Chen X, Bargonetti J, Prives C
Department of Biological Sciences, Columbia University, New York, New York 10027, USA.
Cancer Res. 1995 Oct 1;55(19):4257-63.
Cells induced to accumulate the p53 tumor suppressor protein have been shown to arrest in G1. This arrest is characterized by accumulation of the cyclin-dependent kinase inhibitor p21 (WAF1/CIP1) and of under-phosphorylated forms of retinoblastoma protein. We show here that accumulation of the wild-type p53 protein in either human or murine cells markedly increases expression of cyclin D1. The induction of cyclin D1 can also be mediated by a target of p53, the p21 (WAF1/CIP1) inhibitor of cyclin-dependent kinases. The relationship between the induction of cyclin D1 and G1 arrest defines a new cellular response to p53.
已证明,被诱导积累p53肿瘤抑制蛋白的细胞会停滞在G1期。这种停滞的特征是细胞周期蛋白依赖性激酶抑制剂p21(WAF1/CIP1)的积累以及视网膜母细胞瘤蛋白的低磷酸化形式的积累。我们在此表明,野生型p53蛋白在人或鼠细胞中的积累会显著增加细胞周期蛋白D1的表达。细胞周期蛋白D1的诱导也可由p53的一个靶点——细胞周期蛋白依赖性激酶的p21(WAF1/CIP1)抑制剂介导。细胞周期蛋白D1的诱导与G1期停滞之间的关系定义了一种对p53的新细胞反应。