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http://purl.uniprot.org/citations/11571252http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11571252http://www.w3.org/2000/01/rdf-schema#comment"

Background

Activity of voltage-gated K(+) (K(v)) channels controls membrane potential (E(m)) that regulates cytosolic free Ca(2+) concentration ([Ca(2+)](cyt)) by regulating voltage-dependent Ca(2+) channel function. A rise in [Ca(2+)](cyt) in pulmonary artery smooth muscle cells (PASMCs) triggers vasoconstriction and stimulates PASMC proliferation. Whether c-Jun, a transcription factor that stimulates cell proliferation, affects K(v) channel activity in PASMCs was investigated.

Methods and results

Infection of primary cultured PASMCs with an adenoviral vector expressing c-jun increased the protein level of c-Jun and reduced K(v) currents (I(K(V))) compared with control cells (infected with an empty adenovirus). Using single-cell reverse transcription-polymerase chain reaction, we observed that the mRNA level of Kv1.5 and the current density of I(K(V)) were both attenuated in c-jun-infected PASMCs compared with control cells and cells infected with antisense c-jun. Overexpression of c-Jun also upregulated protein expression of Kvbeta(2) and accelerated I(K(V)) inactivation. Furthermore, E(m) was more depolarized and [(3)H]thymidine incorporation was greater in PASMCs infected with c-jun than in control cells and cells infected with antisense c-jun.

Conclusions

These results suggest that c-Jun-mediated PASMC proliferation is associated with a decrease in I(K(V)). The resultant membrane depolarization increases [Ca(2+)](cyt) and enhances PASMC growth."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.org/dc/terms/identifier"doi:10.1161/hc3801.095662"xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Yu Y."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Zhao Y."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Yuan J.X."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Krick S."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Rothman A."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Platoshyn O."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/author"Rubin L.J."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/name"Circulation"xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/pages"1557-1563"xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/title"c-Jun decreases voltage-gated K(+) channel activity in pulmonary artery smooth muscle cells."xsd:string
http://purl.uniprot.org/citations/11571252http://purl.uniprot.org/core/volume"104"xsd:string
http://purl.uniprot.org/citations/11571252http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11571252
http://purl.uniprot.org/citations/11571252http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11571252
http://purl.uniprot.org/uniprot/P17325#attribution-F185C7A4313E85CCBE7115597F01CB1Dhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/11571252
http://purl.uniprot.org/uniprot/#_P17325-mappedCitation-11571252http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11571252
http://purl.uniprot.org/uniprot/P17325http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11571252