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

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

1
Institut National de la Santé et de la Recherche Médicale (Inserm), UMR866, Dijon F-21079, France
2
Institut Fédératif de Recherche (IFR), Université de Bourgogne, 100, Dijon F-21079, France
3
Ecole Pratique des Hautes Etudes (EPHE) EA 7269, Dijon, F-21079, France
*
Author to whom correspondence should be addressed.
Received: 31 July 2012 / Revised: 14 September 2012 / Accepted: 27 September 2012 / Published: 10 October 2012
(This article belongs to the Special Issue Cellular Stress Response)
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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 IAPs; apoptosis; caspases; NF-kB; TNFR; UPR; DNA damage response; cancer; neurodegenerative disease
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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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.

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