ReviewJournal of bioenergetics and biomembranes1991
Calcium-activated K+ channels: metabolic regulation.
Review in Journal of bioenergetics and biomembranes, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 42 citations in OpenAlex.
- Reciprocal regulation of the Ca2+ and H+ sensitivity in the SLO1 BK channel conferred by the RCK1 domain.Nature structural & molecular biology · 2008Article
- Oxidative regulation of large conductance calcium-activated potassium channels.The Journal of general physiology · 2001Article
- A novel type of ATP block on a Ca(2+)-activated K(+) channel from bullfrog erythrocytes.Biophysical journal · 2000Article
- Synthesis of models for excitable membranes, synaptic transmission and neuromodulation using a common kinetic formalism.Journal of computational neuroscience · 1994Review
- Highly co-operative Ca2+ activation of intermediate-conductance K+ channels in granulocytes from a human cell line.The Journal of physiology · 1993Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-activated potassium (KCa) channels are highly modulated by a large spectrum of metabolites. Neurotransmitters, hormones, lipids, and nucleotides are capable of activating and/or inhibiting KCa channels. Studies from the last few years have shown that metabolites modulate the activity of KCa channels via: (1) a change in the affinity of the channel for Ca2+ (K 1/2 is modified), (2) a parallel shift in the voltage axis of the activation curves, or (3) a change in the slope (effective valence) of the voltage dependence curve. The shift of the voltage dependence curve can be a direct consequence of the change in the affinity for Ca2+. Recently, the mechanistic steps involved in the modulation of KCa channels are being uncovered. Some interactions may be direct on KCa channels and others may be mediated via G-proteins, second messengers, or phosphorylation. The information given in this review highlights the possibility that KCa channels can be activated or inhibited by metabolites without a change in the intracellular Ca2+ concentration.
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What OpenQuestion holds
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.