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Inhibition of TRPM2 function by PARP inhibitors protects cells from oxidative stress‐induced death
Author(s) -
Miller Barbara A
Publication year - 2004
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705923
Subject(s) - trpm2 , poly adp ribose polymerase , transient receptor potential channel , oxidative stress , programmed cell death , microbiology and biotechnology , oxidative phosphorylation , chemistry , calcium , cancer research , biology , receptor , biochemistry , apoptosis , polymerase , enzyme , organic chemistry
TRPM2 is a member of the transient receptor potential (TRP) protein superfamily of calcium‐permeable, voltage‐independent ion channels expressed in nonexcitable cells. Activation of TRPM2 by oxidative stress results in calcium influx and susceptibility to cell death, whereas inhibition of TRPM2 function enhances cell survival. In the present edition of this journal, Fonfria et al . demonstrate a role for poly(ADP ribose) polymerase (PARP) as a mediator between oxidative stress and TRPM2 activation. They present evidence that inhibition of either PARP or TRPM2 protects cells from plasma membrane damage and cell death. The therapeutic implications of this important observation are discussed. British Journal of Pharmacology (2004) 143 , 515–516. doi: 10.1038/sj.bjp.0705923