LTRPC2 Ca2+-Permeable channel activated by changes in redox status confers susceptibility to cell death

Yuji Hara, Minoru Wakamori, Masakazu Ishii, Emi Maeno, Motohiro Nishida, Takashi Yoshida, Hisanobu Yamada, Shunichi Shimizu, Emiko Mori, Jun Kudoh, Nobuyoshi Shimizu, Hitoshi Kurose, Yasunobu Okada, Keiji Imoto, Yasuo Mori

Research output: Contribution to journalArticlepeer-review

643 Citations (Scopus)


Redox status changes exert critical impacts on necrotic/apoptotic and normal cellular processes. We report here a widely expressed Ca2+-permeable cation channel, LTRPC2, activated by micromolar levels of H2O2 and agents that produce reactive oxygen/nitrogen species. This sensitivity of LTRPC2 to redox state modifiers was attributable to an agonistic binding of nicotinamide adenine dinucleotide (β-NAD+) to the MutT motif. Arachidonic acid and Ca2+ were important positive regulators for LTRPC2. Heterologous LTRPC2 expression conferred susceptibility to death on HEK cells. Antisense oligonucleotide experiments revealed physiological involvement of "native" LTRPC2 in H2O2- and TNFα-induced Ca2+ influx and cell death. Thus, LTRPC2 represents an important intrinsic mechanism that mediates Ca2+ and Na+ overload in response to disturbance of redox state in cell death.

Original languageEnglish
Pages (from-to)163-173
Number of pages11
JournalMolecular Cell
Issue number1
Publication statusPublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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