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 journalArticle

65 Citations (Scopus)

Abstract

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
Volume102
Issue number5
DOIs
StatePublished - Feb 1 2005

Fingerprint

Inositol 1,4,5-Trisphosphate Receptors
NAD
Calcium Signaling
Calcium
Endoplasmic Reticulum
Cysteine

All Science Journal Classification (ASJC) codes

  • General

Cite this

@article{5cf51d24a25a4514bb4a269c13a575d5,
title = "Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca 2+ release via locally derived NADH",
abstract = "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.",
author = "Patterson, {Randen L.} and {Van Rossum}, {Damian B.} and Kaplin, {Adam I.} and Barrow, {Roxanne K.} and Snyder, {Solomon H.}",
year = "2005",
month = "2",
day = "1",
doi = "10.1073/pnas.0409657102",
language = "English (US)",
volume = "102",
pages = "1357--1359",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "5",

}

Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca 2+ release via locally derived NADH. / Patterson, Randen L.; Van Rossum, Damian B.; Kaplin, Adam I.; Barrow, Roxanne K.; Snyder, Solomon H.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, No. 5, 01.02.2005, p. 1357-1359.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca 2+ release via locally derived NADH

AU - Patterson, Randen L.

AU - Van Rossum, Damian B.

AU - Kaplin, Adam I.

AU - Barrow, Roxanne K.

AU - Snyder, Solomon H.

PY - 2005/2/1

Y1 - 2005/2/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=13444255991&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=13444255991&partnerID=8YFLogxK

U2 - 10.1073/pnas.0409657102

DO - 10.1073/pnas.0409657102

M3 - Article

C2 - 15677321

AN - SCOPUS:13444255991

VL - 102

SP - 1357

EP - 1359

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 5

ER -