Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors

Calcium release via intracellular Ca2+ release channels is a central event underpinning the generation of numerous, often divergent physiological processes. In electrically non-excitable cells, this Ca2+ release is brought about primarily through activation of inositol 1,4,5-trisphosphate receptors...

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Autores principales:	STRAUB,STEPHEN V, WAGNER II,LARRY E, BRUCE,JASON I.E, YULE,DAVID I
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2004
Materias:	Inositol 1,4,5-trisphosphate receptor protein kinase A calcium signaling pancreatic acinar cells parotid acinar cells
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400013
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spelling	oai:scielo:S0716-976020040004000132005-06-02Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptorsSTRAUB,STEPHEN VWAGNER II,LARRY EBRUCE,JASON I.EYULE,DAVID I Inositol 1,4,5-trisphosphate receptor protein kinase A calcium signaling pancreatic acinar cells parotid acinar cells Calcium release via intracellular Ca2+ release channels is a central event underpinning the generation of numerous, often divergent physiological processes. In electrically non-excitable cells, this Ca2+ release is brought about primarily through activation of inositol 1,4,5-trisphosphate receptors and typically takes the form of calcium oscillations. It is widely believed that information is carried in the temporal and spatial characteristics of these signals. Furthermore, stimulation of individual cells with different agonists can generate Ca2+ oscillations with dramatically different spatial and temporal characteristics. Thus, mechanisms must exist for the acute regulation of Ca2+ release such that agonist-specific Ca2+ signals can be generated. One such mechanism by which Ca2+ signals can be modulated is through simultaneous activation of multiple second messenger pathways. For example, activation of both the InsP3 and cAMP pathways leads to the modulation of Ca2+ release through protein kinase A mediated phosphoregulation of the InsP3R. Indeed, each InsP3R subtype is a potential substrate for PKA, although the functional consequences of this phosphorylation are not clear. This review will focus on recent advances in our understanding of phosphoregulation of InsP3R, as well as the functional consequences of this modulation in terms of eliciting specific cellular events.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.37 n.4 20042004-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400013en10.4067/S0716-97602004000400013
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Inositol 1,4,5-trisphosphate receptor protein kinase A calcium signaling pancreatic acinar cells parotid acinar cells
spellingShingle	Inositol 1,4,5-trisphosphate receptor protein kinase A calcium signaling pancreatic acinar cells parotid acinar cells STRAUB,STEPHEN V WAGNER II,LARRY E BRUCE,JASON I.E YULE,DAVID I Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
description	Calcium release via intracellular Ca2+ release channels is a central event underpinning the generation of numerous, often divergent physiological processes. In electrically non-excitable cells, this Ca2+ release is brought about primarily through activation of inositol 1,4,5-trisphosphate receptors and typically takes the form of calcium oscillations. It is widely believed that information is carried in the temporal and spatial characteristics of these signals. Furthermore, stimulation of individual cells with different agonists can generate Ca2+ oscillations with dramatically different spatial and temporal characteristics. Thus, mechanisms must exist for the acute regulation of Ca2+ release such that agonist-specific Ca2+ signals can be generated. One such mechanism by which Ca2+ signals can be modulated is through simultaneous activation of multiple second messenger pathways. For example, activation of both the InsP3 and cAMP pathways leads to the modulation of Ca2+ release through protein kinase A mediated phosphoregulation of the InsP3R. Indeed, each InsP3R subtype is a potential substrate for PKA, although the functional consequences of this phosphorylation are not clear. This review will focus on recent advances in our understanding of phosphoregulation of InsP3R, as well as the functional consequences of this modulation in terms of eliciting specific cellular events.
author	STRAUB,STEPHEN V WAGNER II,LARRY E BRUCE,JASON I.E YULE,DAVID I
author_facet	STRAUB,STEPHEN V WAGNER II,LARRY E BRUCE,JASON I.E YULE,DAVID I
author_sort	STRAUB,STEPHEN V
title	Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
title_short	Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
title_full	Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
title_fullStr	Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
title_full_unstemmed	Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
title_sort	modulation of cytosolic calcium signaling by protein kinase a-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors
publisher	Sociedad de Biología de Chile
publishDate	2004
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400013
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Modulation of cytosolic calcium signaling by protein kinase A-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors

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