JBC Anatrace, Inc.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published In Press as doi:10.1074/jbc.M800102200 on February 15, 2008

J. Biol. Chem., Vol. 283, Issue 16, 10892-10903, April 18, 2008
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Data
Right arrow All Versions of this Article:
283/16/10892    most recent
M800102200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Zhang, H.
Right arrow Articles by Semenza, G. L.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, H.
Right arrow Articles by Semenza, G. L.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia*Formula

Huafeng Zhang{ddagger}§, Marta Bosch-Marce{ddagger}§, Larissa A. Shimoda, Yee Sun Tan{ddagger}§, Jin Hyen Baek{ddagger}§, Jacob B. Wesley{ddagger}§, Frank J. Gonzalez||, and Gregg L. Semenza{ddagger}§**{ddagger}{ddagger}§§1

From the {ddagger}Vascular Program, Institute for Cell Engineering, §McKusick-Nathans Institute of Genetic Medicine, and Department of Medicine, **Pediatrics, {ddagger}{ddagger}Oncology, and §§Radiation Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 and ||Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892

Autophagy is a process by which cytoplasmic organelles can be catabolized either to remove defective structures or as a means of providing macromolecules for energy generation under conditions of nutrient starvation. In this study we demonstrate that mitochondrial autophagy is induced by hypoxia, that this process requires the hypoxia-dependent factor-1-dependent expression of BNIP3 and the constitutive expression of Beclin-1 and Atg5, and that in cells subjected to prolonged hypoxia, mitochondrial autophagy is an adaptive metabolic response which is necessary to prevent increased levels of reactive oxygen species and cell death.


Received for publication, January 4, 2008 , and in revised form, February 8, 2008.

* This work was supported by funds from the Johns Hopkins Institute for Cell Engineering and National Institutes of Health Public Health Service Grant P50-CA103175. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Formula The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. 1-6 and Tables 1 and 2.

1 To whom correspondence should be addressed: Broadway Research Bldg., Suite 671, 733 North Broadway, Baltimore, MD 21205. Fax: 443-287-5618; E-mail: gsemenza{at}jhmi.edu.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2008 by the American Society for Biochemistry and Molecular Biology.