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 hMutSα, 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 HCT-15 cells appear to be free of hMSH2 mutations, this selective repair defect is likely a result of a deficiency of the hMutSα 160-kilodalton subunit, and mutations in the corresponding gene may confer hypermutability and cancer predisposition.
Original language | English (US) |
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Pages (from-to) | 1909-1912 |
Number of pages | 4 |
Journal | Science |
Volume | 268 |
Issue number | 5219 |
DOIs | |
State | Published - 1995 |
ASJC Scopus subject areas
- General