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http://purl.uniprot.org/citations/20887894http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20887894http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20887894http://www.w3.org/2000/01/rdf-schema#comment"Ca(2+) is an essential and ubiquitous second messenger. Changes in cytosolic Ca(2+) trigger events critical for tumorigenesis, such as cellular motility, proliferation, and apoptosis. We show that an isoform of Secretory Pathway Ca(2+)-ATPase, SPCA2, is upregulated in breast cancer-derived cells and human breast tumors, and suppression of SPCA2 attenuates basal Ca(2+) levels and tumorigenicity. Contrary to its conventional role in Golgi Ca(2+) sequestration, expression of SPCA2 increased Ca(2+) influx by a mechanism dependent on the store-operated Ca(2+) channel Orai1. Unexpectedly, SPCA2-Orai1 signaling was independent of ER Ca(2+) stores or STIM1 and STIM2 sensors and uncoupled from Ca(2+)-ATPase activity of SPCA2. Binding of the SPCA2 amino terminus to Orai1 enabled access of its carboxyl terminus to Orai1 and activation of Ca(2+) influx. Our findings reveal a signaling pathway in which the Orai1-SPCA2 complex elicits constitutive store-independent Ca(2+) signaling that promotes tumorigenesis."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2010.08.040"xsd:string
http://purl.uniprot.org/citations/20887894http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2010.08.040"xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Nguyen N."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Nguyen N."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Feng M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Feng M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Rao R."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Rao R."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Kenny P.A."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Kenny P.A."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Sukumar S."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Sukumar S."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Faddy H.M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Faddy H.M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Grice D.M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Grice D.M."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Leitch S."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Leitch S."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Monteith G.R."xsd:string
http://purl.uniprot.org/citations/20887894http://purl.uniprot.org/core/author"Monteith G.R."xsd:string