Journal article

Fas death receptor signalling: roles of Bid and XIAP

T Kaufmann, A Strasser, PJ Jost

CELL DEATH AND DIFFERENTIATION | NATURE PUBLISHING GROUP | Published : 2012

Abstract

Fas (also called CD95 or APO-1), a member of a subgroup of the tumour necrosis factor receptor superfamily that contain an intracellular death domain, can initiate apoptosis signalling and has a critical role in the regulation of the immune system. Fas-induced apoptosis requires recruitment and activation of the initiator caspase, caspase-8 (in humans also caspase-10), within the death-inducing signalling complex. In so-called type 1 cells, proteolytic activation of effector caspases (-3 and -7) by caspase-8 suffices for efficient apoptosis induction. In so-called type 2 cells, however, killing requires amplification of the caspase cascade. This can be achieved through caspase-8-mediated pro..

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University of Melbourne Researchers

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Awarded by Australian NHMRC


Awarded by NIH


Awarded by Leukemia and Lymphoma Society (LLS)


Awarded by JDRF/NHMRC


Awarded by Swiss National Science Foundation


Awarded by NATIONAL CANCER INSTITUTE


Funding Acknowledgements

We dedicate this review to the memory of Juerg Tschopp, wonderfully generous human being and outstanding scientist, who left behind not only important scientific discoveries, but also, importantly, the novel treatments for several inflammatory diseases. He will be solely missed. We thank all the present and the past members of the apoptosis research programs at WEHI, particularly Drs JM Adams, S Cory, D Vaux, J Silke, D Huang, P Colman, P Bouillet, R Kluck and C Scott, for their outstanding contributions and stimulating discussions. Research in our laboratories is supported by fellowships and grants from the Australian NHMRC (257502, 461299), NIH (CA 043540), Leukemia and Lymphoma Society (LLS SCOR 7413), JDRF/NHMRC (466658), the Max-Eder Program grant from the Mildred Scheel-Stiftung/Deutsche Krebshilfe, the Novartis Foundation for Medicine and Biology, and the Swiss National Science Foundation (PP00A-119203).