Mitochondrial Regulation of Apoptosis-Reference-Cited by-同舟云学术

Mitochondrial Regulation of Apoptosis

Published:2003-06 Issue:3 Volume:18 Page:89-94
ISSN:1548-9213
Container-title:Physiology
language:en
Short-container-title:Physiology

Author:

Mayer Bernd¹,Oberbauer Rainer²

Affiliation:

1. Emergentec Analytics and

2. Internal Medicine III, Department of Nephrology, University of Vienna, A-1090 Vienna, Austria

Abstract

Mitochondria play a central part in cellular survival and apoptotic death. These processes are highly regulated by pro- and antiapoptotic Bcl-2 superfamily members. A key feature within apoptosis cascades is disruption of mitochondrial transmembrane potential and apoptogenic protein release, caused by opening of the permeability transition pore (PT). New data, however, indicate that mitochondrial apoptosis may occur without PT involvement.

Publisher

American Physiological Society

Subject

Physiology

Link

https://www.physiology.org/doi/pdf/10.1152/nips.01433.2002

Reference14 articles.

1. Apoptosis-inducing factor (AIF): key to the conserved caspase-independent pathways of cell death?

2. The Bcl2 family: regulators of the cellular life-or-death switch

3. Collapse of the Inner Mitochondrial Transmembrane Potential Is Not Required for Apoptosis of HL60 Cells

4. Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c

5. Bid, Bax, and Lipids Cooperate to Form Supramolecular Openings in the Outer Mitochondrial Membrane

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