Axin localizes to mitotic spindles and centrosomes in mitotic cells
- Authors
- Kim, Slli-Mun; Choi, Eun-Jin; Song, Ki-Joon; Kim, Sewoon; Seo, Eunjeong; Jho, Eek-Hoon; Kee, Sun-Ho
- Issue Date
- 1-4월-2009
- Publisher
- ELSEVIER INC
- Keywords
- Axin; Aurora kinase; Mitosis; Cytokinesis
- Citation
- EXPERIMENTAL CELL RESEARCH, v.315, no.6, pp.943 - 954
- Indexed
- SCIE
SCOPUS
- Journal Title
- EXPERIMENTAL CELL RESEARCH
- Volume
- 315
- Number
- 6
- Start Page
- 943
- End Page
- 954
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/120264
- DOI
- 10.1016/j.yexcr.2009.01.013
- ISSN
- 0014-4827
- Abstract
- Writ signaling plays critical roles in cell proliferation and carcinogenesis. In addition, numerous recent Studies have shown that various Writ signaling components are involved in mitosis and chromosomal instability. However, the role of Axin, a negative regulator of Writ signaling, in mitosis has remained unclear. Using Monoclonal antibodies against Axin, we found that Axin localizes to the centrosome and along mitotic spindles. This localization was suppressed by siRNA specific for Aurora A kinase and by Aurora kinase inhibitor. Interestingly, Axin over-expression altered the subcellular distribution of Plk1 and of phosphorylated glycogen synthase kinase (GSK3 beta) without producing any notable changes in cellular phenotype. In the presence of Aurora kinase inhibitor, Axin over-expression induced the formation of cleavage furrow-like structures and of prominent astral microtubules lacking midbody formation in a subset of cells. Our results suggest that Axin modulates distribution of Axin-associated proteins such as Plk1 and GSK3 beta in an expression level-dependent manner and these interactions affect the mitotic process, including cytokinesis under certain conditions, such as in the presence of Aurora kinase inhibitor. (C) 2009 Elsevier Inc. All rights reserved.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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