肿瘤抑制候选基因p33(ING1)介导紫外线损伤DNA的修复。

The tumor suppressor candidate p33(ING1) mediates repair of UV-damaged DNA.

作者信息

Cheung K J, Mitchell D, Lin P, Li G

机构信息

Division of Dermatology, Department of Medicine, University of British Columbia, and Vancouver Hospital and Health Sciences Center, Vancouver, British Columbia V6H 3Z6, Canada.

出版信息

Cancer Res. 2001 Jul 1;61(13):4974-7.

PMID:11431327

Abstract

The biological functions of the tumor suppressor, ING1, have been studied extensively in the last 5 years since it was cloned. It shares many biological functions with those of p53 and has been reported to mediate growth arrest, senescence, apoptosis, anchorage-dependent growth, and chemosensitivity. Some of these functions, such as cell cycle arrest and apoptosis, have been shown to be dependent on the activity of both ING1 and p53 proteins. In this study, we report that p33(ING1) (one of ING1 isoforms) is also involved in the modulation of DNA repair. We found that overexpression of p33(ING1) enhances repair of UV-damaged DNA and that p53 is required for the repair process. Furthermore, binding between ING1 and GADD45 has been detected. These observations suggest that p33(ING1) cooperates with p53 in nucleotide excision repair and that GADD45 may be one of its components.

摘要

肿瘤抑制因子ING1自克隆以来，其生物学功能在过去5年中得到了广泛研究。它与p53具有许多共同的生物学功能，据报道可介导生长停滞、衰老、凋亡、锚定依赖性生长和化学敏感性。其中一些功能，如细胞周期停滞和凋亡，已被证明依赖于ING1和p53蛋白的活性。在本研究中，我们报告p33(ING1)（ING1异构体之一）也参与DNA修复的调节。我们发现p33(ING1)的过表达增强了紫外线损伤DNA的修复，并且修复过程需要p53。此外，已检测到ING1与GADD45之间的结合。这些观察结果表明，p33(ING1)在核苷酸切除修复中与p53协同作用，并且GADD45可能是其组成部分之一。