| http://purl.uniprot.org/citations/11160515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11160515 | http://www.w3.org/2000/01/rdf-schema#comment | "Voltage-dependent calcium channels (VDCCs) are multimeric complexes composed of a pore-forming alpha(1) subunit together with several accessory subunits, including alpha(2)delta, beta, and, in some cases, gamma subunits. A family of VDCCs known as the L-type channels are formed specifically from alpha(1S) (skeletal muscle), alpha(1C) (in heart and brain), alpha(1D) (mainly in brain, heart, and endocrine tissue), and alpha(1F) (retina). Neuroendocrine L-type currents have a significant role in the control of neurosecretion and can be inhibited by GTP-binding (G-) proteins. However, the subunit composition of the VDCCs underlying these G-protein-regulated neuroendocrine L-type currents is unknown. To investigate the biophysical and pharmacological properties and role of G-protein modulation of alpha(1D) calcium channels, we have examined calcium channel currents formed by the human neuronal L-type alpha(1D) subunit, co-expressed with alpha(2)delta-1 and beta(3a), stably expressed in a human embryonic kidney (HEK) 293 cell line, using whole cell and perforated patch-clamp techniques. The alpha(1D)-expressing cell line exhibited L-type currents with typical characteristics. The currents were high-voltage activated (peak at +20 mV in 20 mM Ba2+) and showed little inactivation in external Ba2+, while displaying rapid inactivation kinetics in external Ca2+. The L-type currents were inhibited by the 1,4 dihydropyridine (DHP) antagonists nifedipine and nicardipine and were enhanced by the DHP agonist BayK S-(-)8644. However, alpha(1D) L-type currents were not modulated by activation of a number of G-protein pathways. Activation of endogenous somatostatin receptor subtype 2 (sst2) by somatostatin-14 or activation of transiently transfected rat D2 dopamine receptors (rD2(long)) by quinpirole had no effect. Direct activation of G-proteins by the nonhydrolyzable GTP analogue, guanosine 5'-0-(3-thiotriphospate) also had no effect on the alpha(1D) currents. In contrast, in the same system, N-type currents, formed from transiently transfected alpha(1B)/alpha(2)delta-1/beta(3), showed strong G-protein-mediated inhibition. Furthermore, the I-II loop from the alpha(1D) clone, expressed as a glutathione-S-transferase (GST) fusion protein, did not bind Gbetagamma, unlike the alpha(1B) I-II loop fusion protein. These data show that the biophysical and pharmacological properties of recombinant human alpha(1D) L-type currents are similar to alpha(1C) currents, and these currents are also resistant to modulation by G(i/o)-linked G-protein-coupled receptors."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.org/dc/terms/identifier | "doi:10.1152/jn.2001.85.2.816"xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Brust P.F."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Butcher A.J."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Bell D.C."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Page K.M."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Stauderman K.A."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Dolphin A.C."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Nurnberg B."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Berrow N.S."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Seabrook G.R."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/author | "Nesterova A."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/name | "J Neurophysiol"xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/pages | "816-827"xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/title | "Biophysical properties, pharmacology, and modulation of human, neuronal L-type (alpha(1D), Ca(V)1.3) voltage-dependent calcium currents."xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://purl.uniprot.org/core/volume | "85"xsd:string |
| http://purl.uniprot.org/citations/11160515 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11160515 |
| http://purl.uniprot.org/citations/11160515 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11160515 |
| http://purl.uniprot.org/uniprot/P54289#attribution-689DCC31563A2C8271A10CDFB4B5DCBB | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11160515 |
| http://purl.uniprot.org/uniprot/Q01668#attribution-689DCC31563A2C8271A10CDFB4B5DCBB | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11160515 |
| http://purl.uniprot.org/uniprot/P54284#attribution-689DCC31563A2C8271A10CDFB4B5DCBB | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/11160515 |