Calcium signaling 2219538 221224612 2008-06-23T16:25:53Z DOI bot 6652755 Citation maintenance. You can [[WP:DOI|use this bot]] yourself! Please [[User:DOI_bot/bugs|report any bugs]]. {{expansion|date=January 2007}} Calcium can act in [[signal transduction]] after influx resulting from activation of [[ion channels]] or as a second messenger caused by indirect signal transduction pathways such as [[G protein-coupled receptors]]. Calcium is a common signaling mechanism, as once it enters the cytoplasm it exerts allosteric regulatory affects on many enzymes and proteins. ==Calcium signaling through ion channels== Movement of calcium ions from the extracellular compartment to the intracellular compartment alters membrane depolarisation. This is seen in the heart, during the plateau phase of ventricular contraction. In this example, calcium acts to maintain depolarisation of the heart. ==Calcium as a secondary messenger== Important physiological roles for calcium signaling include [[muscle contraction]], and cellular [[motility]], including the movement of [[flagella]] and [[cilia]]. Other biochemical roles of calcium include regulating [[enzyme]] activity, [[Ion pump (biology)|ion pump]]s, and components of the [[cytoskeleton]].<ref>Koolman, Roehm. ''Color Atlas of Biochemistry''. Thieme, 2005 ISBN 1-58890-247-1</ref> Signaling occurs when the cell is stimulated to release calcium ions (Ca<sup>2+</sup>) from intracellular stores. The resting concentration of Ca<sup>2+</sup> in the [[cytoplasm]] is normally maintained in the range of 10 - 100 nM. To maintain this low concentration, Ca<sup>2+</sup> is actively pumped from the cytosol and accumulated in the [[endoplasmic reticulum]] (ER), and sometimes in the [[mitochondria]]. Certain proteins of the cytoplasm and organelles act as buffers by binding Ca<sup>2+</sup>. Specific signals can trigger a sudden increase in the cytoplasmic Ca<sup>2+</sup> level up to 500 - 1 000 nM by opening channels in the [[endoplasmic reticulum]] or the [[plasma membrane]]. Many of Ca<sup>2+</sup>-mediated events occur when the released Ca<sup>2+</sup> binds to and activates the regulatory protein [[calmodulin]]. After cytoplasmic calcium has been depleted, Ca<sup>2+</sup> can be imported from outside the cell by activation of "Store Operated Channels" ([[SOC channels|SOCs]]). This inflowing calcium current that results after stored calcium reserves have been released is referred to as Ca2+-release-activated Ca2+ current ([[ICRAC]]). The mechanisms through which ICRAC occurs are currently still under investigation, although two candidate molecules, Orai1 and [[STIM1]] have been linked by several studies, and a model of store-operated [[calcium influx]], involving these molecules, has been proposed. Recent studies have cited the [[phospholipase]] A2 beta,<ref>Csutora P, Zarayskiy V, Peter K, Monje F, Smani T, Zakharov S, Litvinov D, Bolotina VM (2006) ''J Biol Chem'' 281 :34926-34945. </ref> nicotinic acid adenine dinucleotide phosphate (NAADP),<ref>Moccia F, Lim D, Nusco GA, Ercolano E, Santella L (2003) ''FASEB'' J 17: 1907-1909</ref> and the protein STIM 1<ref>Baba Y, et al. (2006) ''Proc Natl Acad Sci USA'' 103:16704-9</ref> as possible mediators of ICRAC. ==History== *{{cite journal | quotes = yes |last=Petersen |first=Ole H |authorlink= |year=[[2005]] |month= |title=Ca2+ signalling and Ca2+-activated ion channels in exocrine acinar cells |journal=Cell Calcium |volume=38 |issue=3-4 |pages=171–200 | publisher = | location = | issn = | pmid = 16107275 |doi = 10.1016/j.ceca.2005.06.024 | bibcode = | oclc =| id = | url = | language = | format = | accessdate = | laysummary = | laysource = | laydate = | quote = }} ==References== <references/> {{Cell_signaling}} {{Calcium signaling}} [[Category:Cell signaling]] [[Category:Signal transduction]]