Перегляд вихідного коду сторінки Five Important And Vital Elements Of Ribonucleotide reductase

, 2007). However, this interesting possibility has not been tested and, importantly, there is no corresponding information on either global or gene-specific functions of H3K4me3-TAF3 interactions or on their underlying mechanism of action. Following a global analysis of H3K4me3-TAF3 interactions, we focus on possible gene-specific effects of these interactions in the regulation of gene expression by the tumor suppressor p53. As a transcriptional activator, p53 strikes a balance between cell-cycle arrest and programmed cell death through the differential activation of cognate genes (reviewed in Vousden and Prives, 2009). The kinetics of p53 target gene activation vary, ranging from a rapid induction of cell-cycle control genes to a delayed induction of proapoptotic genes (Zhao et?al., 2000). However, the mechanisms that regulate the distinct transcription programs remain to be fully elucidated. A potential [http://www.selleckchem.com/products/Cisplatin.html selleck] role for H3K4me3 in p53-mediated gene activation is supported by a DNA damage-enhanced accumulation of H3K4me3 at the GADD45A promoter ( An and Roeder, 2004). Also, ubiquitylated H2B, which directly stimulates hSET1-dependent [http://en.wikipedia.org/wiki/Ribonucleotide_reductase Ribonucleotide reductase] H3K4 di- and trimethylation ( Shilatifard, 2006), accumulates at the p21 promoter in response to DNA damage ( Kim et?al., 2009). However, the downstream mechanisms underlying H3K4me3 function in p53-dependent activation remain to be determined. Here, we show that H3K4me3, through interactions with [http://www.selleckchem.com/products/Vorinostat-saha.html Vorinostat mw] TAF3, directs global TFIID recruitment. In subsequent biochemical and cell-based analyses of p53 function, we show that H3K4me3-TAF3/TFIID interactions both enhance p53-dependent transcription by directly stimulating PIC formation and facilitate selective gene activation by p53 in response to DNA damage. To investigate a role for H3K4me3 in the genome-wide recruitment of TAF3, we employed chromatin immunoprecipitation sequencing (ChIP-seq) to examine the distribution of TAF3, RNAPII, and H3K4me3 in human colorectal carcinoma HCT116 cells (Bunz et?al., 1998). Stringent TAF3 binding peaks (n?= 11,765, p?