| First Author | Hublitz P | Year | 2005 |
| Journal | Genes Dev | Volume | 19 |
| Issue | 23 | Pages | 2912-24 |
| PubMed ID | 16322561 | Mgi Jnum | J:103923 |
| Mgi Id | MGI:3610870 | Doi | 10.1101/gad.351205 |
| Citation | Hublitz P, et al. (2005) NIR is a novel INHAT repressor that modulates the transcriptional activity of p53. Genes Dev 19(23):2912-24 |
| abstractText | Most transcriptional repression pathways depend on the targeted deacetylation of histone tails. In this report, we characterize NIR, a novel transcriptional corepressor with inhibitor of histone acetyltransferase (INHAT) activity. NIR (Novel INHAT Repressor) is ubiquitously expressed throughout embryonic development and adulthood. NIR is a potent transcriptional corepressor that is not blocked by histone deacetylase inhibitors and is capable of silencing both basal and activator-driven transcription. NIR directly binds to nucleosomes and core histones and prevents acetylation by histone acetyltransferases, thus acting as a bona fide INHAT. Using a tandem affinity purification approach, we identified the tumor suppressor p53 as a NIR-interacting partner. Association of p53 and NIR was verified in vitro and in vivo. Upon recruitment by p53, NIR represses transcription of both p53-dependent reporters and endogenous target genes. Knock-down of NIR by RNA interference significantly enhances histone acetylation at p53-regulated promoters. Moreover, p53-dependent apoptosis is robustly increased upon depletion of NIR. In summary, our findings describe NIR as a novel INHAT that plays an important role in the control of p53 function. |
