ArticleThe Journal of physiology2001
Functional characterization of the C-terminus of the human ether-à-go-go-related gene K(+) channel (HERG).
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 62 citations in OpenAlex.
- Detection of a novel pathogenic variant in KCNH2 associated with long QT syndrome 2 using whole exome sequencing.BMC medical genomics · 2024Article
- Development of automated patch clamp assays to overcome the burden of variants of uncertain significance in inheritable arrhythmia syndromes.Frontiers in physiology · 2023Review
- Multiple mechanisms underlie reduced potassium conductance in the p.T1019PfsX38 variant of hERG.Physiological reports · 2022Article
- Functional study of a KCNH2 mutant: Novel insights on the pathogenesis of the LQT2 syndrome.Journal of cellular and molecular medicine · 2019Article
- Express with caution: Epitope tags and cDNA variants effects on hERG channel trafficking, half-life and function.Journal of cardiovascular electrophysiology · 2017Article
- The subfamily-specific assembly of Eag and Erg K+ channels is determined by both the amino and the carboxyl recognition domains.The Journal of biological chemistry · 2014Article
- Role of the cytoplasmic N-terminal Cap and Per-Arnt-Sim (PAS) domain in trafficking and stabilization of Kv11.1 channels.The Journal of biological chemistry · 2014Article
- Insights into hERG K+ channel structure and function from NMR studies.European biophysics journal : EBJ · 2013Review
- Voltage-dependent gating of HERG potassium channels.Frontiers in pharmacology · 2012Article
- Cytoplasmic domains and voltage-dependent potassium channel gating.Frontiers in pharmacology · 2012Article
- Distal end of carboxyl terminus is not essential for the assembly of rat Eag1 potassium channels.The Journal of biological chemistry · 2011Article
- Trafficking defect and proteasomal degradation contribute to the phenotype of a novel KCNH2 long QT syndrome mutation.PloS one · 2011Article
- hERG potassium channel gating is mediated by N- and C-terminal region interactions.The Journal of general physiology · 2011Article
- Absence of direct cyclic nucleotide modulation of mEAG1 and hERG1 channels revealed with fluorescence and electrophysiological methods.The Journal of biological chemistry · 2009Article
- A recombinant N-terminal domain fully restores deactivation gating in N-truncated and long QT syndrome mutant hERG potassium channels.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Functional properties of human neuronal Kv11 channels.Pflugers Archiv : European journal of physiology · 2009Article
- A new C-terminal hERG mutation A915fs+47X associated with symptomatic LQT2 and auditory-trigger syncope.Heart rhythm · 2008Article
- Characterization of hERG1a and hERG1b potassium channels-a possible role for hERG1b in the I (Kr) current.Pflugers Archiv : European journal of physiology · 2008Article
- Identification of a posttranslational mechanism for the regulation of hERG1 K+ channel expression and hERG1 current density in tumor cells.Molecular and cellular biology · 2008Article
- Thermodynamic and kinetic properties of amino-terminal and S4-S5 loop HERG channel mutants under steady-state conditions.Biophysical journal · 2008Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
1. In the present study the functional role of the C-terminus of the human ether-à-go-go-related gene K(+) channel HERG was investigated using a series of C-terminal deletion constructs expressed in Xenopus oocytes. 2. Constructs with deletions of 311 or more amino acid residues failed to form functional channels. Truncation by 215 amino acid residues or fewer had no discernable effects on channel activity. Truncation by 236 or 278 amino acid residues accelerated deactivation, and caused a faster recovery from inactivation. 3. In high extracellular K(+), channel deactivation of HERG results from the binding of the N-terminus to a site within the pore. This slows channel deactivation by a knock-off mechanism. Here, it was shown that C-terminal deletions also abolished this effect of high extracellular K(+). Mutants containing deletions in both the N- and C-termini deactivated with rates similar to those observed in individual deletion mutants. 4. In contrast, experiments with double-deletion constructs showed additive effects of the N- and C-termini on the voltage dependence of activation, and on the kinetics of inactivation and recovery from inactivation. The reduction of inactivation in these mutants contributed to an increase in peak current amplitude. 5. These results indicate that residues within the C-terminus of HERG play a role in channel expression as well as in most aspects of channel gating. The regulation of channel deactivation is likely to be mediated by an interaction with the N-terminus, but the regulation of the voltage dependence of activation, and of rate processes associated with inactivation, does not require the N-terminus.
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