JBC INTERFERin siRNA transfection reagent

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on October 6, 2006
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
281/40/29468    most recent
M602533200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Veereshwarayya, V.
Right arrow Articles by Querfurth, H. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Veereshwarayya, V.
Right arrow Articles by Querfurth, H. W.
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?

Papers In Press, published online ahead of print August 3, 2006
J. Biol. Chem, 10.1074/jbc.M602533200
Submitted on March 17, 2006
Accepted on August 3, 2006

Differential effects of mitochondrial HSP60 and related molecular chaperones to prevent intracellular beta -amyloid - induced inhibition of complex IV and limit apoptosis

Vimal Veereshwarayya, Pravir Kumar, Kenneth M. Rosen, Ruben Mestril, and Henry W. Querfurth

Department of Neurology, Caritas St. Elizabeth's Med. Ctr., Boston, MA 02135

Corresponding Author: henry.querfurth{at}tufts.edu

Defects in mitochondrial oxidative metabolism, in particular decreased activity of cytochrome c oxidase, have been reported in Alzheimer’s disease (AD) tissue and in cultured cells that over-express Amyloid Precursor Protein (APP). Mitochondrial dysfunction contributes to neurodegeneration in AD partly through formation of reactive oxygen species (ROS) and the release of sequestered molecules that initiate programmed cell death pathways. The heat shock proteins (HSP) are cytoprotective against a number of stressors, including accumulations of misfolded proteins and reactive oxygen species. Previously we reported on the property of Hsp70 to protect neuroblastoma and mixed neuronal cultures from cell death caused by intraneuronal beta -amyloid (Abeta ). Here we demonstrate that Hsp60, Hsp70 and Hsp90, both alone and in combination, provide differential protection against intracellular beta -amyloid stress through the maintenance of mitochondrial oxidative phosphorylation and functionality of tricarboxylic acid (TCA) cycle enzymes. Notably, beta -amyloid was found to selectively inhibit complex IV activity-an effect selectively neutralized by Hsp60.The combined effect of HSPs was to reduce the free radical burden, preserve ATP generation, decrease cytochrome c release and prevent caspase-9 activation, all important mediators of beta -amyloid-induced neuronal dysfunction and death.


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?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
D. Chandra, G. Choy, and D. G. Tang
Cytosolic Accumulation of HSP60 during Apoptosis with or without Apparent Mitochondrial Release: EVIDENCE THAT ITS PRO-APOPTOTIC OR PRO-SURVIVAL FUNCTIONS INVOLVE DIFFERENTIAL INTERACTIONS WITH CASPASE-3
J. Biol. Chem., October 26, 2007; 282(43): 31289 - 31301.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
P. Kumar, R. K. Ambasta, V. Veereshwarayya, K. M. Rosen, K. S. Kosik, H. Band, R. Mestril, C. Patterson, and H. W. Querfurth
CHIP and HSPs interact with {beta}-APP in a proteasome-dependent manner and influence A{beta} metabolism
Hum. Mol. Genet., April 1, 2007; 16(7): 848 - 864.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.