Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells.
Journal Article (Journal Article)
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.
- Drummond, JT; Li, GM; Longley, MJ; Modrich, P
- June 30, 1995
Volume / Issue
- 268 / 5219
Start / End Page
- 1909 - 1912
International Standard Serial Number (ISSN)
Digital Object Identifier (DOI)
- United States