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Coordination of a transcriptional switch by HMGI(Y) acetylation | N Munshi
; T Agalioti
; S Lomvardas
; M Merika
; G Chen
; D Thanos
; | Date: |
10 Aug 2001 | Journal: | Science, 293 (5532), 1133-6 | Abstract: | Dynamic control of interferon-beta (IFN-beta) gene expression requires the regulated assembly and disassembly of the enhanceosome, a higher-order nucleoprotein complex formed in response to virus infection. The enhanceosome activates transcription by recruiting the histone acetyltransferase proteins CREB binding protein (CBP) and p300/CBP-associated factors (PCAF)/GCN5, which, in addition to modifying histones, acetylate HMGI(Y), the architectural component required for enhanceosome assembly. We show that the accurate execution of the IFN-beta transcriptional switch depends on the ordered acetylation of the high-mobility group I protein HMGI(Y) by PCAF/GCN5 and CBP, which acetylate HMGI(Y) at distinct lysine residues on endogenous promoters. Whereas acetylation of HMGI(Y) by CBP at lysine-65 destabilizes the enhanceosome, acetylation of HMGI(Y) by PCAF/GCN5 at lysine-71 potentiates transcription by stabilizing the enhanceosome and preventing acetylation by CBP. | Source: | PubMed, pmid11498590 doi: 10.1126/science.293.5532.1133 | Services: | Forum | Review | Favorites |
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