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Carcinogenesis Advance Access originally published online on September 11, 2009
Carcinogenesis 2009 30(10):1710-1716; doi:10.1093/carcin/bgp204
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Involvement of p29 in DNA damage responses and Fanconi anemia pathway

Po-Chen Chu1, Tao-Yeuan Wang2,3, Yen-Ta Lu3,4, Chuan-Kai Chou5, Yuh-Cheng Yang3,6 and Mau-Sun Chang1,7,*

1 Institute of Biochemical Sciences, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei 10617, Taiwan
2 Department of Pathology, Mackay Memorial Hospital, Taipei County 251, Taiwan
3 Mackay Medicine, Nursing and Management College, Taipei County 251, Taiwan
4 Chest Division, Medical Department, Mackay Memorial Hospital, Taipei County 251, Taiwan
5 National Laboratory Animal Center, Taipei 115, Taiwan
6 Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei County 251, Taiwan
7 Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan

* To whom correspondence should be addressed. Tel: +886 2 3366 9837; Fax: +886 2 2363 5038; Email: mschang{at}ntu.edu.tw

Human p29 is a chromatin-associated protein and the silencing of p29 expression increases cell population in G1 phase and decreases phosphorylation levels of Chk1 and Chk2 in response to UV treatment. To further characterize the function of p29, U2OS and Fanconi anemia complementation group G (FA-G) cells with constitutive p29 expression have been established. Analyses of these cells identified increased phosphorylation levels of Chk1 and Chk2, which were accompanied by elevated amounts of chromatin-associated Mre11–Rad50–Nbs1 complex and ATR-IP. Monoubiquitination of the FA ID complex was restored in p29 stably expressing FA-G cells. Moreover, lower tumor incidence was observed in mp29 transgenic mice after UV irradiation. These results suggest the involvement of p29 in the DNA damage responses and Fanconi anemia pathway.

Abbreviations: ATM, ataxia telangiectasia mutated; ATR, ataxia-telangiectasia and Rad3-related; ATRIP, ATR-interacting protein; CSK, cytoskeletal; DDR, DNA damage response; FA, Fanconi anemia; FA-G, Fanconi anemia complementation group G; GCIP, grap2 cyclin-D interacting protein; GST, glutathione S-transferase; IR, ionizing radiation; MMC, mitomycin C; MRN, Mre11–Rad50–Nbs1; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; ssDNA-RPA, single stranded DNA-replication protein A; TopBP1, topoisomerase II binding protein 1

Received April 19, 2009; revised July 27, 2009; accepted August 1, 2009.


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