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Diabetic neuropathy: inhibitory G protein dysfunction involves PKC-dependent phosphorylation of G oα
dc.contributor.authorShangguan, Yuen_US
dc.contributor.authorHall, Karen E.en_US
dc.contributor.authorNeubig, Richard R.en_US
dc.contributor.authorWiley, John W.en_US
dc.date.accessioned2010-04-01T15:53:18Z
dc.date.available2010-04-01T15:53:18Z
dc.date.issued2003-08en_US
dc.identifier.citationShangguan, Yu; Hall, Karen E.; Neubig, Richard R.; Wiley, John W. (2003). "Diabetic neuropathy: inhibitory G protein dysfunction involves PKC-dependent phosphorylation of G oα ." Journal of Neurochemistry 86(4): 1006-1014. <http://hdl.handle.net/2027.42/66385>en_US
dc.identifier.issn0022-3042en_US
dc.identifier.issn1471-4159en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/66385
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12887697&dopt=citationen_US
dc.description.abstractWe examined the hypothesis that decreased inhibitory G protein function in diabetic neuropathy is associated with increased protein kinase C (PKC)-dependent phosphorylation of the G oα subunit. Streptozotocin-induced diabetic rats were studied between 4 and 8 weeks after onset of diabetes and compared with aged-matched healthy animals as controls. Opioid-mediated inhibition of forskolin-stimulated cyclic AMP was significantly less in dorsal root ganglia (DRGs) from diabetic rats compared with controls. Activation of PKC in DRGs from control rats was associated with a significant decrease in opioid-mediated inhibition of forskolin-stimulated cyclic AMP that was similar to the decrease in inhibition observed in DRGs from diabetic rats. Both basal and PKC-mediated labeling of G oα with 32 P i was significantly less in DRGs from diabetic rats, supporting increased endogenous PKC-dependent phosphorylation of G oα . Probing of immunoprecipitated G oα with an anti-phospho-serine/threonine specific antibody revealed a significant increase in baseline phosphorylation in diabetic DRGs. Activation of PKC produced a significant increase in phosphorylation in control DRGs but no significant increase in G oα in diabetic DRGs. Phosphorylation of PKC-α was increased, PKC-β II was unchanged and PKC-δ decreased in diabetic DRGs. These results suggest that diminished inhibitory G protein function observed in DRGs neurons from diabetic rats involves an isoform-specific PKC-dependent pathway.en_US
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dc.format.extent3110 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Science Ltden_US
dc.rights2003 International Society for Neurochemistryen_US
dc.subject.otherDiabetes Mellitusen_US
dc.subject.otherDiabetic Neuropathyen_US
dc.subject.otherG Proteinen_US
dc.subject.otherPKCen_US
dc.titleDiabetic neuropathy: inhibitory G protein dysfunction involves PKC-dependent phosphorylation of G oαen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum† Ann Arbor VA Medical Center, University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationotherDepartments of * Internal Medicine anden_US
dc.contributor.affiliationother† Pharmacology,en_US
dc.identifier.pmid12887697en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/66385/1/j.1471-4159.2003.01912.x.pdf
dc.identifier.doi10.1046/j.1471-4159.2003.01912.xen_US
dc.identifier.sourceJournal of Neurochemistryen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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