Document Detail


Oncoprotein v-Myb and retinoic acid receptor alpha are mutual antagonists.
MedLine Citation:
PMID:  9714701     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The process of hematopoiesis is critically dependent on correct interactions of multiple regulatory molecules and transcription factors. We have studied the interactions of the v-Myb and retinoic acid receptor proteins which have opposing effects on hematopoiesis. While v-myb acts as a transforming oncogene preventing differentiation of monoblasts to macrophages, RAR alpha functions as an anti-oncogene arresting the growth of v-myb-transformed cells and allowing their final myeloid differentiation steps to occur. We found that the retinoic acid receptor alpha inhibits v-Myb transformation by suppressing the expression of v-Myb target genes typified by the mim-1 gene. Conversely, v-Myb protein interferes with RAR alpha transactivation function as well as with retinoic acid-induced apoptosis of HL-60 cells. These results demonstrate that retinoic acid receptor and v-Myb proteins act in antagonistic ways and reciprocally modify each other's functions.
Authors:
K Zemanová; J Smarda
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Blood cells, molecules & diseases     Volume:  24     ISSN:  1079-9796     ISO Abbreviation:  Blood Cells Mol. Dis.     Publication Date:  1998 Jun 
Date Detail:
Created Date:  1998-11-23     Completed Date:  1998-11-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9509932     Medline TA:  Blood Cells Mol Dis     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  239-50     Citation Subset:  IM    
Affiliation:
Department of Cellular and Molecular Oncology, Masaryk Institute of Oncology, Brno, Czech Republic.
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MeSH Terms
Descriptor/Qualifier:
Acetyltransferases*
Animals
Apoptosis / drug effects
Cell Differentiation / drug effects,  physiology
Cell Transformation, Neoplastic
Chlorides / pharmacology
Coturnix
Fibroblasts / drug effects
Gene Expression Regulation / drug effects,  physiology
Gene Expression Regulation, Leukemic / drug effects
HL-60 Cells / drug effects
Hematopoiesis / drug effects,  physiology*
Hematopoietic Stem Cells / cytology,  drug effects,  metabolism
Humans
Oncogene Proteins v-myb
Protein Biosynthesis
Proteins / genetics
Receptors, Retinoic Acid / antagonists & inhibitors,  physiology*
Retroviridae Proteins, Oncogenic / antagonists & inhibitors,  physiology*
Transcription, Genetic / drug effects,  physiology*
Tretinoin / pharmacology
Zinc Compounds / pharmacology
Grant Support
ID/Acronym/Agency:
R03 TW00749/TW/FIC NIH HHS
Chemical
Reg. No./Substance:
0/Chlorides; 0/Oncogene Proteins v-myb; 0/Proteins; 0/Receptors, Retinoic Acid; 0/Retroviridae Proteins, Oncogenic; 0/Zinc Compounds; 0/retinoic acid receptor alpha; 302-79-4/Tretinoin; 7646-85-7/zinc chloride; EC 2.3.1.-/Acetyltransferases; EC 2.3.1.-/mim-1 protein, Gallus gallus

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


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