| http://purl.uniprot.org/citations/11245614 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11245614 | http://www.w3.org/2000/01/rdf-schema#comment | "Intracellular K+ plays an important role in controlling the cytoplasmic ion homeostasis for maintaining cell volume and inhibiting apoptotic enzymes in the cytosol and nucleus. Cytoplasmic K+ concentration is mainly regulated by K+ uptake via Na+-K+-ATPase and K+ efflux through K+ channels in the plasma membrane. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), a protonophore that dissipates the H+ gradient across the inner membrane of mitochondria, induces apoptosis in many cell types. In rat and human pulmonary artery smooth muscle cells (PASMC), FCCP opened the large-conductance, voltage- and Ca2+-sensitive KK+ (maxi-K) channels, increased K+ currents through maxi-K channels [I(K(Ca))], and induced apoptosis. Tetraethylammonia (1 mM) and iberiotoxin (100 nM) decreased I(K(Ca)) by blocking the sarcolemmal maxi-K channels and inhibited the FCCP-induced apoptosis in PASMC cultured in media containing serum and growth factors. Furthermore, inhibition of K+ efflux by raising extracellular K+ concentration from 5 to 40 mM also attenuated PASMC apoptosis induced by FCCP and the K+ ionophore valinomycin. These results suggest that FCCP-mediated apoptosis in PASMC is partially due to an increase of maxi-K channel activity. The resultant K+ loss through opened maxi-K channels may serve as a trigger for cell shrinkage and caspase activation, which are major characteristics of apoptosis in pulmonary vascular smooth muscle cells."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpcell.2001.280.4.c970"xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/author | "Kim H."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/author | "Yuan J.X."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/author | "Sweeney M."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/author | "Krick S."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/author | "Platoshyn O."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/name | "Am J Physiol Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/pages | "C970-9"xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/title | "Activation of K+ channels induces apoptosis in vascular smooth muscle cells."xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://purl.uniprot.org/core/volume | "280"xsd:string |
| http://purl.uniprot.org/citations/11245614 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11245614 |
| http://purl.uniprot.org/citations/11245614 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11245614 |
| http://purl.uniprot.org/uniprot/Q12791#attribution-676B5AE7FE0895EFEC51CF9CA41CC58E | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11245614 |
| http://purl.uniprot.org/uniprot/Q12791#attribution-AE5DC86E2357E56EFF1C088277F98B55 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11245614 |