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http://purl.uniprot.org/citations/17982259http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17982259http://www.w3.org/2000/01/rdf-schema#comment"Volume-sensitive outwardly rectifying (VSOR) Cl(-) channels participate in several physiological processes such as regulatory volume decrease, cell cycle regulation, proliferation and apoptosis. Recent evidence points to a significant role of hydrogen peroxide (H(2)O(2)) in VSOR Cl(-) channel activation. The aim of this study was to determine the signalling pathways responsible for H(2)O(2)-induced VSOR Cl(-) channel activation. In rat hepatoma (HTC) cells, H(2)O(2) elicited a transient increase in tyrosine phosphorylation of phospholipase Cgamma1 (PLCgamma1) that was blocked by PP2, a Src-family protein kinases inhibitor. Also, H(2)O(2) triggered an increase in cytosolic [Ca(2+)] that paralleled the time course of PLCgamma1 phosphorylation. The H(2)O(2)-induced [Ca(2+)](i) rise was prevented by the generic phospholipase C (PLC) inhibitor U73122 and the inositol 1,4,5-trisphosphate-receptor (IP(3)R) blocker 2-APB. In line with these results, manoeuvres that prevented PLCgamma1 activation and/or [Ca(2+)](i) rise, abolished H(2)O(2)-induced VSOR Cl(-) currents. Furthermore, in cells that overexpress a phosphorylation-defective dominant mutant of PLCgamma1, H(2)O(2) did not induce activation of VSOR Cl(-) currents. All these H(2)O(2)-induced effects were independent of extracellular Ca(2+). Our findings suggest that activation of PLCgamma1 and subsequent Ca(2+)(i) mobilisation mediate H(2)O(2)-induced VSOR Cl(-) currents, indicating that H(2)O(2) operates via redox-sensitive signalling pathways akin to those activated by osmotic challenges."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.org/dc/terms/identifier"doi:10.1159/000110437"xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Sala F."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Simon F."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Varela D."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Jorgensen F."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Armisen R."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Stutzin A."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Olivero P."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/author"Leiva-Salcedo E."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/name"Cell Physiol Biochem"xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/pages"773-780"xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/title"Activation of H2O2-induced VSOR Cl- currents in HTC cells require phospholipase Cgamma1 phosphorylation and Ca2+ mobilisation."xsd:string
http://purl.uniprot.org/citations/17982259http://purl.uniprot.org/core/volume"20"xsd:string
http://purl.uniprot.org/citations/17982259http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17982259
http://purl.uniprot.org/citations/17982259http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17982259
http://purl.uniprot.org/uniprot/P10686#attribution-FC16E3C819168F11A8DFCED074527DB8http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/#_A0A8I6ACY2-mappedCitation-17982259http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/#_G3V845-mappedCitation-17982259http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/#_P10686-mappedCitation-17982259http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/P10686http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/A0A8I6ACY2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17982259
http://purl.uniprot.org/uniprot/G3V845http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17982259