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From androgen receptor to the general transcription factor TFIIH. Identification of cdk activating kinase (CAK) as an androgen receptor NH(2)-terminal associated coactivator.

The androgen receptor (AR), like other steroid receptors, modulates the activity of the general transcription machinery on the core promoter to exert its function as a regulator. Co-immunoprecipitation of prostate cancer LNCaP cell extract using protein A-Sepharose coupled with anti-AR antibody indicates that the AR interacts with the general transcription factor TFIIH in a physiological condition. Co-transfection of cdk activating kinase (CAK), the kinase moiety of TFIIH, enhanced AR-mediated transcription in a ligand-dependent manner in human prostate cancer PC-3 and LNCaP cells, and in a ligand-independent manner in human prostate cancer DU145 cells. Detailed interaction studies further revealed that the AR NH(2)-terminal domain interacting with CAK was essential for the CAK-induced AR transactivation. Together, our data suggest that the AR may interact with TFIIH for efficient communication with the general transcription factors/RNA polymerase II on the core promoter.

Pubmed ID: 10734072 RIS Download

Mesh terms: Cyclin H | Cyclin-Dependent Kinases | Cyclins | DNA-Binding Proteins | Fungal Proteins | Humans | Male | Prostatic Neoplasms | Protein-Serine-Threonine Kinases | Receptors, Androgen | Recombinant Fusion Proteins | Saccharomyces cerevisiae Proteins | TATA-Binding Protein Associated Factors | Transcription Factor TFIID | Transcription Factor TFIIH | Transcription Factors | Transcription Factors, TFII | Tumor Cells, Cultured

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Associated grants

  • Agency: NCI NIH HHS, Id: CA55639
  • Agency: NCI NIH HHS, Id: CA68568
  • Agency: NIDDK NIH HHS, Id: DK51346

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