期刊
CELL CYCLE
卷 1, 期 5, 页码 343-350出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.1.5.153
关键词
p21; p300; CBP; TATA box; Transcription
类别
资金
- BBSRC
- Royal Society University Fellowship
- US National Cancer Institute
- BBSRC Integrated Cellular Responses Initiative from the US National Institutes of Health [R01 CA89636, R01 AG17921]
- Cancer Research Campaign from the US National Institutes of Health [R01 CA89636, R01 AG17921]
The tumor suppressors p300 and CREB-binding protein (CBP) are both multifunctional transcriptional coactivators. We have previously found that the cyclin dependent kinase (CDK) inhibitor p21(WAF1/CIP1) can stimulate transactivation by p300 and CBP through inhibiting transcriptional repression by a discrete domain within these proteins termed CRD1. Given the large number of p300/CBP associated functions, it is unlikely that p21 regulates the expression of every gene under their control, however. Here we have investigated the factors that help determine this specificity. We have discovered that while CRD1 can repress the activity of p300 at multiple promoters, induction of transcription by p21 though this motif is highly variable. Analysis of this effect revealed that p21 inducibility is determined by sequences flanking the TATA box. Significantly, p21 regulation of CRD1 domain function is independent of Cyclin /CDK inhibition suggesting a novel function of this protein. p21 does not interact directly with the CRD1 motif, however. These results give further insight into how regulators of cell growth and tumorigenesis, such as p21, can specifically target and induce the expression of select groups of genes.
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