Partial correction of the single-strand break repair defect in the CHO mutant EM9 by electroporated recombinant XRCC1 protein
Conference
·
OSTI ID:134871
- Lawrence Livermore National Lab., CA (United States)
The CHO mutant EM9 is hypersentitive to simple alkylating agents and is unable to rejoin efficiently the DNA single-strand breaks that arise during base excision repair. In addition, EM9 exhibits a reduced frequency of homologous recombination and a 10-fold increase in sister chromatid exchange, similar to that observed in cells from individuals afflicted with Bloom`s syndrome. The human gene that fully corrects EM9 has been cloned and is denoted XRCC1, and fully functional XRCC1 cDNA minigenes have been constructed. To further examine the biochemical role of XRCC1, the human XRCCq ORF was inserted into the E. coli expression vector pMAL-cRI (New England Biolabs, Beverly, MA) to generate pMAL-cRIX, which encodes a fusion protein.
- Research Organization:
- New York Academy of Sciences, New York, NY (United States)
- DOE Contract Number:
- W-7405-ENG-48
- OSTI ID:
- 134871
- Report Number(s):
- CONF-9307221--
- Country of Publication:
- United States
- Language:
- English
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