Survivin initiates cell cycle entry by the competitive interaction with Cdk4/p16INK4a and Cdk2/Cyclin E complex activation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2000-07

AUTHORS

Atsushi Suzuki, Midori Hayashida, Takeshi Ito, Hirokazu Kawano, Takeshi Nakano, Masayuki Miura, Kouichi Akahane, Katsuya Shiraki

ABSTRACT

Survivin is observed uniquely in tumor cells and developmental cells, which undergo either inappropriate or programmed cell growth. In the current study, we investigated the influence of Survivin on cell cycle. Overexpression of Survivin resulted in accelerated S phase shift, resistance to G1 arrest, and activated Cdk2/Cyclin E complex leading Rb phosphorylation. In addition, nuclear translocation of Survivin followed by an interaction with Cdk4 was detected. Interestingly, Survivin nuclear translocation coincided with S phase shift, and prevention of nuclear transport suppressed Survivin nuclear translocation and S phase shift. Further, we also observed that Survivin competitively interacted with the Cdk4/p16(INK4a) complex in a cell free system and in vivo. These results suggest that Survivin initiates the cell cycle entry as a result of nuclear translocation followed by an interaction with Cdk4. More... »

PAGES

1203665

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1203665

DOI

http://dx.doi.org/10.1038/sj.onc.1203665

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027293885

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10918579


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