Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca 2+ release via locally derived NADH

Randen L. Patterson, Damian B. Van Rossum, Adam I. Kaplin, Roxanne K. Barrow, Solomon H. Snyder

Research output: Contribution to journalArticlepeer-review

70 Scopus citations


NADH regulates the release of calcium from the endoplasmic reticulum by modulation of inositol 1,4,5-trisphosphate receptors (IP3R), accounting for the augmented calcium release of hypoxic cells. We report selective binding of IP3R to GAPDH, whose activity leads to the local generation of NADH to regulate intracellular calcium signaling. This interaction requires cysteines 992 and 995 of IP3R and C150 of GAPDH. Addition of native GAPDH and NAD+ to WT IP3R stimulates calcium release, whereas no stimulation occurs with C992S/995S IP3R that cannot bind GAPDH. Thus, the IP3R/GAPDH interaction likely enables cellular energy dynamics to impact calcium signaling.

Original languageEnglish (US)
Pages (from-to)1357-1359
Number of pages3
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number5
StatePublished - Feb 1 2005
Externally publishedYes


  • Calcium
  • Hypoxia
  • Metabolism

ASJC Scopus subject areas

  • Genetics
  • General


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