Literature DB >> 19133301

Regulation of inositol 1,4,5-trisphosphate-induced Ca2+ release by reversible phosphorylation and dephosphorylation.

Veerle Vanderheyden1, Benoit Devogelaere, Ludwig Missiaen, Humbert De Smedt, Geert Bultynck, Jan B Parys.   

Abstract

The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) is a universal intracellular Ca2+-release channel. It is activated after cell stimulation and plays a crucial role in the initiation and propagation of the complex spatio-temporal Ca2+ signals that control cellular processes as different as fertilization, cell division, cell migration, differentiation, metabolism, muscle contraction, secretion, neuronal processing, and ultimately cell death. To achieve these various functions, often in a single cell, exquisite control of the Ca2+ release is needed. This review aims to highlight how protein kinases and protein phosphatases can interact with the IP3R or with associated proteins and so provide a large potential for fine tuning the Ca2+-release activity and for creating efficient Ca2+ signals in subcellular microdomains.

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Year:  2008        PMID： 19133301      PMCID： PMC2693466          DOI： 10.1016/j.bbamcr.2008.12.003

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN： 0006-3002


  195 in total

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2.  Ca2+-calmodulin inhibits Ca2+ release mediated by type-1, -2 and -3 inositol trisphosphate receptors.

Authors:  C E Adkins; S A Morris; H De Smedt; I Sienaert; K Török; C W Taylor
Journal:  Biochem J       Date:  2000-01-15       Impact factor: 3.857

3.  Modulation of inositol 1,4,5-trisphosphate binding to the recombinant ligand-binding site of the type-1 inositol 1,4, 5-trisphosphate receptor by Ca2+ and calmodulin.

Authors:  H Sipma; P De Smet; I Sienaert; S Vanlingen; L Missiaen; J B Parys; H De Smedt
Journal:  J Biol Chem       Date:  1999-04-23       Impact factor: 5.157

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Authors:  R K Srivastava; Q S Mi; J M Hardwick; D L Longo
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Authors:  K Yamamoto; H Ichijo; S J Korsmeyer
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6.  Phosphorylation of the inositol 1,4,5-trisphosphate receptor by cyclic nucleotide-dependent kinases in vitro and in rat cerebellar slices in situ.

Authors:  L S Haug; V Jensen; O Hvalby; S I Walaas; A C Ostvold
Journal:  J Biol Chem       Date:  1999-03-12       Impact factor: 5.157

7.  Encoding of Ca2+ signals by differential expression of IP3 receptor subtypes.

Authors:  T Miyakawa; A Maeda; T Yamazawa; K Hirose; T Kurosaki; M Iino
Journal:  EMBO J       Date:  1999-03-01       Impact factor: 11.598

8.  cGMP inhibits IP3-induced Ca2+ release in intact rat megakaryocytes via cGMP- and cAMP-dependent protein kinases.

Authors:  S Tertyshnikova; X Yan; A Fein
Journal:  J Physiol       Date:  1998-10-01       Impact factor: 5.182

9.  Differential distribution of inositol trisphosphate receptor isoforms in mouse oocytes.

Authors:  R A Fissore; F J Longo; E Anderson; J B Parys; T Ducibella
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Review 2.  cGMP-dependent protein kinases and cGMP phosphodiesterases in nitric oxide and cGMP action.

Authors:  Sharron H Francis; Jennifer L Busch; Jackie D Corbin; David Sibley
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3.  InsP3R-associated cGMP kinase substrate determines inositol 1,4,5-trisphosphate receptor susceptibility to phosphoregulation by cyclic nucleotide-dependent kinases.

Authors:  Wataru Masuda; Matthew J Betzenhauser; David I Yule
Journal:  J Biol Chem       Date:  2010-09-27       Impact factor: 5.157

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6.  Functional inositol 1,4,5-trisphosphate receptors assembled from concatenated homo- and heteromeric subunits.

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7.  Loss of activity mutations in phospholipase C zeta (PLCζ) abolishes calcium oscillatory ability of human recombinant protein in mouse oocytes.

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Review 8.  The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.

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10.  Isoform- and species-specific control of inositol 1,4,5-trisphosphate (IP3) receptors by reactive oxygen species.

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