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dc.contributor.authorPrabhakar, Bellur S.
dc.contributor.authorMulherkar, Nirupama
dc.contributor.authorPrasad, Kanteti V.
dc.date.accessioned2009-08-08T16:13:17Z
dc.date.available2009-08-08T16:13:17Z
dc.date.issued2008-01
dc.identifier.bibliographicCitationPrabhakar BS, Mulherkar N, Prasad KV. Role of IG20 splice variants in TRAIL resistance. Clin Cancer Res. 2008 Jan 15;14(2):347-51. http://clincancerres.aacrjournals.org/cgi/reprint/14/2/347en
dc.identifier.issn1078-0432
dc.identifier.otherdoi: 10.1158/1078-0432.CCR-07-0493
dc.identifier.urihttp://hdl.handle.net/10027/6206
dc.descriptionPostprint version of article may differ from published versionen
dc.description.abstractTumor necrosis factor receptor–related apoptosis-inducing ligand (TRAIL) can induce apoptosis primarily in cancer cells with little or no effect on normal cells; therefore, it has the potential for use in cancer therapy. TRAIL binding to death receptors DR4 and DR5 triggers the death-inducing signal complex formation and activation of procaspase-8, which in turn activates caspase-3, leading to cell death. Like FasL, TRAIL can trigger type 1 (caspase-8 caspase-3) or type 2 (caspase-8 Bid cleavage capsase-9 caspase-3) apoptotic pathways depending on the cell type. Some cancers are resistant to TRAIL treatment because most molecules in the TRAIL signaling pathway, including FLIPs and IAPs, can contribute to resistance. In addition, we have identified an essential role for splice variants of the IG20 gene in TRAIL resistance.en
dc.language.isoen_USen
dc.publisherAmerican Association for Cancer Researchen
dc.titleResistance to TRAIL-induced apoptosis: role of IG20 splice variantsen
dc.title.alternativeRole of IG20 splice variants in TRAIL resistanceen
dc.typeArticleen


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