生物
癌症研究
P300-CBP转录因子
癌变
遗传学
组蛋白乙酰转移酶
突变
生殖系
种系突变
髓系白血病
癌症
组蛋白
CREB结合蛋白
转录因子
基因
奶油
作者
N. Gopalakrishna Iyer,Hilal Özdağ,Carlos Caldas
出处
期刊:Oncogene
[Springer Nature]
日期:2004-05-24
卷期号:23 (24): 4225-4231
被引量:566
标识
DOI:10.1038/sj.onc.1207118
摘要
p300 and cyclic AMP response element-binding protein (CBP) are adenoviral E1A-binding proteins involved in multiple cellular processes, and function as transcriptional co-factors and histone acetyltransferases. Germline mutation of CBP results in Rubinstein-Taybi syndrome, which is characterized by an increased predisposition to childhood malignancies. Furthermore, somatic mutations of p300 and CBP occur in a number of malignancies. Chromosome translocations target CBP and, less commonly, p300 in acute myeloid leukemia and treatment-related hematological disorders. p300 mutations in solid tumors result in truncated p300 protein products or amino-acid substitutions in critical protein domains, and these are often associated with inactivation of the second allele. A mouse model confirms that p300 and CBP function as suppressors of hematological tumor formation. The involvement of these proteins in critical tumorigenic pathways (including TGF-beta, p53 and Rb) provides a mechanistic route as to how their inactivation could result in cancer.
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