Mismatch repair proteins as sensors of alkylation DNA damage

Jean Y.J. Wang; Winfried Edelmann

doi:10.1016/j.ccr.2006.05.013

Mismatch repair proteins as sensors of alkylation DNA damage

Jean Y.J. Wang, Winfried Edelmann

Cell Biology

Research output: Contribution to journal › Short survey › peer-review

65 Scopus citations

Abstract

The DNA mismatch repair (MMR) system maintains genome integrity by correcting replication errors. MMR also stimulates checkpoint and cell death responses to DNA damage suggested by the resistance of MMR-defective tumor cells to several chemotherapeutic agents. MMR-dependent cytotoxic response may result from futile repair; however, MMR-mediated apoptosis has been genetically separated from its repair function. In a recent issue of Molecular Cell, Yoshioka and coworkers show that MMR complexes (MutSα and MutLα) are required for the recruitment of ATR-ATRIP to sites of alkylation damage, demonstrating that MMR complexes can function as sensors in DNA damage signal transduction.

Original language	English (US)
Pages (from-to)	417-418
Number of pages	2
Journal	Cancer Cell
Volume	9
Issue number	6
DOIs	https://doi.org/10.1016/j.ccr.2006.05.013
State	Published - Jun 13 2006

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.ccr.2006.05.013

Cite this

@article{8335e50665f74ce2a775ccf0c0449980,

title = "Mismatch repair proteins as sensors of alkylation DNA damage",

abstract = "The DNA mismatch repair (MMR) system maintains genome integrity by correcting replication errors. MMR also stimulates checkpoint and cell death responses to DNA damage suggested by the resistance of MMR-defective tumor cells to several chemotherapeutic agents. MMR-dependent cytotoxic response may result from futile repair; however, MMR-mediated apoptosis has been genetically separated from its repair function. In a recent issue of Molecular Cell, Yoshioka and coworkers show that MMR complexes (MutSα and MutLα) are required for the recruitment of ATR-ATRIP to sites of alkylation damage, demonstrating that MMR complexes can function as sensors in DNA damage signal transduction.",

author = "Wang, {Jean Y.J.} and Winfried Edelmann",

note = "Funding Information: The authors are supported by NIH grants CA43054 to J.Y.J.W., CA76329 to W.E., and ES-11040 to J.Y.J.W. and W.E. We apologize to those whose important contributions to the field could not be cited due to restrictions in the number of references.",

year = "2006",

month = jun,

day = "13",

doi = "10.1016/j.ccr.2006.05.013",

language = "English (US)",

volume = "9",

pages = "417--418",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "6",

}

TY - JOUR

T1 - Mismatch repair proteins as sensors of alkylation DNA damage

AU - Wang, Jean Y.J.

AU - Edelmann, Winfried

N1 - Funding Information: The authors are supported by NIH grants CA43054 to J.Y.J.W., CA76329 to W.E., and ES-11040 to J.Y.J.W. and W.E. We apologize to those whose important contributions to the field could not be cited due to restrictions in the number of references.

PY - 2006/6/13

Y1 - 2006/6/13

N2 - The DNA mismatch repair (MMR) system maintains genome integrity by correcting replication errors. MMR also stimulates checkpoint and cell death responses to DNA damage suggested by the resistance of MMR-defective tumor cells to several chemotherapeutic agents. MMR-dependent cytotoxic response may result from futile repair; however, MMR-mediated apoptosis has been genetically separated from its repair function. In a recent issue of Molecular Cell, Yoshioka and coworkers show that MMR complexes (MutSα and MutLα) are required for the recruitment of ATR-ATRIP to sites of alkylation damage, demonstrating that MMR complexes can function as sensors in DNA damage signal transduction.

AB - The DNA mismatch repair (MMR) system maintains genome integrity by correcting replication errors. MMR also stimulates checkpoint and cell death responses to DNA damage suggested by the resistance of MMR-defective tumor cells to several chemotherapeutic agents. MMR-dependent cytotoxic response may result from futile repair; however, MMR-mediated apoptosis has been genetically separated from its repair function. In a recent issue of Molecular Cell, Yoshioka and coworkers show that MMR complexes (MutSα and MutLα) are required for the recruitment of ATR-ATRIP to sites of alkylation damage, demonstrating that MMR complexes can function as sensors in DNA damage signal transduction.

UR - http://www.scopus.com/inward/record.url?scp=33744928856&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33744928856&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2006.05.013

DO - 10.1016/j.ccr.2006.05.013

M3 - Short survey

C2 - 16766259

AN - SCOPUS:33744928856

SN - 1535-6108

VL - 9

SP - 417

EP - 418

JO - Cancer Cell

JF - Cancer Cell

IS - 6

ER -

Mismatch repair proteins as sensors of alkylation DNA damage

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this