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dc.contributor.authorKane, J. K.en_US
dc.contributor.authorKonu, Özlemen_US
dc.contributor.authorMa, J. Z.en_US
dc.contributor.authorLi, M. D.en_US
dc.coverage.spatialNew Orleans, USAen_US
dc.date.accessioned2016-02-08T11:52:24Zen_US
dc.date.available2016-02-08T11:52:24Zen_US
dc.date.issued2004en_US
dc.identifier.issn0169-328Xen_US
dc.identifier.urihttp://hdl.handle.net/11693/27400en_US
dc.descriptionDate of Conference: 6-7 November 2003en_US
dc.descriptionConference Name: 5th Brain Research Symposium, 2003en_US
dc.description.abstractPreviously, we used cDNA microarrays to demonstrate that the phosphatidylinositol and MAP kinase signaling pathways are regulated by nicotine in different rat brain regions. In the present report, we show that, after exposure to nicotine for 14 days, ubiquitin, ubiquitin-conjugating enzymes, 20S and 19S proteasomal subunits, and chaperonin-containing TCP-1 protein (CCT) complex members are upregulated in rat prefrontal cortex (PFC) while being downregulated in the medial basal hypothalamus (MBH). In particular, relative to saline controls, ubiquitins B and C were upregulated by 33% and 47% (P<0.01), respectively, in the PFC. The proteasome beta subunit 1 (PSMB1) and 26S ATPase 3 (PSMC3) genes were upregulated in the PFC by 95% and 119% (P<0.001), respectively. In addition to the protein degradation pathway of the ubiquitin-proteasome complexes, we observed in the PFC an increase in the expression of small, ubiquitin-related modifiers (SUMO) 1 and 2 by 80% and 33%, respectively (P<0.001), and in 3 of 6 CCT subunits by up to 150% (P<0.0001). To a lesser extent, a change in the opposite direction was obtained in the expression of the same gene families in the MBH. Quantitative real-time RT-PCR was used to validate the microarray results obtained with some representative genes involved in these pathways. Taken together, our results suggest that, in response to systemic nicotine administration, the ubiquitin-proteasome, SUMO, and chaperonin complexes provide an intricate control mechanism to maintain cellular homeostasis, possibly by regulating the composition and signaling of target neurons in a region-specific manner.en_US
dc.language.isoEnglishen_US
dc.source.titleMolecular Brain Researchen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.molbrainres.2004.09.010en_US
dc.subjectcDNA microarraysen_US
dc.subjectNicotineen_US
dc.subjectProteasomesen_US
dc.subjectReal-time RT-PCRen_US
dc.subjectUbiquitinen_US
dc.subjectPrefrontal cortexen_US
dc.subjectHypothalamusen_US
dc.subjectUbiquitin conjugating enzymeen_US
dc.subjectNeurotransmissionen_US
dc.subjectNucleotide sequenceen_US
dc.subjectProtein modificationen_US
dc.subjectQuantitative analysisen_US
dc.subjectNicotinic agonistsen_US
dc.subjectOligonucleotide array sequence analysisen_US
dc.subjectProteasome endopeptidase complexen_US
dc.titleNicotine coregulates multiple pathways involved in protein modification/degradation in rat brainen_US
dc.typeConference Paperen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.citation.spage181en_US
dc.citation.epage191en_US
dc.citation.volumeNumber132en_US
dc.citation.issueNumber2en_US
dc.identifier.doi10.1016/j.molbrainres.2004.09.010en_US
dc.publisherElsevieren_US


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