Abstract：
:Cancer-prone diseases ataxia-telangiectasia (AT), Nijmegen breakage syndrome (NBS) and ataxia-telangiectasia-like disorder (ATLD) are defective in the repair of DNA double-stranded break (DSB). On the other hand, arsenic (As) has been reported to cause DSB and to be involved in the occurrence of skin, lung and bladder cancers. To dissect the repair mechanism of As-induced DSB, wild type, AT and NBS cells were treated with sodium arsenite to study the complex formation and post-translational modification of Rad50/NBS1/Mre11 repair proteins. Our results showed that Mre11 went through cell cycle-dependent phosphorylation upon sodium arsenite treatment and this post-translational modification required NBS1 but not ATM. Defective As-induced Mre11 phosphorylation was rescued by reconstitution with full length NBS1 in NBS cells. Although As-induced Mre11 phosphorylation was not required for Rad50/NBS1/Mre11 complex formation, it might be required for the formation of Rad50/NBS1/Mre11 nuclear foci upon DNA damage.
journal_name
DNA Repair (Amst)journal_title
DNA repairauthors
Yuan SS,Su JH,Hou MF,Yang FW,Zhao S,Lee EYdoi
10.1016/s1568-7864(01)00009-xkeywords:
subject
Has Abstractpub_date
2002-02-28 00:00:00pages
137-42issue
2eissn
1568-7864issn
1568-7856pii
S156878640100009Xjournal_volume
1pub_type
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