Araki M, Masutani C, Takemura M, Uchida A, Sugasawa K, Kondoh J, Ohkuma Y, Hanaoka F
Institute for Molecular and Cellular Biology and The Graduate School of Pharmaceutical Sciences, Osaka University and CREST, Japan.
J Biol Chem. 2001 Jun 1;276(22):18665-72. doi: 10.1074/jbc.M100855200. Epub 2001 Feb 27.
Nucleotide excision repair (NER) is carried out by xeroderma pigmentosum (XP) factors. Before the excision reaction, DNA damage is recognized by a complex originally thought to contain the XP group C responsible gene product (XPC) and the human homologue of Rad23 B (HR23B). Here, we show that centrin 2/caltractin 1 (CEN2) is also a component of the XPC repair complex. We demonstrate that nearly all XPC complexes contain CEN2, that CEN2 interacts directly with XPC, and that CEN2, in cooperation with HR23B, stabilizes XPC, which stimulates XPC NER activity in vitro. CEN2 has been shown to play an important role in centrosome duplication. Thus, those findings suggest that the XPC-CEN2 interaction may reflect coupling of cell division and NER.
核苷酸切除修复（NER）由着色性干皮病（XP）因子执行。在切除反应之前，DNA损伤由一个最初认为包含XP C组负责基因产物（XPC）和Rad23 B的人类同源物（HR23B）的复合物识别。在此，我们表明中心蛋白2/钙牵蛋白1（CEN2）也是XPC修复复合物的一个组成部分。我们证明几乎所有的XPC复合物都包含CEN2，CEN2直接与XPC相互作用，并且CEN2与HR23B协同作用，稳定XPC，这在体外刺激了XPC的NER活性。已证明CEN2在中心体复制中起重要作用。因此，这些发现表明XPC-CEN2相互作用可能反映了细胞分裂和NER的偶联。
