| http://purl.uniprot.org/citations/18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18065659 | http://www.w3.org/2000/01/rdf-schema#comment | "Prolonged exposure to decreased oxygen tension causes contraction and proliferation of pulmonary arterial smooth muscle cells (PASMCs) and pulmonary hypertension. Hypoxia-induced inhibition of voltage-gated K(+) (K(v)) channels may contribute to the development of pulmonary hypertension by increasing intracellular calcium concentration ([Ca(2+)](i)). The peptide endothelin-1 (ET-1) has been implicated in the development of pulmonary hypertension and acutely decreases K(v) channel activity. ET-1 also activates several transcription factors, although whether ET-1 alters K(V) channel expression is unclear. The hypoxic induction of ET-1 is regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1), which we demonstrated to regulate hypoxia-induced decreases in K(V) channel activity. In this study, we tested the hypothesis that HIF-1-dependent increases in ET-1 lead to decreased K(v) channel expression and subsequent elevation in [Ca(2+)](i). Resting [Ca(2+)](i) and K(v) channel expression were measured in cells exposed to control (18% O(2), 5% CO(2)) and hypoxic (4% O(2), 5% CO(2)) conditions. Hypoxia caused a decrease in expression of K(v)1.5 and K(v)2.1 and a significant increase in resting [Ca(2+)](i). The increase in [Ca(2+)](i) was reduced by nifedipine, an inhibitor of voltage-dependent calcium channels, and removal of extracellular calcium. Treatment with BQ-123, an ET-1 receptor inhibitor, prevented the hypoxia-induced decrease in K(v) channel expression and blunted the hypoxia-induced increase in [Ca(2+)](i) in PASMCs, whereas ET-1 mimicked the effects of hypoxia. Both hypoxia and overexpression of HIF-1 under normoxic conditions increased ET-1 expression. These results suggest that the inhibition of K(v) channel expression and rise in [Ca(2+)](i) during chronic hypoxia may be the result of HIF-1-dependent induction of ET-1."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajplung.00091.2007"xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Semenza G.L."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Shimoda L.A."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Luke T."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Sylvester J.T."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Fallon M."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Pisarcik S."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/author | "Whitman E.M."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/name | "Am J Physiol Lung Cell Mol Physiol"xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/pages | "L309-18"xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/title | "Endothelin-1 mediates hypoxia-induced inhibition of voltage-gated K+ channel expression in pulmonary arterial myocytes."xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://purl.uniprot.org/core/volume | "294"xsd:string |
| http://purl.uniprot.org/citations/18065659 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18065659 |
| http://purl.uniprot.org/citations/18065659 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18065659 |
| http://purl.uniprot.org/uniprot/#_A0A0R4J1E9-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |
| http://purl.uniprot.org/uniprot/#_A0A0R4J1F0-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |
| http://purl.uniprot.org/uniprot/#_P15387-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |
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| http://purl.uniprot.org/uniprot/#_A6J756-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |
| http://purl.uniprot.org/uniprot/#_A6JXI9-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |
| http://purl.uniprot.org/uniprot/#_A6ILV3-mappedCitation-18065659 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18065659 |