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Tyrosine Kinase Inhibitors Attenuate "Capacitative" Ca2+ Influx in Rat Pancreatic Acinar Cells

dc.contributor.authorYule D. I. ,en_US
dc.contributor.authorKim E. T. ,en_US
dc.contributor.authorWilliams J. A. ,en_US
dc.date.accessioned2006-05-10T15:36:59Z
dc.date.available2006-05-10T15:36:59Z
dc.date.issued1994-08-15en_US
dc.identifier.citationYule D. I., , Kim E. T., , Williams J. A., (1994/08/15)."Tyrosine Kinase Inhibitors Attenuate "Capacitative" Ca2+ Influx in Rat Pancreatic Acinar Cells." Biochemical and Biophysical Research Communications 202(3): 1697-1704. <http://hdl.handle.net/2027.42/31389>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6WBK-45PMMDV-RM/2/8c24736374888998fcb80a75fa669438en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/31389
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8060359&dopt=citationen_US
dc.description.abstractThe effect of several tyrosine kinase inhibitors was tested on Ca2+ influx mediated by thapsigargin-and CCh-induced intracellular store depletion. Genestein inhibited Ca2+ influx in a concentration dependent manner without affecting Ca2+ release or Ca2+ pumping activity. A measureable effect was observed at 3 [mu]M with total inhibition of influx seen at 100 [mu]M. Tyrphostin A25 (300 [mu]M; 78% inhibition) and methyl 2,5 dihydroxycinnamate (10 [mu]M; 51% inhibition) also inhibited Ca2+ influx. The degree of attenuation was not markedly altered by preincubation of the inhibitors. Genestein also inhibited Ca2+ influx induced by CCh. These data indicate that inhibition of Ca2+ influx could in part underlie the previously reported inhibition of enzyme secretion by these agents.en_US
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dc.format.extent3118 bytes
dc.format.extent428435 bytes
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dc.format.mimetypeapplication/pdf
dc.language.isoen_USen_US
dc.publisherElsevieren_US
dc.titleTyrosine Kinase Inhibitors Attenuate "Capacitative" Ca2+ Influx in Rat Pancreatic Acinar Cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNatural Resources and Environmenten_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelEcology and Evolutionary Biologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan, Sch Med, Dept Physiol, Ann Arbor, MI 48109, USA and Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109, USAen_US
dc.contributor.affiliationumUniversity of Michigan, Sch Med, Dept Physiol, Ann Arbor, MI 48109, USA and Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109, USAen_US
dc.contributor.affiliationumUniversity of Michigan, Sch Med, Dept Physiol, Ann Arbor, MI 48109, USA and Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109, USAen_US
dc.identifier.pmid8060359en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/31389/3/0000303.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1006/bbrc.1994.2130en_US
dc.identifier.sourceBiochemical and Biophysical Research Communicationsen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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