ArticleThe Journal of membrane biology2007
Charges in the cytoplasmic pore control intrinsic inward rectification and single-channel properties in Kir1.1 and Kir2.1 channels.
Article in The Journal of membrane biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Modular architecture of KEMBO reports · 2025Review
- Gating and modulation of an inward-rectifier potassium channel.The Journal of general physiology · 2023Article
- A small viral potassium ion channel with an inherent inward rectification.Channels (Austin, Tex.) · 2019Article
- Mechanism for attenuated outward conductance induced by mutations in the cytoplasmic pore of Kir2.1 channels.Scientific reports · 2015Article
- The bundle crossing region is responsible for the inwardly rectifying internal spermine block of the Kir2.1 channel.Pflugers Archiv : European journal of physiology · 2014Article
- Control of KirBac3.1 potassium channel gating at the interface between cytoplasmic domains.The Journal of biological chemistry · 2014Article
- Revisiting inward rectification: K ions permeate through Kir2.1 channels during high-affinity block by spermidine.The Journal of general physiology · 2012Article
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
An E224G mutation of the Kir2.1 channel generates intrinsic inward rectification and single-channel fluctuations in the absence of intracellular blockers. In this study, we showed that positively charged residues H226, R228 and R260, near site 224, regulated the intrinsic inward rectification and single-channel properties of the E224G mutant. By carrying out systematic mutations, we found that the charge effect on the intrinsic inward rectification and single-channel conductance is consistent with a long-range electrostatic mechanism. A Kir1.1 channel where the site equivalent to E224 in the Kir2.1 channel is a glycine residue does not show inward rectification or single-channel fluctuations. The G223K and N259R mutations of the Kir1.1 channel induced intrinsic inward rectification and reduced the single-channel conductance but did not generate large open-channel fluctuations. Substituting the cytoplasmic pore of the E224G mutant into the Kir1.1 channel induced open-channel fluctuations and intrinsic inward rectification. The single-channel conductance of the E224G mutant showed inward rectification. Also, a voltage-dependent gating mechanism decreased open probability during depolarization and contributed to the intrinsic inward rectification in the E224G mutant. In addition to an electrostatic effect, a close interaction of K(+) with channel pore may be required for generating open-channel fluctuations in the E224G mutant.
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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.