The PCNA-associated factor KIAA0101/p15PAF binds the potential tumor suppressor product p33ING1b

被引:52
作者
Simpson, F
van Bueren, KL
Butterfield, N
Bennetts, JS
Bowles, J
Adolphe, C
Simms, LA
Young, J
Walsh, MD
Leggett, B
Fowles, LF
Wicking, C [1 ]
机构
[1] Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia
[2] Royal Brisbane & Womens Hosp Res Fdn, Conjoint Gastroenterol Lab, Brisbane, Qld 4029, Australia
[3] Queensland Inst Med Res, Brisbane, Qld 4029, Australia
基金
英国医学研究理事会;
关键词
p15(PAF); KIAA0101; colorectal tumor; PCNA; p33ING1b; UV irradiation; OEATC-1;
D O I
10.1016/j.yexcr.2005.09.020
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The KIAA0101/p15(PAF)/OEATC-1 protein was initially isolated in a yeast two-hybrid screen for proliferating cell nuclear antigen (PCNA) binding partners, and was shown to bind PCNA competitively with the cell cycle regulator p21(WAF). PCNA is involved in DNA replication and damage repair. Using polyclonal antisera raised against a p15(PAF) fusion protein, we have shown that in a range of mammalian tumor and non-tumor cell lines the endogenous p15(PAF) protein localises to the nucleus and the mitochondria. Under normal conditions no co-localisation with PCNA could be detected, however following exposure to UV it was possible to co-immunoprecipitate p15(PAF) and PCNA from a number of cell lines, suggesting a UV-enhanced association of the two proteins. Overexpression of p15(PAF) in mammalian cells was also found to protect cells from UV-induced cell death. Based on similarities between the behaviour of p15(PAF) and the potential tumor suppressor product p33ING1b, we have further shown that these two proteins interact in the same complex in cell cultures. This suggests that p15(PAF) forms part of a larger protein complex potentially involved in the regulation of DNA repair, apoptosis and cell cycle progression. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:73 / 85
页数:13
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