Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-10-24
pubmed:abstractText
The mechanism of rectification of HERG, the human cardiac delayed rectifier K+ channel, was studied after heterologous expression in Xenopus oocytes. Currents were measured using two-microelectrode and macropatch voltage clamp techniques. The fully activated current-voltage (I-V) relationship for HERG inwardly rectified. Rectification was not altered by exposing the cytoplasmic side of a macropatch to a divalent-free solution, indicating this property was not caused by voltage-dependent block of outward current by Mg2+ or other soluble cytosolic molecules. The instantaneous I-V relationship for HERG was linear after removal of fast inactivation by a brief hyperpolarization. The time constants for the onset of and recovery from inactivation were a bell-shaped function of membrane potential. The time constants of inactivation varied from 1.8 ms at +50 mV to 16 ms at -20 mV; recovery from inactivation varied from 4.7 ms at -120 mV to 15 ms at -50 mV. Truncation of the NH2-terminal region of HERG shifted the voltage dependence of activation and inactivation by +20 to +30 mV. In addition, the rate of deactivation of the truncated channel was much faster than wild-type HERG. The mechanism of HERG rectification is voltage-gated fast inactivation. Inactivation of channels proceeds at a much faster rate than activation, such that no outward current is observed upon depolarization to very high membrane potentials. Fast inactivation of HERG and the resulting rectification are partly responsible for the prolonged plateau phase typical of ventricular action potentials.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-13449874, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-1570292, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-1899980, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-2122519, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-2170562, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-2436236, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-2443680, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-2717377, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-3790689, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7604285, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7629068, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7692301, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7729538, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7736582, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7769379, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7813010, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7889573, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7915826, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-7973666, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-8001043, http://linkedlifedata.com/resource/pubmed/commentcorrection/8740374-8078584
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1295
pubmed:author
pubmed:issnType
Print
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
611-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Fast inactivation causes rectification of the IKr channel.
pubmed:affiliation
Cardiology Division, University of Utah, Salt Lake City 84112, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.