
Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells.
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.
Duke Scholars
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- Tumor Cells, Cultured
- Sequence Deletion
- Nucleic Acid Heteroduplexes
- Mutation
- Molecular Weight
- Molecular Sequence Data
- Humans
- Hela Cells
- HeLa Cells
- General Science & Technology
Citation

Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Tumor Cells, Cultured
- Sequence Deletion
- Nucleic Acid Heteroduplexes
- Mutation
- Molecular Weight
- Molecular Sequence Data
- Humans
- Hela Cells
- HeLa Cells
- General Science & Technology