Document Detail


Acetyl-CoA carboxylase beta expression mediated by MyoD and muscle regulatory factor 4 is differentially affected by retinoic acid receptor and retinoid X receptor.
MedLine Citation:
PMID:  12642900     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mammals have two major isoforms of acetyl-CoA carboxyase (ACC). The 275 kDa beta-form (ACCbeta) is predominantly in heart and skeletal muscle while the 265 kDa alpha-form (ACCalpha) is the major isoform in lipogenic tissues such as liver and adipose tissue. ACCbeta is thought to control fatty acid oxidation by means of the ability of malonyl-CoA to inhibit carnitine palmitoyl-CoA transferase-1 (CPT-1), which is a rate-limiting enzyme of fatty acid oxidation in mitochondria. Previously, it was reported that MyoD and other muscle regulating factors (MRFs) up-regulate the expression of ACCbeta by interactions between these factors and several cis-elements of ACCbeta promoter. We described here that ACCbeta expression mediated by MRFs is regulated by retinoic acids. Endogenous expression of ACCbeta in differentiated H9C2 myotube was significantly increased by retinoic acid treatment. However, on transient transfection assay in H9C2 myoblast, ACCbeta promoter activity was suppressed by RXRalpha and more severely by RARalpha. These effects on ACCbeta expression in myoblasts and myotubes by RXRalpha and RARalpha seem to be mediated by their interactions with MRFs because no consensus sequence for RXRalpha and RARalpha has been found in ACCbeta promoter and retinoic acid receptors did not affect this promoter activities by itself. In transient transfection in NIH3T3 fibroblast, the activation of ACCbeta promoter by MyoD, main MRF in myoblast, was significantly suppressed by RARalpha and to a less extent by RXRalpha while the RXRalpha drastically augmented the activation by MRF4, major MRF in myotube. These results explained that retinoic acids differentially affected the action of MRFs according to their types and RXRalpha specially elevates the expression of muscle specific genes by stimulating the action of MRF4.
Authors:
Ju-Youn Kim; Jae-Jung Lee; Kyung-Sup Kim
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental & molecular medicine     Volume:  35     ISSN:  1226-3613     ISO Abbreviation:  Exp. Mol. Med.     Publication Date:  2003 Feb 
Date Detail:
Created Date:  2003-03-18     Completed Date:  2003-10-20     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9607880     Medline TA:  Exp Mol Med     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  23-9     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Molecular Biology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
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MeSH Terms
Descriptor/Qualifier:
3T3 Cells
Acetyl-CoA Carboxylase / genetics,  metabolism*
Animals
Cell Differentiation
Cells, Cultured
Gene Expression Regulation, Enzymologic / drug effects
Mice
MyoD Protein / metabolism*
Myoblasts / drug effects,  metabolism
Myogenic Regulatory Factors / metabolism*
Promoter Regions, Genetic / drug effects
Receptors, Retinoic Acid / genetics,  metabolism*
Retinoid X Receptors
Transcription Factors / genetics,  metabolism*
Transcriptional Activation
Tretinoin / pharmacology
Chemical
Reg. No./Substance:
0/MyoD Protein; 0/Myogenic Regulatory Factors; 0/Receptors, Retinoic Acid; 0/Retinoid X Receptors; 0/Transcription Factors; 0/myogenic factor 6; 302-79-4/Tretinoin; EC 6.4.1.2/Acetyl-CoA Carboxylase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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