ArticleThe Journal of biological chemistry2010
Zn2+ activates large conductance Ca2+-activated K+ channel via an intracellular domain.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Zinc is a key regulator of the sperm-specific KeLife · 2026Article
- Mechanism of Kch activation by ZnPNAS nexus · 2026Article
- Article
- What Are the Functions of Zinc in the Nervous System?Neurology · 2023Article
- Pathophysiological Roles of Transient Receptor Potential (Trp) Channels and Zinc Toxicity in Brain Disease.International journal of molecular sciences · 2023Review
- Region-Specific and Pregnancy-Enhanced Vasodilator Effects of Hydrogen Sulfide.Obstetrics and gynecology research · 2023Article
- The Function and Regulation of Zinc in the Brain.Neuroscience · 2021Review
- New Insights of the Zn(II)-Induced P2 × 4R Positive Allosteric Modulation: Role of Head Receptor Domain SS2/SS3, E160 and D170.International journal of molecular sciences · 2020Article
- FeACS chemical biology · 2020Article
- CO-independent modification of KEuropean journal of pharmacology · 2017Article
- The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.The Biochemical journal · 2017Review
- Mechanistic insight into the heme-independent interplay between iron and carbon monoxide in CFTR and Slo1 BKMetallomics : integrated biometal science · 2017Review
- Zinc transporters and dysregulated channels in cancers.Frontiers in bioscience (Landmark edition) · 2017Review
- Zinc as Allosteric Ion Channel Modulator: Ionotropic Receptors as Metalloproteins.International journal of molecular sciences · 2016Review
- SLO2 Channels Are Inhibited by All Divalent Cations That Activate SLO1 K+ Channels.The Journal of biological chemistry · 2016Article
- The direct modulatory activity of zinc toward ion channels.Integrative medicine research · 2015Review
- Permeation, regulation and control of expression of TRP channels by trace metal ions.Pflugers Archiv : European journal of physiology · 2015Review
- Zn(2+) induces hyperpolarization by activation of a K(+) channel and increases intracellular Ca(2+) and pH in sea urchin spermatozoa.Developmental biology · 2014Review
- BK channel activators and their therapeutic perspectives.Frontiers in physiology · 2014Review
- Divalent cations modulate TMEM16A calcium-activated chloride channels by a common mechanism.The Journal of membrane biology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Zinc is an essential trace element and plays crucial roles in normal development, often as an integral structural component of transcription factors and enzymes. Recent evidence suggests that intracellular Zn(2+) functions as a signaling molecule, mediating a variety of important physiological phenomena. However, the immediate effectors of intracellular Zn(2+) signaling are not well known. We show here that intracellular Zn(2+) potently and reversibly activates large-conductance voltage- and Ca(2+)-activated Slo1 K(+) (BK) channels. The full effect of Zn(2+) requires His(365) in the RCK1 (regulator of conductance for K(+)) domain of the channel. Furthermore, mutation of two nearby acidic residues, Asp(367) and Glu(399), also reduced activation of the channel by Zn(2+), suggesting a possible structural arrangement for Zn(2+) binding by the aforementioned residues. Extracellular Zn(2+) activated Slo1 BK channels when coexpressed with Zn(2+)-permeable TRPM7 (transient receptor potential melastatin 7) channels. The results thus demonstrate that Slo1 BK channels represent a positive and direct effector of Zn(2+) signaling and may participate in sculpting cellular response to an increase in intracellular Zn(2+) concentration.
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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.