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Silencing of p29 Affects DNA Damage Responses with UV Irradiation

¹ Institute of Biochemical Sciences, National Taiwan University; ² Department of Medical Research, Mackay Memorial Hospital; Departments of ³ Obstetrics and Gynecology and ⁴ Respiratory Care, Taipei Medical University; ⁵ Mackay Medicine, Nursing and Management College; and ⁶ National Taipei University of Technology, Taipei, Taiwan

Requests for reprints: Mau-Sun Chang, Department of Medical Research, Mackay Memorial Hospital, 45 Minshen Road, Tamshui, Taipei, Taiwan. Phone: 886-2-2809-4661, ext. 3081; Fax: 886-2-2808-5952; E-mail: mschang{at}ms1.mmh.org.tw.

Human p29 is a newly identified nuclear protein whose function is largely undetermined. We found that p29 associated with chromatin, interacted with MCM3, and localized with proliferating cell nuclear antigen foci in the S phase. Silencing of p29 using small interfering RNA duplexes reduced DNA synthesis and increased the expression of p107, a member of the RB family, and of cyclin-dependent kinase inhibitor p21, accompanied with a decreased expression of DNA polymerase . Lethal events consisting of premature chromatin condensation with a reduced Chk1 phosphorylation were observed in p29-depleted cells in response to UV irradiation. Intriguingly, the phosphorylation of ataxia telangectasia-mutated kinases at S1981 was suppressed in p29-depleted HeLa cells with UV irradiation, but not in hydroxyurea- and ionizing radiation-treated cells. Taken together, these results reveal a novel function of p29 in the regulation of DNA replication checkpoint responses. (Cancer Res 2006; 66(17): 8484-91)