ArticleThe Journal of general physiology2004
State-dependent block of CNG channels by dequalinium.
Article in The Journal of general physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Bis-Quinolinium Cyclophane Blockers of SK Potassium Channels Are Antagonists of M3 Muscarinic Acetylcholine Receptors.Frontiers in pharmacology · 2020Article
- PP2B/calcineurin-mediated desensitization of TRPV1 does not require AKAP150.The Biochemical journal · 2010Article
- Role of the S4-S5 linker in CNG channel activation.Biophysical journal · 2010Article
- On the mechanism of TBA block of the TRPV1 channel.Biophysical journal · 2007Article
- State-independent block of BK channels by an intracellular quaternary ammonium.The Journal of general physiology · 2006Article
- Access of quaternary ammonium blockers to the internal pore of cyclic nucleotide-gated channels: implications for the location of the gate.The Journal of general physiology · 2006Article
- The pharmacology of cyclic nucleotide-gated channels: emerging from the darkness.Current pharmaceutical design · 2006Review
- Defining the retinoid binding site in the rod cyclic nucleotide-gated channel.The Journal of general physiology · 2005Article
- Mutation of the pore glutamate affects both cytoplasmic and external dequalinium block in the rat olfactory CNGA2 channel.European biophysics journal : EBJ · 2005Article
- All-trans-retinal is a closed-state inhibitor of rod cyclic nucleotide-gated ion channels.The Journal of general physiology · 2004Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cyclic nucleotide-gated (CNG) ion channels are nonselective cation channels with a high permeability for Ca(2+). Not surprisingly, they are blocked by a number of Ca(2+) channel blockers including tetracaine, pimozide, and diltiazem. We studied the effects of dequalinium, an extracellular blocker of the small conductance Ca(2+)-activated K(+) channel. We previously noted that dequalinium is a high-affinity blocker of CNGA1 channels from the intracellular side, with little or no state dependence at 0 mV. Here we examined block by dequalinium at a broad range of voltages in both CNGA1 and CNGA2 channels. We found that dequalinium block was mildly state dependent for both channels, with the affinity for closed channels 3-5 times higher than that for open channels. Mutations in the S4-S5 linker did not alter the affinity of open channels for dequalinium, but increased the affinity of closed channels by 10-20-fold. The state-specific effect of these mutations raises the question of whether/how the S4-S5 linker alters the binding of a blocker within the ion permeation pathway.
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Registered trials
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.