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http://purl.uniprot.org/SHA-384/95F6516227C107061BE5A83E3C277854DCB2BCD30749F06A6D5178724E95E45AC3D2E0D10094EF79713FBD143D8A4F2Ehttp://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/95F6516227C107061BE5A83E3C277854DCB2BCD30749F06A6D5178724E95E45AC3D2E0D10094EF79713FBD143D8A4F2Ehttp://www.w3.org/2000/01/rdf-schema#comment"TRPC3 deletion prevents mechanical stress-induced ROS production and left ventricular dysfunction in pressure-overloaded heart. TRPC3 specifically contributed to the upregulation of Nox2 in pressure-overloaded heart. TRPC3 participates in pressure overload-induced LV dysfunction in 129 Sv mice."xsd:string
http://purl.uniprot.org/uniprot/#_89F42AC049B8C9E6CB2A4173EF68D859ECA77D552D78EA9F9898A3AAE5B2B518308478BF2FAA7DE4303BBA9438331757http://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/95F6516227C107061BE5A83E3C277854DCB2BCD30749F06A6D5178724E95E45AC3D2E0D10094EF79713FBD143D8A4F2E
http://purl.uniprot.org/uniprot/Q9QZC1http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/95F6516227C107061BE5A83E3C277854DCB2BCD30749F06A6D5178724E95E45AC3D2E0D10094EF79713FBD143D8A4F2E
http://purl.uniprot.org/uniprot/#_Q9QZC1-mappedCitation-27833156http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/95F6516227C107061BE5A83E3C277854DCB2BCD30749F06A6D5178724E95E45AC3D2E0D10094EF79713FBD143D8A4F2E