/CBP by the hypoxia-inducible factor, HIF-1, is essential for the transcriptional response to hypoxia and requires an interaction between the p300/CBP CH1 region and HIF-1α. A new p300-CH1 interacting protein, p35srj, has been identified and cloned. p35srj is an alternatively spliced isoform of MRG1, a human protein of unknown function. Virtually all endogenous p35srj is bound to p300/CBP in vivo, and it inhibits HIF-1 transactivation by blocking the HIF-1α/p300 CH1 interaction. p35srj did not affect transactivation by transcription factors that bind p300/CBP outside the CH1 region. Endogenous p35srj is up-regulated markedly by the HIF-1 activators hypoxia or deferoxamine, suggesting that it could operate in a negative-feedback loop. In keeping with this notion, a p300 CH1 mutant domain, defective in HIF-1 but not p35srj binding, enhanced endogenous HIF-1 function. In hypoxic cells, p35srj may regulate HIF-1 transactivation by controlling access of HIF-1α to p300/CBP, and may keep a significant portion of p300/CBP available for interaction with other transcription factors by partially sequestering and functionally compartmentalizing cellular p300/CBP. |
| Starting Page | 64 |
| File Format | |
| ISSN | 08909369 |
| Journal | Genes & Development |
| Issue Number | 1 |
| Volume Number | 13 |
| Language | English |
| Publisher | Cold Spring Harbor Laboratory Press |
| Publisher Date | 1999-01-01 |
| Access Restriction | Open |
| Rights Holder | Cold Spring Harbor Laboratory Press |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Developmental Biology |
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