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Mol Cell Biol. 2004 Feb;24(3):1044-57.

ARA67/PAT1 functions as a repressor to suppress androgen receptor transactivation.

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Department of Pathology, Urology, and Radiation Oncology and Cancer Center, George Whipple Laboratory for Cancer Research, University of Rochester Medical Center, Rochester, New York 14642, USA.

Erratum in

  • Mol Cell Biol. 2004 Jun;24(12):5635.


The androgen receptor (AR) may recruit multiple coregulators for proper or optimal transactivation. Here we report the identification and characterization of ARA67/PAT1 as an AR coregulator from a prostate cDNA library. ARA67/PAT1 was screened out as an AR N terminus interacting protein. Interaction mapping shows that the cooperation of multiple domains within ARA67/PAT1 may be required for the maximal interaction with AR. ARA67/PAT1 functions as a repressor with better suppressive effects on AR compared to glucocorticoid receptor and estrogen receptor. Further mechanism dissection reveals that the interrupted AR cytoplasmic-nuclear shuttling may play a major role in ARA67/PAT1 mediated suppression on AR. Together, these results suggest that ARA67/PAT1 may function as a novel repressor that can modulate AR function in prostate cancer.

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