Functional availability of γ-herpesvirus K-cyclin is regulated by cellular CDK6 and p16INK4a

Hidenori Yoshioka, Kohji Noguchi, Kazuhiro Katayama, Junko Mitsuhashi, Satoshi Yamagoe, Masahiro Fujimuro, Yoshikazu Sugimoto

研究成果: Article査読

3 被引用数 (Scopus)

抄録

Viral K-cyclin derived from Kaposi's sarcoma-associated herpesvirus is homologous with mammalian D-type cyclins. Here, we demonstrated the regulatory mechanisms for K-cyclin function and degradation in human embryonic kidney HEK293 and primary effusion lymphoma JSC-1 cell lines. Proteasome inhibitor MG132 treatment induced an accumulation of ubiquitinated K-cyclin in these cells, and co-expression of CDK6 prevented K-cyclin ubiquitination. Also K-cyclin mutants incompetent for CDK6-binding were destabilized by proteasome pathway. Furthermore, silencing of p16INK4a promoted K-cyclin-CDK6 complex formation and hence induced K-cyclin-associated kinase activity in HEK293 cells. These observations indicate that CDK6-bound K-cyclin is functionally stable but monomeric K-cyclin is targeted to ubiquitin-dependent degradation pathway in these cells. Our data suggest that the balance between CDK6 and p16INK4a regulates the availability of functional K-cyclin in human cells.

本文言語English
ページ(範囲)1000-1005
ページ数6
ジャーナルBiochemical and Biophysical Research Communications
394
4
DOI
出版ステータスPublished - 2010 4月 16

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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