Exercise, PGC-1α, and metabolic adaptation in skeletal muscle

Appl. Physiol. Nutr. Metab. 34(3): 424–427 (2009) doi:10.1139/H09-030 Published by NRC Research Press / Publié par les Presses scientifiques du CNRC

Full text: http://article.pubs.nrc-cnrc.gc.ca/RPAS/rpv?hm=HInit&journal=apnm&volume=34&calyLang=eng&afpf=h09-030.pdf

Exercise, PGC-1α, and metabolic adaptation in skeletal muscle

Zhen Yan

Endurance exercise is protective for mice with mitochondrial myopathy

J Appl Physiol 106: 1712-1719, 2009. First published March 12, 2009; doi:10.1152/japplphysiol.91571.2008 8750-7587/09 $8.00

HIGHLIGHTED TOPIC Regulation of Protein Metabolism in Exercise and Recovery

Endurance exercise is protective for mice with mitochondrial myopathy

Tina Wenz,1 Francisca Diaz,1 Dayami Hernandez,1 and Carlos T. Moraes1,2
Departments of 1Neurology and of 2Cell Biology and Anatomy, University of Miami School of Medicine, Miami, Florida
Submitted 8 December 2008 ; accepted in final form 9 March 2009

Address for reprint requests and other correspondence: C. T. Moraes, Dept. of Neurology, Miller School of Medicine, Univ. of Miami, 1095 NW 14th Terrace, Miami, FL 33136 (e-mail: cmoraes@med.miami.edu

p53/CEP-1 Increases or Decreases Lifespan, Depending on Level of Mitochondrial Bioenergetic Stress.

Aging Cell. 2009 Apr 22. [Epub ahead of print]

p53/CEP-1 Increases or Decreases Lifespan, Depending on Level of Mitochondrial Bioenergetic Stress.

Ventura N, Rea SL, Schiavi A, Torgovnick A, Testi R, Johnson TE.
Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80309, USA.

Oxidative stress induces degradation of mitochondrial DNA

http://nar.oxfordjournals.org/cgi/content/short/37/8/2539?rss=1

http://nar.oxfordjournals.org/cgi/reprint/37/8/2539 (Full text)

Nucleic Acids Research Advance Access originally published online on March 5, 2009 Nucleic Acids Research 2009 37(8):2539-2548; doi:10.1093/nar/gkp100

Oxidative stress induces degradation of mitochondrial DNA

Inna Shokolenko, Natalia Venediktova, Alexandra Bochkareva, Glenn L. Wilson and Mikhail F. Alexeyev*
Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, AL 36688, USA
*To whom correspondence should be addressed. Tel: +1 251 460 6789; Fax: +1 251 460 6771; Email: malexeye@jaguar1.usouthal.edu

Received September 4, 2008. Revised January 25, 2009. Accepted February 8, 2009.

Fly Study Suggests That Gene May 'Bypass' Disease-Linked Mitochondrial Defects

Fly Study Suggests That Gene May 'Bypass' Disease-Linked Mitochondrial Defects

Article Date: 06 May 2009 - 6:00 PDT
http://www.medicalnewstoday.com/articles/149070.php

Matching Supply and Demand

Science 24 April 2009:Vol. 324. no. 5926, p. 440DOI: 10.1126/science.324_440b
Editors' Choice: Highlights of the recent literature

http://www.sciencemag.org/cgi/content/full/324/5926/440-b?rss=1

Biochemistry:

Matching Supply and Demand

Valda Vinson

Nat. Struct. Mol. Biol. 16, 390 (2009).

J. Chem. Phys. 130, 155101 (2009); DOI:10.1063/1.3109902 Published 16 April 2009

N. K. Voulgarakis, K. Ø. Rasmussen, and P. M. Welch
Theoretical Division and Center for Nonlinear Studies, Los Alamos National Laboratory, Los Alamos, New Mexico 87545, USA

Dendrimers as synthetic gene vectors: Cell membrane attachment

http://www.medicalnewstoday.com/articles/148319.php

First Large-Scale Computer Simulation Of Gene Therapy

Effectiveness and safety of treatments for degenerative ataxias: A systematic review

http://www3.interscience.wiley.com/journal/122371107/abstract?CRETRY=1&SRETRY=0

Effectiveness and safety of treatments for degenerative ataxias: A systematic review

M.Mar Trujillo-Martín, PhD 1 *, Pedro Serrano-Aguilar, MD, PhD 2 3, Fernando Monton-Álvarez, MD, PhD 4, Romen Carrillo-Fumero, PhD 1

1Canary Islands Research and Health Foundation (Fundación Canaria de Investigación y Salud-FUNCIS), Santa Cruz de Tenerife, Canary Islands, Spain 2Planning and Evaluation Unit, Canary Islands Health Authority, Santa Cruz de Tenerife, Canary Islands, Spain 3CIBER Epidemiología y Salud Pública (CIBERESP), Spain 4Department of Neurology, University Hospital of Na Sa de la Candelaria, Santa Cruz de Tenerife, Canary Islands, Spain

email: M.Mar Trujillo-Martín (matrumar@gobiernodecanarias.org)

^*Correspondence to M.Mar Trujillo-Martín, Servicio de Evaluación y Planificación, Servicio Canario de la Salud, Pérez de Rozas, 5-4^a planta, 38004 Santa Cruz de Tenerife, España

Potential conflict of interest: None reported.

Funded by:
Spanish Ministry of Health
Consumption in cooperation
Fundación Canaria de Investigación y Salud (FUNCIS)

Keywords

rare diseases • degenerative ataxia • systematic review • treatment effectiveness • treatment safety

Received: 13 October 2008; Accepted: 3 March 2009

Digital Object Identifier (DOI)

Evidence That Phosphorylation of Iron Regulatory Protein 1 at Serine 138 Destabilizes the [4Fe-4S] Cluster in Cytosolic Aconitase by Enhancing 4Fe-3Fe

Originally published In Press as doi:10.1074/jbc.M807717200 on March 6, 2009 J. Biol. Chem., Vol. 284, Issue 19, 12701-12709, May 8, 2009

Evidence That Phosphorylation of Iron Regulatory Protein 1 at Serine 138 Destabilizes the [4Fe-4S] Cluster in Cytosolic Aconitase by Enhancing 4Fe-3Fe Cycling^*

Kathryn M. Deck, Aparna Vasanthakumar, Sheila A. Anderson, Jeremy B. Goforth¹, M. Claire Kennedy, William E. Antholine^¶, and Richard S. Eisenstein²

From the Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706, the Biochemistry Department, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, and the ^¶National Biomedical ESR Center, Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226-3548

Received for publication, October 6, 2008 , and in revised form, March 5, 2009.

This paper is dedicated to the memory of Helmut Beinert.

^* This work was supported in part by National Institutes of Health Grants DK 66600 (to R. S. E.) and National Biomedical ESR Center Grant EB001980. This work was also supported by United States Department of Agriculture Cooperative States Research Education and Extension Service Grant 2006-35200-16604 and University of Wisconsin-Madison Hatch Project 4885 (to R. S. E.).

The on-line version of this article (available at http://www.jbc.org/) contains supplemental Figs. S1 and S2.

¹ Supported by National Institutes of Health Training Grant T32 DK007665.

² To whom correspondence should be addressed: University of Wisconsin, Dept. of Nutritional Sciences, 1415 Linden Dr., Madison, WI 53706. Tel.: 608-262-5830; Fax: 608-262-5860; E-mail: eisenste@nutrisci.wisc.edu
.