4.5 Article

Down-regulation of Aurora B kinase induces cellular senescence in human fibroblasts and endothelial cells through a p53-dependent pathway

期刊

FEBS LETTERS
卷 585, 期 22, 页码 3569-3576

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2011.10.022

关键词

Cellular senescence; Aurora B kinase; p53; Human primary cells

资金

  1. National Research Foundation of Korea (NRF)
  2. Korea government (MEST) [2011-0001241]
  3. National Research Foundation of Korea [2005-0049473] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Aurora B kinase (Aurora-B) functions in chromosome segregation and cleavage of polar spindle microtubules. However, its role in cellular senescence remains elusive. Here, we investigated Aurora-B effects on cellular senescence in human fibroblasts and endothelial cells. Aurora-B levels were reduced during replicative senescence and premature senescence by adriamycin. Aurora-B overexpression in old cells partially reversed senescence phenotypes. In contrast, Aurora-B down-regulation accelerated cellular senescence. p53 knockdown but not p16 knockdown inhibited cellular senescence by Aurora-B reduction. These results suggest that Aurora-B might function in the regulation of cellular senescence of human primary cells via a p53-dependent pathway. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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