Document Detail


B-myb rescues ras-induced premature senescence, which requires its transactivation domain.
MedLine Citation:
PMID:  11485831     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
B-myb, a ubiquitously expressed member of the myb gene family, is highly regulated throughout the cell cycle and appears to be required for cell cycle progression. In contrast to its relatives A-myb, c-myb, and v-myb, no transforming activity of B-myb has been reported thus far. We report here that B-myb can rescue senescence induced by an activated ras oncogene in rodent cells in vitro. We show that transformation by B-Myb involves its ability to activate transcription. Similar to other oncogenic transcription factors, such as c-Myc and E2F, we show that B-Myb also has repression activity. We demonstrate that the C-terminus of B-Myb can function as a repressor of transcription, that B-Myb interacts with the repressor molecules BS69 and N-CoR and that the repression function, like the transactivation domain, contributes to B-myb transformation.
Authors:
H Masselink; N Vastenhouw; R Bernards
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer letters     Volume:  171     ISSN:  0304-3835     ISO Abbreviation:  Cancer Lett.     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-08-03     Completed Date:  2001-09-20     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7600053     Medline TA:  Cancer Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  87-101     Citation Subset:  IM    
Affiliation:
Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
3T3 Cells
Animals
Carrier Proteins / physiology
Cell Aging / physiology*
Cell Cycle Proteins*
DNA-Binding Proteins / chemistry,  physiology*
Gene Expression Regulation*
Humans
Mice
Nuclear Proteins / metabolism,  physiology
Nuclear Receptor Co-Repressor 1
Protein Structure, Tertiary
Proteins / metabolism
Recombinant Fusion Proteins / metabolism
Repressor Proteins / physiology*
Retinoblastoma-Like Protein p107
Trans-Activators / chemistry,  physiology*
Transcriptional Activation*
Transfection
Tumor Cells, Cultured
Tumor Suppressor Protein p14ARF
Tumor Suppressor Protein p53 / metabolism
ras Proteins / physiology*
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/MYBL2 protein, human; 0/Mybl2 protein, mouse; 0/NCOR1 protein, human; 0/Ncor1 protein, mouse; 0/Nuclear Proteins; 0/Nuclear Receptor Co-Repressor 1; 0/Proteins; 0/Rbl1 protein, mouse; 0/Recombinant Fusion Proteins; 0/Repressor Proteins; 0/Retinoblastoma-Like Protein p107; 0/Trans-Activators; 0/Tumor Suppressor Protein p14ARF; 0/Tumor Suppressor Protein p53; 0/ZMYND11 protein, human; 0/Zmynd11 protein, mouse; EC 3.6.5.2/ras Proteins

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