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B-MYB delays cell aging by repressing p16 ( INK4α ) transcription.
MedLine Citation:
PMID:  20734103     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
p16 ( INK4α ), an inhibitor of cyclin-dependent kinase 4 and 6, has been proposed to play an important role in cellular aging and in premature senescence. The expression of the p16 ( INK4α ) is primarily under transcriptional control. Our previous data showed that a negative regulation element lies in its promoter. In that element, a MYB-binding site (MBS) was uncovered by transcription analysis. Here, we report that MBS is a negative regulation element and B-MYB binds to this site in vivo. In human embryonic lung fibroblast cells, B-MYB downregulated p16 ( INK4α ) expression, whereas knocking down of B-MYB upregulated it. Evidence also showed that overexpression of B-MYB in cells could increase the number of utmost passage and decrease G1 block, whereas knocking down of B-MYB could impair their replicative ability. This study provides evidence of the capacity of B-MYB not only to regulate p16 ( INK4α ) expression but also the phenotypic consequence on cellular senescence.
Authors:
Yu Huang; Junfeng Wu; Renzhong Li; Peichang Wang; Limin Han; Zongyu Zhang; Tanjun Tong
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Publication Detail:
Type:  Journal Article     Date:  2010-08-25
Journal Detail:
Title:  Cellular and molecular life sciences : CMLS     Volume:  68     ISSN:  1420-9071     ISO Abbreviation:  Cell. Mol. Life Sci.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9705402     Medline TA:  Cell Mol Life Sci     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  893-901     Citation Subset:  IM    
Affiliation:
Peking University Research Center on Aging, Peking University Health Science Center, 100083, Beijing, People's Republic of China.
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