Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells
- PMID: 7604264
- DOI: 10.1126/science.7604264
Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells
Abstract
A mismatch-binding heterodimer of hMSH2 and a 160-kilodalton polypeptide has been isolated from HeLa cells by virtue of its ability to restore mismatch repair to nuclear extracts of hMSH2-deficient LoVo colorectal tumor cells. This heterodimer, designated hMutS alpha, also restores mismatch repair to extracts of alkylation-tolerant MT1 lymphoblastoid cells and HCT-15 colorectal tumor cells, which are selectively defective in the repair of base-base and single-nucleotide insertion-deletion mismatches. Because HOT-15 cells appear to be free of hMSH2 mutations, this selective repair defect is likely a result of a deficiency of the hMutS alpha 160-kilodalton subunit, and mutations in the corresponding gene may confer hypermutability and cancer predisposition.
Comment in
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Appropriate partners make good matches.Science. 1995 Jun 30;268(5219):1857-8. doi: 10.1126/science.7604258. Science. 1995. PMID: 7604258 Review. No abstract available.
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