Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function

Shih Shun Chen, Pi Chu Chang, Yu Wen Cheng, Fen Mei Tang, Young Sun Lin

Research output: Contribution to journalArticle

102 Citations (Scopus)

Abstract

Using a transactivation-defective p53 derivative as bait, STK15, a centrosome-associated oncogenic serine/threonine kinase, was isolated as a p53 partner. The p53-STK15 interaction was confirmed further by co-immunoprecipitation and GST pull-down studies. In co-transfection experiments, p53 suppressed STK15-induced centrosome amplification and cellular transformation in a transactivation-independent manner. The suppression of STK15 oncogenic activity by p53 might be explained in part by the finding that p53 inhibited STK15 kinase activity via direct interaction with the latter's Aurora box. Taken together, these findings revealed a novel mechanism for the tumor suppressor function of p53.

Original languageEnglish
Pages (from-to)4491-4499
Number of pages9
JournalEMBO Journal
Volume21
Issue number17
DOIs
Publication statusPublished - Sep 2 2002
Externally publishedYes

Fingerprint

Aurora Kinase A
Centrosome
Protein-Serine-Threonine Kinases
Transcriptional Activation
Amplification
Tumors
Derivatives
Immunoprecipitation
Transfection
Experiments
Neoplasms

Keywords

  • Aurora box
  • Centrosome amplification
  • Oncogenic kinase
  • P53
  • STK15

ASJC Scopus subject areas

  • Genetics
  • Cell Biology

Cite this

Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function. / Chen, Shih Shun; Chang, Pi Chu; Cheng, Yu Wen; Tang, Fen Mei; Lin, Young Sun.

In: EMBO Journal, Vol. 21, No. 17, 02.09.2002, p. 4491-4499.

Research output: Contribution to journalArticle

Chen, Shih Shun ; Chang, Pi Chu ; Cheng, Yu Wen ; Tang, Fen Mei ; Lin, Young Sun. / Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function. In: EMBO Journal. 2002 ; Vol. 21, No. 17. pp. 4491-4499.
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