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 publication also includes supplementary data on AR and 14-3-3 ζ interacting proteins identified by mass spectrometry and spectra counts, proteins that overlap between AR and 14-3-3 ζ, and the amount of AR pulled down by 14-3-3 ζ and vice versa. In addition, there are source data for the figures in the publication.
Access
- Restrictions
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Free to All
- Instructions
- The mass spectrometry data have been deposited to the ProteomeXchange Consortium via the Proteomics Identifications (PRIDE) database and the sequencing data have been deposited in the Gene Expression Omnibus (GEO) database. All other data generated or analyzed during this study are included in this article on PubMed Central (PMC) under Supplementary Information.
- Grant Support
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Howard Hughes Medical Institute/Howard Hughes Medical InstituteBlavatnik Family Foundation/Blavatnik Family Foundation