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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

Authors

  • Lee DK
  • Duan HO
  • Chang C

Journal

The Journal of biological chemistry

Publication Data

March 31, 2000

Associated Grants

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

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