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http://purl.uniprot.org/citations/21190959http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21190959http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21190959http://www.w3.org/2000/01/rdf-schema#comment"Epidermal growth factor through the stimulation of epidermal growth factor receptor (EGFR) plays a critical role in the activation of MAPKs and phosphatidylinositol-3-protein kinase/AKT cell survival pathways attributed in many pathological conditions. At the cellular level, such functions involve EGFR overactivation and phosphorylation. In the present study, we describe that human embryonic kidney-293 cells transfected with somatostatin (SST) receptor 5 (SSTR5) exhibit inhibition of EGFR phosphorylation and modulate MAPK and phosphatidylinositol-3-protein kinase/AKT cell survival signaling. Furthermore, suppression of EGFR by using small interference RNA and an antagonist (AG1478) potentiates the SST effect via activation of SSTR5 on signaling molecules. In wild-type human embryonic kidney-293 cells, EGFR/ErbB2 exists as constitutive heterodimers. The presence of SSTR5 leads to the dissociation of the heteromeric complex of EGFR/ErbB2 and display preferential heterodimerization between SSTR5 and EGFR in an agonist-dependent manner. These findings highlight a new undiscovered mechanism and potential role of SSTR5 to attenuate the EGFR-mediated signaling pathways involved in tumorigenesis. Our data indicate that the activation and/or overexpression of SST receptors along with the inhibition of EGFR will serve as an important therapeutic approach in the treatment of ErbB-positive tumors."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.org/dc/terms/identifier"doi:10.1210/en.2010-0940"xsd:string
http://purl.uniprot.org/citations/21190959http://purl.org/dc/terms/identifier"doi:10.1210/en.2010-0940"xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Qiu X."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Qiu X."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Chaudhari N."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Chaudhari N."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Kumar U."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Kumar U."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Somvanshi R.K."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Somvanshi R.K."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Kharmate G."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Kharmate G."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Rajput P.S."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Rajput P.S."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Watt H.L."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/author"Watt H.L."xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/name"Endocrinology"xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/name"Endocrinology"xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/pages"931-945"xsd:string
http://purl.uniprot.org/citations/21190959http://purl.uniprot.org/core/pages"931-945"xsd:string