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Mitotic centromere‐associated kinase (MCAK/Kif2C) regulates cellular senescence in human primary cells through a p53‐dependent pathway
Author(s) -
Gwon Mi-Ri,
Cho Jung Hee,
Kim Jae-Ryong
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.10.012
Subject(s) - microbiology and biotechnology , senescence , mitosis , biology , gene knockdown , chromosome segregation , cell culture , genetics , chromosome , gene
Mitotic centromere‐associated kinase (MCAK/Kif2C) plays a critical role in chromosome movement and segregation with ATP‐dependent microtubule depolymerase activity. However, its role in cellular senescence remains unclear. MCAK/Kif2C expression decreased in human primary cells under replicative and premature senescence. MCAK/Kif2C down‐regulation in young cells induced premature senescence. MCAK/Kif2C overexpression in old cells partially reversed cell senescence. Senescence phenotypes by MCAK/Kif2C knockdown were observed in p16‐knockdown cells, but not in p53‐knockdown cells. These results suggest that MCAK/Kif2C plays an important role in the regulation of cellular senescence through a p53‐dependent pathway and might contribute to tissue/organism aging and protection of cellular transformation.