Regulation of Mitochondrial Integrity, Autophagy and Cell Survival by BNIP3

Understanding the role of BNIP3 in the systemic response to hypoxia has been complicated by conflicting results that indicate on the one hand that BNIP3 promotes cell death, and other data, including our own that BNIP3 is not sufficient for cell death, but rather plays a critical role in hypoxia-ind...

Full description

Saved in:
Bibliographic Details
Published inAutophagy Vol. 3; no. 6; pp. 616 - 619
Main Authors Tracy, Kristin, Macleod, Kay F.
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 01.11.2007
Subjects
Animals
Autophagy - physiology
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cell Survival - physiology
Cycle
Gene Expression Regulation
Humans
Landes
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mitochondria - genetics
Mitochondria - metabolism
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Models, Biological
Organogenesis
Proteins
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Online AccessGet full text

Cover

More Information
Summary:Understanding the role of BNIP3 in the systemic response to hypoxia has been complicated by conflicting results that indicate on the one hand that BNIP3 promotes cell death, and other data, including our own that BNIP3 is not sufficient for cell death, but rather plays a critical role in hypoxia-induced autophagy. This work suggests that rather than promoting death, BNIP3 may actually allow survival either by preventing ATP depletion or by eliminating damaged mitochondria. However, the function of BNIP3 may be subverted under unusual conditions associated with acidosis that arise following extended periods of hypoxia and anaerobic glycolysis. Despite this novel insight into BNIP3 function, much remains to be done in terms of pinning down a molecular activity for BNIP3 that explains both its role in autophagy and how this may be subverted to induce cell death. As a target of the RB tumor suppressor, our work also places BNIP3 at the center of efforts to exploit autophagy to better treat human cancers in which tumor hypoxia is implicated as a progression factor. Addendum to: BNIP3 is an RB/E2F Target Gene Required for Hypoxia-Induced Autophagy K. Tracy, B.C. Dibling, BT. Spike, J. Knabb, P. Schumacker and K.F. Macleod Mol Cell Biol 2007; In press
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1554-8627
1554-8635
DOI:10.4161/auto.4892