http://purl.uniprot.org/citations/16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16449965 | http://www.w3.org/2000/01/rdf-schema#comment | "Hormones acting through G protein-coupled receptors (GPCRs) can cause androgen-independent activation of androgen receptor (AR) in prostate cancer cells. Regulators of G-protein signaling (RGS) proteins, through their GTPase activating protein (GAP) activities, inhibit GPCR-mediated signaling by inactivating G proteins. Here, we identified RGS2 as a gene specifically downregulated in androgen-independent prostate cancer cells. Expression of RGS2, but not other RGS proteins, abolished androgen-independent AR activity in androgen-independent LNCaP cells and CWR22Rv1 cells. In LNCaP cells, RGS2 inhibited G(q)-coupled GPCR signaling. Expression of exogenous wild-type RGS2, but not its GAP-deficient mutant, significantly reduced AR activation by constitutively activated G(q)Q209L mutant whereas silencing endogenous RGS2 by siRNA enhanced G(q)Q209L-stimulated AR activity. RGS2 had no effect on RGS-insensitive G(q)Q209L/G188S-induced AR activation. Furthermore, extracellular signal-regulated kinase 1/2 (ERK1/2) was found to be involved in RGS2-mediated regulation of androgen-independent AR activity. In addition, RGS2 functioned as a growth suppressor for androgen-independent LNCaP cells whereas androgen-sensitive LNCaP cells with RGS2 silencing had a growth advantage under steroid-reduced conditions. Finally, RGS2 expression level was significantly decreased in human prostate tumor specimens. Taken together, our results suggest RGS2 as a novel regulator of AR signaling and its repression may be an important step during prostate tumorigenesis and progression."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.org/dc/terms/identifier | "doi:10.1038/sj.onc.1209408"xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Cao X."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Xie Y."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Tu Y."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Qin J."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Lin M.F."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Scofield M."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Khan O."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/author | "Dowd F."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/pages | "3719-3734"xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/title | "Regulator of G-protein signaling 2 (RGS2) inhibits androgen-independent activation of androgen receptor in prostate cancer cells."xsd:string |
http://purl.uniprot.org/citations/16449965 | http://purl.uniprot.org/core/volume | "25"xsd:string |
http://purl.uniprot.org/citations/16449965 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16449965 |
http://purl.uniprot.org/citations/16449965 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16449965 |
http://purl.uniprot.org/uniprot/#_A0A087WUX9-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_D2KF13-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_C0JKD5-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_A0A3G2C3P2-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_A0A6H0MAB3-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_C0JKD6-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |
http://purl.uniprot.org/uniprot/#_C0JKD7-mappedCitation-16449965 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16449965 |