
Overview:
CHK2 is rapidly phosphorylated and activated in response to replication blocks and DNA damage; the response to DNA damage occurs in an ataxia telangiectasia mutated (ATM)-dependent manner (1). Expression of wild-type Chk2 leads to increased p53 stabilization after DNA damage, whereas expression of a dominant-negative Chk2 mutant abrogated both phosphorylation of p53 on Ser-20 and p53 stabilization (2).
References:
1. Matsuoka, S. et al: Linkage of ATM to cell cycle regulation by the Chk2 protein kinase. Science. 1998 Dec 4; 282(5395):1893-7.2. Chehab NH. et al: Chk2/hCds1 functions as a DNA damage checkpoint in G(1) by stabilizing p53. Genes Dev. 2000 Feb 1; 14(3):278-88.
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二、补体(complement,C)是存在于正常人和动物血清与组织液中的一组经活化后具有酶活性的蛋白质。早在19世纪末Bordet即证实,新鲜血液中含有一种不耐热的成分,可辅助和补充特异性抗体,介导免疫溶菌、溶血作用,故称为补体。补体是由30余种可溶性蛋白、膜结合性蛋白和补体受体组成的多分子系统,故称为补体系统(complementsystem)。根据补体系统各成分的生物学功能,可将其分为补体固有成分、补体调控成分和补体受体(CR)。

