{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chan SC"],"funding":["NCI NIH HHS"],"pagination":["19736-49"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3366007"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["287(23)"],"pubmed_abstract":["Synthesis of truncated androgen receptor (AR) splice variants has emerged as an important mechanism of prostate cancer (PCa) resistance to AR-targeted therapy and progression to a lethal castration-resistant phenotype. However, the precise role of these factors at this stage of the disease is not clear due to loss of multiple COOH-terminal AR protein domains, including the canonical nuclear localization signal (NLS) in the AR hinge region. Despite loss of this NLS, we show that diverse truncated AR variant species have a basal level of nuclear localization sufficient for ligand-independent transcriptional activity. Whereas full-length AR requires Hsp90 and importin-β for active nuclear translocation, basal nuclear localization of truncated AR variants is independent of these classical sign"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Androgen receptor splice variants activate androgen receptor target genes and support aberrant prostate cancer cell growth independent of canonical androgen receptor nuclear localization signal."],"pmcid":["PMC3366007"],"funding_grant_id":["PC094384","CA141011","R21 CA141011"],"pubmed_authors":["Li Y","Dehm SM","Chan SC"],"additional_accession":[]},"is_claimable":false,"name":"Androgen receptor splice variants activate androgen receptor target genes and support aberrant prostate cancer cell growth independent of canonical androgen receptor nuclear localization signal.","description":"Synthesis of truncated androgen receptor (AR) splice variants has emerged as an important mechanism of prostate cancer (PCa) resistance to AR-targeted therapy and progression to a lethal castration-resistant phenotype. However, the precise role of these factors at this stage of the disease is not clear due to loss of multiple COOH-terminal AR protein domains, including the canonical nuclear localization signal (NLS) in the AR hinge region. Despite loss of this NLS, we show that diverse truncated AR variant species have a basal level of nuclear localization sufficient for ligand-independent transcriptional activity. Whereas full-length AR requires Hsp90 and importin-β for active nuclear translocation, basal nuclear localization of truncated AR variants is independent of these classical sign","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jun","modification":"2025-06-26T03:06:52.225Z","creation":"2025-06-26T03:06:52.225Z"},"accession":"S-EPMC3366007","cross_references":{"pubmed":["22532567"],"doi":["10.1074/jbc.m112.352930","10.1074/jbc.M112.352930"]}}