PIM1 Phosphorylation Regulates Gene Transcription in Prostate Cancer
- Description
Previous study showed that PIM1 phosphorylates the androgen receptor (AR), the primary therapeutic target in prostate cancer. This study examined the mechanism how PIM1 phosphorylation of AR alters its transcriptional activity. They identified the AR co-activator, 14-3-3 ζ, as an endogenous PIM1 substrate in LNCaP cells. Rapid immunoprecipitation and mass spectrometry of endogenous proteins on chromatin was used to find that select AR co-regulators interact with both AR and 14-3-3 ζ in PIM1 over-expressing cells. This dataset includes mass spectrometry and sequencing data. The study indicates that PIM1 phosphorylation of AR and 14-3-3 ζ coordinates their interaction, which recruits additional co-regulatory proteins to alter AR transcriptional activity.
Access
- Restrictions
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Free to All
- Instructions
- The mass spectrometry data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository and the sequencing data have been deposited in the Gene Expression Omnibus (GEO) database.
- Grant Support
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Howard Hughes Medical Institute/Howard Hughes Medical InstituteBlavatnik Family Foundation/Blavatnik Family Foundation