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

James T. Drummond, Guo Min Li, Matthew J. Longley, Paul Modrich

Research output: Contribution to journalArticlepeer-review

510 Scopus citations

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 languageEnglish (US)
Pages (from-to)1909-1912
Number of pages4
JournalScience
Volume268
Issue number5219
DOIs
StatePublished - 1995

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells'. Together they form a unique fingerprint.

Cite this