Please use this identifier to cite or link to this item:
Title: FLIP: A flop for execution signals
Authors: Subramaniam, K.
Hirpara, J.L. 
Tucker-Kellogg, L. 
Tucker-Kellogg, G. 
Pervaiz, S.
Keywords: Apoptosis
Issue Date: 28-May-2013
Citation: Subramaniam, K., Hirpara, J.L., Tucker-Kellogg, L., Tucker-Kellogg, G., Pervaiz, S. (2013-05-28). FLIP: A flop for execution signals. Cancer Letters 332 (2) : 151-155. ScholarBank@NUS Repository.
Abstract: Resistance to apoptosis is one of the established hallmarks of cancer cells. This is a function of an imbalance between the proteins that facilitate death execution and those that inhibit apoptosis or promote cell proliferation. The anti-apoptotic protein, FLICE inhibitory protein (FLIP), first identified as a viral protein, is over-expressed in a variety of human pathologies. Initial observations linked FLIP expression to inhibition of death receptor induced apoptosis, due to its structural homology to the cysteine protease, caspase-8. FLIP impedes full processing of pro-caspase-8 to its active form and its release to the cytosol, and by doing so blocks apoptotic signaling downstream of the membrane death initiating signaling complex (DISC). Recent observations have highlighted the complex regulation of this protein and its cross talk with diverse signaling networks and metabolic processes. As FLIP expression is directly associated with chemotherapy resistance, a better understanding of its genomic organization, gene transcription, as well as post-transcriptional regulation could yield novel targets with potential therapeutic implications against drug refractory cancers. In this short review, we provide a brief overview of the structural and functional biology of this somewhat complex protein with direct relevance to carcinogenesis. © 2012 Elsevier Ireland Ltd.
Source Title: Cancer Letters
ISSN: 03043835
DOI: 10.1016/j.canlet.2012.07.005
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.