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Medicine, College of >
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Microbiology and Immunology, Department of >
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Please use this identifier to cite or link to this item: http://hdl.handle.net/10027/6206

Title:	Resistance to TRAIL-induced apoptosis: role of IG20 splice variants
Other Titles:	Role of IG20 splice variants in TRAIL resistance
Authors:	Prabhakar, Bellur S. Mulherkar, Nirupama Prasad, Kanteti V.
Issue Date:	Jan-2008
Publisher:	American Association for Cancer Research
Citation:	Prabhakar 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/14/2/347
Abstract:	Tumor 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.
Description:	Postprint version of article may differ from published version
URI:	http://hdl.handle.net/10027/6206
ISSN:	1078-0432
Appears in Collections:	Publications - Microbiology and Immunology

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