Document Detail


p120-v-Abl expression overcomes TGF-beta1 negative regulation of c-myc transcription but not cell growth.
MedLine Citation:
PMID:  8875988     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transformation of interleukin-3 dependent (IL-3) 32D-123 myeloid cells by p120-v-Abl produced the factor-independent 32D-abl cell line. In 32D-abl cells, myc expression was found to be significantly higher than in the parental cells and was correlated with increased E2F-1 protein expression and DNA binding ability. Surprisingly, in 32D-abl cells, TGF-beta1, a potent G1/S inhibitor of 32D-123 and 32D-abl cell growth, increased E2F transactivation as shown by increased c-myc promoter-CAT and GAL4-E2F-1 activity. In addition, TGF-beta1 was also found to increase E2F-1 protein levels but had no effect on steady-state retinoblastoma (RB) protein levels or phosphorylation state. In the absence of TGF-beta1, transient expression of RB in v-Abl expressing cells resulted in decreased c-myc transcription, inhibition of GAL4-E2F-1 driven transactivation and inhibition of cellular proliferation. RB and v-Abl were found to physically associate in vivo and in vitro via v-Abl's ATP binding region. In summary, these studies established that in myeloid cells: (1) v-Abl binds RB resulting in increased E2F-1-driven c-myc transcription, and (2) an alternative pathway exists for TGF-beta1-mediated growth inhibition of v-Abl-transformed cells, in which increased rather than decreased E2F-mediated c-myc transcription is observed.
Authors:
M C Birchenall-Roberts; S J Kim; D C Bertolette; J M Turley; T Fu; O S Bang; J J Kasper; Y D Yoo; F W Ruscetti
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Oncogene     Volume:  13     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1996 Oct 
Date Detail:
Created Date:  1996-12-09     Completed Date:  1996-12-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1499-509     Citation Subset:  IM    
Affiliation:
Intramural Research Support Program, SAIC Frederick, Maryland 21702, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carrier Proteins*
Cell Cycle Proteins*
Cell Line, Transformed
DNA / metabolism*
DNA-Binding Proteins*
E2F Transcription Factors
E2F1 Transcription Factor
Mice
Proto-Oncogene Proteins c-myc / metabolism*
Recombinant Fusion Proteins / metabolism
Retinoblastoma Protein / genetics,  metabolism*
Retinoblastoma-Binding Protein 1
Transcription Factor DP1
Transcription Factors / genetics,  metabolism*
Transcription, Genetic
Transfection
Transforming Growth Factor beta / physiology*
Chemical
Reg. No./Substance:
0/Arid4a protein, mouse; 0/Carrier Proteins; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/E2F Transcription Factors; 0/E2F1 Transcription Factor; 0/E2f1 protein, mouse; 0/Proto-Oncogene Proteins c-myc; 0/Recombinant Fusion Proteins; 0/Retinoblastoma Protein; 0/Retinoblastoma-Binding Protein 1; 0/Transcription Factor DP1; 0/Transcription Factors; 0/Transforming Growth Factor beta; 9007-49-2/DNA

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


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