细胞周期蛋白D1
细胞周期蛋白D
细胞周期蛋白依赖激酶
细胞周期蛋白依赖激酶复合物
细胞周期蛋白
细胞周期蛋白A2
癌症研究
葛兰素史克-3
细胞周期蛋白B
细胞生物学
周期素
细胞周期蛋白依赖激酶6
细胞周期
细胞周期蛋白依赖激酶2
视网膜母细胞瘤蛋白
细胞生长
蛋白激酶B
基因敲除
细胞周期蛋白
生物
PI3K/AKT/mTOR通路
分子生物学
GSK3B公司
Wnt信号通路
激酶
蛋白激酶A
生物化学
基因
作者
Fumi Takahashi-Yanaga,Toshiyuki Sasaguri
标识
DOI:10.1016/j.cellsig.2007.10.018
摘要
Cyclin D1 is known as a proto-oncogene whose gene amplification and protein overexpression are frequently observed in tumor cells. It acts as a mitogenic signal sensor and is expressed as a delayed-early response to many mitogenic signals. Cyclin-dependent kinases (CDKs) 4 and 6 are cyclin D1 binding partners, and activated cyclin D1/CDK4 and cyclin D1/CDK6 complex phosphorylate the retinoblastoma protein to induce the expression of target genes essential for S phase entry, resulting in facilitation of the progression from G1 to S phase. As well as acting as a positive regulator of the cell cycle, cyclin D1 is known to bind and modulate the actions of several transcription factors. Since the protein level of cyclin D1 reflects cell cycle progression, the rates of protein production and degradation are strictly regulated. Glycogen synthase kinase-3beta (GSK-3beta), a serine/threonine protein kinase, has been shown to play an important role in the determination of cyclin D1 expression level by regulating mRNA transcription and protein degradation. This review highlights the regulatory mechanisms of cyclin D1 expression level, with special attention to the involvement of GSK-3beta.
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