ArticlePflugers Archiv : European journal of physiology1996
Modification of C-type inactivating Shaker potassium channels by chloramine-T.
Article in Pflugers Archiv : European journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Closed state-coupled C-type inactivation in BK channels.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014Review
- ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K⁺ o-dependent resting inactivation.Pflugers Archiv : European journal of physiology · 2013Article
- C-type inactivation of voltage-gated K+ channels: pore constriction or dilation?The Journal of general physiology · 2013Article
- Mechanism of Cd2+ coordination during slow inactivation in potassium channels.Structure (London, England : 1993) · 2012Article
- Hydrogen peroxide differentially affects activity in the pre-Bötzinger complex and hippocampus.Journal of neurophysiology · 2011Article
- Article
- Oxidation of multiple methionine residues impairs rapid sodium channel inactivation.Pflugers Archiv : European journal of physiology · 2008Article
- Functional consequences of methionine oxidation of hERG potassium channels.Biochemical pharmacology · 2007Article
- The binding of kappa-Conotoxin PVIIA and fast C-type inactivation of Shaker K+ channels are mutually exclusive.Biophysical journal · 2004Article
- The physiology and pharmacology of singlet oxygen.Medical hypotheses · 2003Article
- Inactivation and pharmacological properties of sqKv1A homotetramers in Xenopus oocytes cannot account for behavior of the squid "delayed rectifier" K(+) conductance.Biophysical journal · 2002Article
- Oxidative regulation of large conductance calcium-activated potassium channels.The Journal of general physiology · 2001Article
- Regulation of ROMK by extracellular cations.Biophysical journal · 2001Article
- A novel leg-shaking Drosophila mutant defective in a voltage-gated K(+)current and hypersensitive to reactive oxygen species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Voltage dependence of slow inactivation in Shaker potassium channels results from changes in relative K(+) and Na(+) permeabilities.The Journal of general physiology · 2000Article
- Acceleration of P/C-type inactivation in voltage-gated K(+) channels by methionine oxidation.Biophysical journal · 2000Article
- Inactivation gating of Kv4 potassium channels: molecular interactions involving the inner vestibule of the pore.The Journal of general physiology · 1999Article
- Modulation of slow inactivation in human cardiac Kv1.5 channels by extra- and intracellular permeant cations.The Journal of physiology · 1999Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shaker potassium channels undergo a slow C-type inactivation which can be hastened dramatically by single-point mutations in or near the pore region. We found that the oxidizing agent chloramine-T (Chl-T) causes an irreversible loss of current for those mutants which show C-type inactivation. For several mutants at position T449, which show a wide spectrum of inactivation time constants, the time constant of current rundown induced by Chl-T correlated with the speed of inactivation. Rundown was accelerated when the channels were in the inactivated state but rundown also occurred when channels were not opened or inactivated. Apparently, only those channels which can undergo C-type inactivation are accessible to Chl-T. In order to gain information about the target amino-acid residue for the action of Chl-T and the structural rearrangements occurring during C-type inactivation, several mutant channel proteins were compared with respect to their response to Chl-T. Since Chl-T can oxidize cysteine and methionine residues, we mutated the possible targets in and close to the pore region, namely C462 to A, and M440 and M448 to I. While the residues M440 and C462 were not important for channel rundown, mutation of M448 to I made the channels more resistant to Chl-T by about one order of magnitude. While inactivation was accelerated upon application of Chl-T in most mutants, mutation of M448 to I abolished this effect on the time course of inactivation, indicating that M448 is one of the target residues for Chl-T.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.