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    Science. 1995 Jun 30;268(5219):1909-12.

    Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells.

    Drummond JT, Li GM, Longley MJ, Modrich P.

    Source

    Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA.

    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.

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    PMID:
    7604264
    [PubMed - indexed for MEDLINE]

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