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Article: The molecular basis of enzyme secretion

TitleThe molecular basis of enzyme secretion
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1990
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 1990, v. 99 n. 4, p. 1157-1176 How to Cite?
AbstractAcinar cells are one of the best studied models of exocytotic secretion. A number of different hormones and neurotransmitters interact with specific membrane receptors, and it is commonly held that pancreatic secretagogues stimulate enzyme release via the elevation of either cytosolic free Ca2+ or cellular cyclic adenosine monophosphate. The discovery of the pivotal role played by phospholipid metabolism in the chain of events leading to secretion, together with the introduction of sensitive techniques to monitor cytosolic free Ca2+, has generated a series of studies that have challenged this classical model. Thus, several observations in pancreatic acini as well as other cell types have argued against the notion that a generalized increase in cytosolic free Ca2+ represents a sufficient and necessary stimulus for exocytosis in nonexcitable cells. Furthermore, the demonstration that a single agonist activates multiple transduction pathways has served to refute the schematic view that receptor agonists activate only one second messenger system. The aim of this article is to review the recent advances in understanding the molecular and cellular mechanisms of signal transduction, with particular emphasis on the inositol lipid pathway, and to integrate this information into a new working model of enzyme secretion from acinar cells.
Persistent Identifierhttp://hdl.handle.net/10722/132772
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBruzzone, Ren_HK
dc.date.accessioned2011-03-28T09:28:52Z-
dc.date.available2011-03-28T09:28:52Z-
dc.date.issued1990en_HK
dc.identifier.citationGastroenterology, 1990, v. 99 n. 4, p. 1157-1176en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132772-
dc.description.abstractAcinar cells are one of the best studied models of exocytotic secretion. A number of different hormones and neurotransmitters interact with specific membrane receptors, and it is commonly held that pancreatic secretagogues stimulate enzyme release via the elevation of either cytosolic free Ca2+ or cellular cyclic adenosine monophosphate. The discovery of the pivotal role played by phospholipid metabolism in the chain of events leading to secretion, together with the introduction of sensitive techniques to monitor cytosolic free Ca2+, has generated a series of studies that have challenged this classical model. Thus, several observations in pancreatic acini as well as other cell types have argued against the notion that a generalized increase in cytosolic free Ca2+ represents a sufficient and necessary stimulus for exocytosis in nonexcitable cells. Furthermore, the demonstration that a single agonist activates multiple transduction pathways has served to refute the schematic view that receptor agonists activate only one second messenger system. The aim of this article is to review the recent advances in understanding the molecular and cellular mechanisms of signal transduction, with particular emphasis on the inositol lipid pathway, and to integrate this information into a new working model of enzyme secretion from acinar cells.en_HK
dc.languageengen_US
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.titleThe molecular basis of enzyme secretionen_HK
dc.typeArticleen_HK
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hken_HK
dc.identifier.authorityBruzzone, R=rp01442en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2118462-
dc.identifier.scopuseid_2-s2.0-0025077725en_HK
dc.identifier.volume99en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1157en_HK
dc.identifier.epage1176en_HK
dc.identifier.isiWOS:A1990DY35300036-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridBruzzone, R=7006793327en_HK

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