HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tahiliani, A. G. Articles by Neely, J. R. Search for Related Content PubMed PubMed Citation Articles by Tahiliani, A. G. Articles by Neely, J. R. Social Bookmarking                      What's this?

J. Biol. Chem., Vol. 262, Issue 24, 11607-11610, Aug, 1987

A transport system for coenzyme A in isolated rat heart mitochondria [published erratum appears in J Biol Chem 1989 Aug 15;264(23):13962]

AG Tahiliani and JR Neely

The ability of isolated rat heart mitochondria to take up coenzyme A (CoA) from the incubation medium was studied. Mitochondria accumulated CoA in a time- and concentration-dependent manner. The accumulation process occurred in two phases. Within the first 30 s of incubation, mitochondrial content of CoA increased, and this phase did not plateau in the concentration range studied. Following this initial increase, a second slower phase of CoA accumulation occurred which plateaued around 50 microM CoA. The initial phase was decreased significantly by ATP or by carboxyatractyloside. In contrast, the presence of ATP or carboxyatractyloside did not affect the second phase. Decreasing the temperature from 30 to 0 degrees C did not affect the initial phase, but the second phase was almost abolished. In the presence of metabolic inhibitors (either 2,4-dinitrophenol or a combination of rotenone and antimycin), the initial "binding" phase was not affected; but the second "uptake" phase was abolished. These results suggest that the first phase of mitochondrial CoA accumulation is probably CoA binding to adenine recognizing sites on the mitochondria while the second phase may represent a specific uptake process for CoA which, although not directly ATP-dependent, is energy-dependent.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				G. Ramaswamy, M. A. Karim, K. G. Murti, and S. Jackowski PPAR{alpha} controls the intracellular coenzyme A concentration via regulation of PANK1{alpha} gene expression J. Lipid Res., January 1, 2004; 45(1): 17 - 31. [Abstract] [Full Text] [PDF]

				M. Spaniol, P. Kaufmann, K. Beier, J. Wuthrich, M. Torok, H. Scharnagl, W. Marz, and S. Krahenbuhl Mechanisms of liver steatosis in rats with systemic carnitine deficiency due to treatment with trimethylhydraziniumpropionate J. Lipid Res., January 1, 2003; 44(1): 144 - 153. [Abstract] [Full Text] [PDF]

				C. Prohl, W. Pelzer, K. Diekert, H. Kmita, T. Bedekovics, G. Kispal, and R. Lill The Yeast Mitochondrial Carrier Leu5p and Its Human Homologue Graves' Disease Protein Are Required for Accumulation of Coenzyme A in the Matrix Mol. Cell. Biol., February 15, 2001; 21(4): 1089 - 1097. [Abstract] [Full Text]

				C. O. Rock, R. B. Calder, M. A. Karim, and S. Jackowski Pantothenate Kinase Regulation of the Intracellular Concentration of Coenzyme A J. Biol. Chem., January 14, 2000; 275(2): 1377 - 1383. [Abstract] [Full Text] [PDF]