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Article: Protein kinase C delta is not activated by caspase-3 and its inhibition is sufficient to induce apoptosis in the colon cancer line, COLO 205

TitleProtein kinase C delta is not activated by caspase-3 and its inhibition is sufficient to induce apoptosis in the colon cancer line, COLO 205
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cellsig
Citation
Cellular Signalling, 2005, v. 17 n. 2, p. 253-262 How to Cite?
AbstractActivation of protein kinase C δ (PKCδ) is believed to be pro-apoptotic. PKCδ is reported to be reduced in colon cancers. Using a colon cancer cell line, COLO 205, we have examined the roles of PKCδ in apoptosis and of caspase-3 in the activation and inhibition of PKCδ. PKCδ activation with bistratene A and its inhibition with rottlerin induced apoptosis. Effects of PKC activators and inhibitors were additive, suggesting that PKCδ down-regulation was responsible for the effects on apoptosis. Different apoptotic pathways induced PKCδ cleavage, but the fragment produced was inactive in kinase assays. Caspase-3 inhibition did not block DNA fragmentation or PKCδ proteolysis despite blocking intracellular caspase-3 activity. Calpain inhibition with calpeptin did not prevent TPA-induced PKCδ cleavage. We conclude that in colonocytes, inhibition of PKCδ is sufficient to lead to caspase-3-independent apoptosis. Caspase-3 does not cleave PKCδ to an active form, nor does caspase-3 inhibition block apoptosis. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76368
ISSN
2015 Impact Factor: 4.191
2015 SCImago Journal Rankings: 2.289
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLewis, AEen_HK
dc.contributor.authorSusarla, Ren_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorLangman, MJSen_HK
dc.contributor.authorEggo, MCen_HK
dc.date.accessioned2010-09-06T07:20:29Z-
dc.date.available2010-09-06T07:20:29Z-
dc.date.issued2005en_HK
dc.identifier.citationCellular Signalling, 2005, v. 17 n. 2, p. 253-262en_HK
dc.identifier.issn0898-6568en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76368-
dc.description.abstractActivation of protein kinase C δ (PKCδ) is believed to be pro-apoptotic. PKCδ is reported to be reduced in colon cancers. Using a colon cancer cell line, COLO 205, we have examined the roles of PKCδ in apoptosis and of caspase-3 in the activation and inhibition of PKCδ. PKCδ activation with bistratene A and its inhibition with rottlerin induced apoptosis. Effects of PKC activators and inhibitors were additive, suggesting that PKCδ down-regulation was responsible for the effects on apoptosis. Different apoptotic pathways induced PKCδ cleavage, but the fragment produced was inactive in kinase assays. Caspase-3 inhibition did not block DNA fragmentation or PKCδ proteolysis despite blocking intracellular caspase-3 activity. Calpain inhibition with calpeptin did not prevent TPA-induced PKCδ cleavage. We conclude that in colonocytes, inhibition of PKCδ is sufficient to lead to caspase-3-independent apoptosis. Caspase-3 does not cleave PKCδ to an active form, nor does caspase-3 inhibition block apoptosis. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cellsigen_HK
dc.relation.ispartofCellular Signallingen_HK
dc.rightsCellular Signalling. Copyright © Elsevier Inc.en_HK
dc.subject.meshAcetamides - pharmacologyen_HK
dc.subject.meshAcetophenones - pharmacologyen_HK
dc.subject.meshAlkaloidsen_HK
dc.subject.meshAmino Acid Chloromethyl Ketones - pharmacologyen_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshBenzophenanthridinesen_HK
dc.subject.meshBenzopyrans - pharmacologyen_HK
dc.subject.meshCalpain - antagonists & inhibitorsen_HK
dc.subject.meshCaspase 3en_HK
dc.subject.meshCaspases - antagonists & inhibitors - metabolism - physiologyen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshColonic Neoplasms - chemistry - metabolism - pathologyen_HK
dc.subject.meshCysteine Proteinase Inhibitors - pharmacologyen_HK
dc.subject.meshDNA Fragmentation - drug effectsen_HK
dc.subject.meshDipeptides - pharmacologyen_HK
dc.subject.meshEnzyme Activationen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshHistones - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIndomethacin - pharmacologyen_HK
dc.subject.meshKineticsen_HK
dc.subject.meshPhenanthridines - pharmacologyen_HK
dc.subject.meshPhosphorylation - drug effectsen_HK
dc.subject.meshProtein Kinase C - metabolism - physiologyen_HK
dc.subject.meshProtein Kinase C-deltaen_HK
dc.subject.meshPyrans - pharmacologyen_HK
dc.subject.meshSpiro Compounds - pharmacologyen_HK
dc.subject.meshTetradecanoylphorbol Acetate - pharmacologyen_HK
dc.subject.meshTumor Necrosis Factor-alpha - pharmacologyen_HK
dc.titleProtein kinase C delta is not activated by caspase-3 and its inhibition is sufficient to induce apoptosis in the colon cancer line, COLO 205en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0898-6568&volume=17&issue=2&spage=253&epage=262&date=2005&atitle=Protein+kinase+C+delta+is+not+activated+by+caspase-3+and+its+inhibition+is+sufficient+to+induce+apoptosis+in+the+colon+cancer+line,+COLO+205en_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cellsig.2004.07.005en_HK
dc.identifier.pmid15494216-
dc.identifier.scopuseid_2-s2.0-5644266524en_HK
dc.identifier.hkuros99181en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-5644266524&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue2en_HK
dc.identifier.spage253en_HK
dc.identifier.epage262en_HK
dc.identifier.isiWOS:000224930000012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLewis, AE=7403488048en_HK
dc.identifier.scopusauthoridSusarla, R=18838807700en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridLangman, MJS=7102542271en_HK
dc.identifier.scopusauthoridEggo, MC=7006000548en_HK

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