2003
DOI: 10.1093/emboj/cdg023
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A novel inducible transactivation domain in the androgen receptor: implications for PRK in prostate cancer

Abstract: In addition to the classical activation by ligands, nuclear receptor activity is also regulated by ligandindependent signalling. Here, we unravel a novel signal transduction pathway that links the RhoA effector protein kinase C-related kinase PRK1 to the transcriptional activation of the androgen receptor (AR). Stimulation of the PRK signalling cascade results in a ligand-dependent superactivation of AR. We show that AR and PRK1 interact both in vivo and in vitro. The transactivation unit 5 (TAU-5) located in … Show more

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Cited by 103 publications
(134 citation statements)
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References 46 publications
(71 reference statements)
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“…PRK1 also regulates the transcriptional activity of other nuclear receptors such as mineralocorticoid and progesterone receptor 6 , possibly via a mechanism similar to that controlling AR target gene expression. This raises questions whether other transcription factors are regulated by PRK1, and whether there exist other H3T11 kinases that control the activity of specific transcription factors.…”
Section: Discussionmentioning
confidence: 99%
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“…PRK1 also regulates the transcriptional activity of other nuclear receptors such as mineralocorticoid and progesterone receptor 6 , possibly via a mechanism similar to that controlling AR target gene expression. This raises questions whether other transcription factors are regulated by PRK1, and whether there exist other H3T11 kinases that control the activity of specific transcription factors.…”
Section: Discussionmentioning
confidence: 99%
“…Myc-PRK1 and the flag-tagged kinase dead mutant PRK1 K644E 6 were immunoprecipitated from 293 cell lysates with α-myc or α-flag antibody, respectively ( Supplementary Information, Fig. S1g, h) and incubated with bacterially expressed and purified GST-H3 1-44 or GST control protein.…”
Section: Prk1 Phosphorylates H3t11mentioning
confidence: 99%
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“…This is particularly relevant, because previous studies established LSD1 as a potential drug target for cancer treatment. [13][14][15][16][17][18]42 Continuous dox treatment of shLSD1 mice resulted in dramatic changes within different hematopoietic compartments. Mechanistically, enhanced expression of hematopoietic regulatory genes in these mice is presumably caused by the lack of LSD1 repressive activity at H3K4 residues in the gene promoters.…”
Section: Discussionmentioning
confidence: 99%