ArticleThe Journal of general physiology2011
Binding of ATP to the CBS domains in the C-terminal region of CLC-1.
Article in The Journal of general physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Biophysical and Pharmacological Insights to CLC Chloride Channels.Handbook of experimental pharmacology · 2024Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- ClC-1 Chloride Channel: Inputs on the Structure-Function Relationship of Myotonia Congenita-Causing Mutations.Biomedicines · 2023Review
- Molecular mechanism underlying regulation of Arabidopsis CLCa transporter by nucleotides and phospholipids.Nature communications · 2023Article
- Small Molecules Targeting Kidney ClC-K Chloride Channels: Applications in Rare Tubulopathies and Common Cardiovascular Diseases.Biomolecules · 2023Review
- Depletion of ATP Limits Membrane Excitability of Skeletal Muscle by Increasing Both ClC1-Open Probability and Membrane Conductance.Frontiers in neurology · 2020Article
- Defective Gating and Proteostasis of Human ClC-1 Chloride Channel: Molecular Pathophysiology of Myotonia Congenita.Frontiers in neurology · 2020Review
- Structure of the human ClC-1 chloride channel.PLoS biology · 2019Article
- Regulatory Conformational Coupling between CLC Anion Channel Membrane and Cytoplasmic Domains.Biophysical journal · 2016Article
- Role of CBS and Bateman Domains in Phosphorylation-Dependent Regulation of a CLC Anion Channel.Biophysical journal · 2016Article
- Role of physiological ClC-1 Cl- ion channel regulation for the excitability and function of working skeletal muscle.The Journal of general physiology · 2016Review
- ClC-1 mutations in myotonia congenita patients: insights into molecular gating mechanisms and genotype-phenotype correlation.The Journal of physiology · 2015Article
- Regulation of ClC-2 gating by intracellular ATP.Pflugers Archiv : European journal of physiology · 2013Article
- Regulatory phosphorylation induces extracellular conformational changes in a CLC anion channel.Biophysical journal · 2013Article
- Functional characterization of a ClC transporter by solid-supported membrane electrophysiology.The Journal of general physiology · 2013Article
- Dominantly inherited myotonia congenita resulting from a mutation that increases open probability of the muscle chloride channel CLC-1.Neuromolecular medicine · 2012Article
- CLC anion channel regulatory phosphorylation and conserved signal transduction domains.Biophysical journal · 2012Article
- Intracellular β-nicotinamide adenine dinucleotide inhibits the skeletal muscle ClC-1 chloride channel.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The common gating of CLC-1 has been shown to be inhibited by intracellular adenosine triphosphate (ATP) in acidic pH conditions. Such modulation is thought to be mediated by direct binding of ATP to the cystathionine β-synthase (CBS) domains at the C-terminal cytoplasmic region of CLC-1. Guided by the crystal structure of the C-terminal domain of CLC-5, we constructed a homology model of CLC-1's C terminus and mutated critical amino acid residues lining the potential ATP-binding site. The CLC-1 mutations V634A and E865A completely abolished the ATP inhibition of CLC-1, consistent with the loss of ATP binding seen with the corresponding mutations in CLC-5. Mutating two other residues, V613 and V860, also disrupted the ATP modulation of CLC-1. However, placing aromatic amino acids at position 634 increases the apparent ATP affinity. Mutant cycle analyses showed that the modulation effects of ATP and cytidine triphosphate on wild-type CLC-1 and the V634F mutant were nonadditive, suggesting that the side chain of amino acid at position 634 interacts with the base moiety of the nucleotide. The mutation effects of V634F and V613A on the ATP modulation were also nonadditive, which is consistent with the assertion suggested from the homology model that these two residues may both interact with the bound nucleotide. These results provide evidence for a direct ATP binding for modulating the function of CLC-1 and suggest an overall conserved architecture of the ATP-binding sites in CLC-1 and CLC-5. This study also demonstrates that CLC-1 is a convenient experimental model for studying the interaction of nucleotides/nucleosides with the CBS domain.
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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.