Sundqvist A, Sollerbrant K, Svensson C
Department of Medical Biochemistry and Microbiology, BMC, Uppsala University, Sweden.
FEBS Lett. 1998 Jun 12;429(2):183-8. doi: 10.1016/s0014-5793(98)00588-2.
Binding of the C-terminal binding protein, CtBP, to the adenovirus E1A moiety of a Gal4-E1A fusion protein abolishes conserved region (CR) 1-dependent transcription activation. In contrast, a non-promoter targeted E1A peptide, capable of binding CtBP, can induce transcription from the proliferating cell nuclear antigen (PCNA) promoter. CtBP is shown here to bind the histone deacetylase HDAC1, suggesting that a promoter targeted CtBP-HDAC1 complex can silence transcription from the PCNA promoter through a deacetylation mechanism. Expression of the CtBP binding domain of E1A is sufficient to alleviate repression, possibly due to the displacement of the CtBP-HDAC1 complex from the promoter.
C末端结合蛋白(CtBP)与Gal4-E1A融合蛋白的腺病毒E1A部分结合,会消除保守区域(CR)1依赖性转录激活。相反,一种能够结合CtBP的非启动子靶向E1A肽,可以诱导增殖细胞核抗原(PCNA)启动子的转录。本文显示CtBP与组蛋白脱乙酰基酶HDAC1结合,这表明靶向启动子的CtBP-HDAC1复合物可以通过去乙酰化机制使PCNA启动子的转录沉默。E1A的CtBP结合结构域的表达足以缓解抑制作用,这可能是由于CtBP-HDAC1复合物从启动子上被取代所致。