TUMOR-SUPPRESSOR GENES
TUMOR-SUPPRESSOR GENES
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DOI：
10.1016/0959-437x(94)90102-3
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发表时间：
1994-02-01
影响因子：
4
通讯作者：
WEINBERG, RA
中科院分区：
文献类型：
--
作者：
HINDS, PW;WEINBERG, RA
肿瘤抑制基因的突变被认为通过使通常限制细胞增殖的蛋白质失活而促进肿瘤生长。近年来，已经鉴定了几种肿瘤抑制蛋白，但只有其中两种，p53 和 pRb，被详细了解。在过去的一年中，这两种蛋白质在细胞从 G1 期进入 S 期所需的转录和磷酸化事件中的作用变得越来越明显。 pRb 蛋白似乎可以阻止 S 期所需的转录因子和其他蛋白的功能，直到其被 tate G1 中的细胞周期蛋白依赖性激酶失活。 DNA 损伤诱导 p53 可能会通过改变受损细胞的转录程序而导致细胞周期停滞或细胞死亡。对这些生长调节剂的详细分子了解正在浮现，这也是本次综述的主题。
The mutation of tumor suppressor genes is thought to contribute to tumor growth by inactivating proteins that normally act to limit cell proliferation. Several tumor suppressor proteins have been identified in recent years, but only two of them, p53 and pRb, are understood in detail. In the past year, a role has become apparent for both of these proteins in transcription and phosphorylation events required for passage of a cell from G1 to S phase. The pRb protein appears to prevent the function of transcription factors and other proteins needed for S phase until its inactivation by cyclin-dependent kinases in tate G1. Induction of p53 by DNA damage may act to cause cell cycle arrest or cell death by altering the transcription program of damaged cells. A detailed molecular understanding of these growth regulators is now emerging, and is the subject of this review.