ArticleThe Journal of physiology2006
Three methionine residues located within the regulator of conductance for K+ (RCK) domains confer oxidative sensitivity to large-conductance Ca2+-activated K+ channels.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 59 citations in OpenAlex.
- To activate a G protein-coupled receptor permanently with cell surface photodynamic action in the gastrointestinal tract.World journal of gastroenterology · 2025Review
- Incorporating physics to overcome data scarcity in predictive modeling of protein function: A case study of BK channels.PLoS computational biology · 2023Article
- Incorporating physics to overcome data scarcity in predictive modeling of protein function: a case study of BK channels.bioRxiv : the preprint server for biology · 2023Article
- TRPM2 Oxidation Activates Two Distinct Potassium Channels in Melanoma Cells through Intracellular Calcium Increase.International journal of molecular sciences · 2021Article
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Circadian redox rhythms in the regulation of neuronal excitability.Free radical biology & medicine · 2018Review
- Methionine Sulfoxide Reductase B3-Targeted In Utero Gene Therapy Rescues Hearing Function in a Mouse Model of Congenital Sensorineural Hearing Loss.Antioxidants & redox signaling · 2016Article
- Oxidation of K(+) Channels in Aging and Neurodegeneration.Aging and disease · 2016Review
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- CRYPTOCHROME-mediated phototransduction by modulation of the potassium ion channel β-subunit redox sensor.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014Review
- MsrB1 and MICALs regulate actin assembly and macrophage function via reversible stereoselective methionine oxidation.Molecular cell · 2013Article
- Wavelet Analysis of Protein Motion.International journal of wavelets, multiresolution and information processing · 2012Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Methionine sulfoxide reductase B1 (MsrB1) recovers TRPM6 channel activity during oxidative stress.The Journal of biological chemistry · 2010Article
- Structure of the human BK channel Ca2+-activation apparatus at 3.0 A resolution.Science (New York, N.Y.) · 2010Article
- The 1.5-A structure of XplA-heme, an unusual cytochrome P450 heme domain that catalyzes reductive biotransformation of royal demolition explosive.The Journal of biological chemistry · 2009Article
- Modulation of BKCa channel gating by endogenous signaling molecules.Physiology (Bethesda, Md.) · 2009Review
- Oxidation of multiple methionine residues impairs rapid sodium channel inactivation.Pflugers Archiv : European journal of physiology · 2008Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methionine-directed oxidation of the human Slo1 potassium channel (hSlo1) shifts the half-activation voltage by -30 mV and markedly slows channel deactivation at low concentrations of intracellular Ca2+ ([Ca2+]i). We demonstrate here that the contemporaneous mutation of M536, M712 and M739 to leucine renders the channel functionally insensitive to methionine oxidation caused by the oxidant chloramine-T (Ch-T) without altering other functional characteristics. Coexpression with the auxiliary beta1 subunit fails to restore the full oxidative sensitivity to this triple mutant channel. The Ch-T effect is mediated specifically by M536, M712 and M739 because even small changes in this residue combination interfere with the ability to remove the oxidant sensitivity following mutation. Replacement of M712 or M739, but not M536, with the hydrophilic residue glutamate largely mimics oxidation of the channel and essentially removes the Ch-T sensitivity, suggesting that M712 and M739 may be part of a hydrophobic pocket disrupted by oxidation of non-polar methionine to the more hydrophilic methionine sulfoxide. The increase in wild-type hSlo1 open probability caused by methionine oxidation disappears at high [Ca2+]i and biophysical modelling of the Ch-T effect on steady-state activation implicates a decrease in the allosteric coupling between Ca2+ binding and the pore. The dramatic increase in open probability at low [Ca2+]i especially within the physiological voltage range suggests that oxidation of M536, M712 or M739 may enhance the Slo1 BK activity during conditions of oxidative stress, such as those associated with ischaemia-reperfusion and neurodegenerative disease, or in response to metabolic cues.
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