泛素化和蛋白酶体降解 p21(Cip1)、p27(Kip1) 和 p57(Kip2) CDK 抑制剂。
Ubiquitylation and proteasomal degradation of the p21(Cip1), p27(Kip1) and p57(Kip2) CDK inhibitors.
机构信息
Brain Tumor Center and Department of Neuro-Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
出版信息
Cell Cycle. 2010 Jun 15;9(12):2342-52. doi: 10.4161/cc.9.12.11988.
Abstract
The expression levels of the p21(Cip1) family CDK inhibitors (CKIs), p21(Cip1), p27(Kip1) and p57(Kip2), play a pivotal role in the precise regulation of cyclin-dependent kinase (CDK) activity, which is instrumental to proper cell cycle progression. The stabilities of p21(Cip1), p27(Kip1) and p57(Kip2) are all tightly and differentially regulated by ubiquitylation and proteasome-mediated degradation during various stages of the cell cycle, either in steady state or in response to extracellular stimuli, which often elicit site-specific phosphorylation of CKIs triggering their degradation.
摘要
p21(Cip1) 家族细胞周期蛋白依赖性激酶 (CDK) 抑制剂 (CKIs)，包括 p21(Cip1)、p27(Kip1) 和 p57(Kip2) 的表达水平在精确调节 CDK 活性中起着关键作用，这对于细胞周期的正常进行至关重要。p21(Cip1)、p27(Kip1) 和 p57(Kip2) 的稳定性都受到严格的调控，在细胞周期的不同阶段，通过泛素化和蛋白酶体介导的降解进行调控，无论是在稳定状态还是对细胞外刺激的反应中，细胞外刺激通常会引发 CKIs 的特异性磷酸化，从而触发其降解。
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