Cells 2012, 1(4), 711-737; doi:10.3390/cells1040711

The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress

1,2email, 1,2email, 2,3email and 1,2,* email
Received: 31 July 2012; in revised form: 14 September 2012 / Accepted: 27 September 2012 / Published: 10 October 2012
(This article belongs to the Special Issue Cellular Stress Response)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: Cells are constantly exposed to endogenous and exogenous cellular injuries. They cope with stressful stimuli by adapting their metabolism and activating various “guardian molecules.” These pro-survival factors protect essential cell constituents, prevent cell death, and possibly repair cellular damages. The Inhibitor of Apoptosis (IAPs) proteins display both anti-apoptotic and pro-survival properties and their expression can be induced by a variety of cellular stress such as hypoxia, endoplasmic reticular stress and DNA damage. Thus, IAPs can confer tolerance to cellular stress. This review presents the anti-apoptotic and survival functions of IAPs and their role in the adaptive response to cellular stress. The involvement of IAPs in human physiology and diseases in connection with a breakdown of cellular homeostasis will be discussed.
Keywords: IAPs; apoptosis; caspases; NF-kB; TNFR; UPR; DNA damage response; cancer; neurodegenerative disease
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MDPI and ACS Style

Marivin, A.; Berthelet, J.; Plenchette, S.; Dubrez, L. The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress. Cells 2012, 1, 711-737.

AMA Style

Marivin A, Berthelet J, Plenchette S, Dubrez L. The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress. Cells. 2012; 1(4):711-737.

Chicago/Turabian Style

Marivin, Arthur; Berthelet, Jean; Plenchette, Stéphanie; Dubrez, Laurence. 2012. "The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress." Cells 1, no. 4: 711-737.

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