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

Published

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.

Full Text

Duke Authors

Cited Authors

  • Drummond, JT; Li, GM; Longley, MJ; Modrich, P

Published Date

  • June 30, 1995

Published In

Volume / Issue

  • 268 / 5219

Start / End Page

  • 1909 - 1912

PubMed ID

  • 7604264

Pubmed Central ID

  • 7604264

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.7604264

Language

  • eng

Conference Location

  • United States