Document Detail

Aurora B hyperactivation by Bub1 overexpression promotes chromosome missegregation.
MedLine Citation:
PMID:  22033440     Owner:  NLM     Status:  MEDLINE    
High expression of the mitotic kinase Bub1 is associated with a variety of human cancers and correlates with poor clinical prognosis, but whether Bub1 alone can drive tumorigenesis was unknown. We provided conclusive evidence that Bub1 has oncogenic properties by generating transgenic mice that overexpress Bub1 in a wide variety of tissues, resulting in aneuploidization. Consistently, Bub1 transgenic mice developed various kinds of spontaneous tumors as well as accelerated Myc-induced lymphomagenesis. While the mitotic checkpoint was robust in Bub1 overexpressing cells, misaligned and lagging chromosomes were observed. These defects originated from increased Aurora B activity and could be suppressed by inhibition of Aurora B. Taken together, this indicates that Bub1 has oncogenic properties and imply that aneuploidization and tumorigenesis result from Aurora B-dependent missegregation. Here, we focus on the complex relationship between Bub1 and Aurora B and discuss the broader implications of Bub1-dependent Aurora B activation in mediating error correction.
Robin M Ricke; Jan M van Deursen
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-11-01
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  10     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-12-13     Completed Date:  2012-08-28     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3645-51     Citation Subset:  IM    
Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN, USA.
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MeSH Terms
Cell Transformation, Neoplastic / genetics
Chromosome Segregation / genetics*
Gene Expression Regulation, Neoplastic
Models, Biological
Protein-Serine-Threonine Kinases / genetics*,  metabolism*,  physiology
Grant Support
Reg. No./Substance:
EC spindle checkpoint protein; EC Kinases; EC kinase

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

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