XRCC2 is Required for the Formation of Rad51 Foci Induced by Ionizing Radiation and DNA Cross-Linking Agent Mitomycin C
XRCC2 protein shares weak amino acid sequence similarity with Rad51, which is a central player in homologous recombinational repair (HRR). Rad51 proteins assemble at the sites of HRR and form visible nuclear foci in response to DNA damage. Xrcc2 hamster mutant irs1 cells are incapable of forming Rad...
Main Author: | |
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Format: | Article |
Language: | English |
Published: |
Hindawi Limited
2002-01-01
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Series: | Journal of Biomedicine and Biotechnology |
Online Access: | http://dx.doi.org/10.1155/S1110724302204040 |
Summary: | XRCC2 protein shares weak amino acid sequence similarity with
Rad51, which is a central player in homologous recombinational
repair (HRR). Rad51 proteins assemble at the sites of HRR and form
visible nuclear foci in response to DNA damage. Xrcc2
hamster mutant irs1 cells are incapable of forming Rad51 foci
after ionizing irradiation or DNA cross-linking agent mitomycin C
treatment, though the Rad51 protein level is normal in the
mutant. The defect can be corrected in an XRCC2
transformant. Time course study showed that the irs1 cells
primarily lacked the early response (2 hours after
irradiation) to form small Rad51 foci (type 1) and later response
(8 hours after irradiation) to form large foci (type 2).
These results suggested that XRCC2 is essential for the assembly
of the DNA damage-induced Rad51 foci and that XRCC2 may play an
important role in the early stage of HRR. |
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ISSN: | 1110-7243 1110-7251 |