ArticleThe Journal of biological chemistry2017
Free energy landscape remodeling of the cardiac pacemaker channel explains the molecular basis of familial sinus bradycardia.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- A cryptic symmetry switch allosterically controls how the PF4 self-protein turns into a pathogenic antigen.Nature communications · 2026Article
- Aortic disease-linked mutations reveal unexpected convergent allosteric mechanisms of protein kinase G misregulation.Science advances · 2026Article
- A rare HCN4 variant combined with sick sinus syndrome, left ventricular noncompaction, and complex congenital heart disease.Channels (Austin, Tex.) · 2025Article
- Recurrent Acrodysostosis-Related PKA RIα Mutant Reveals a Novel Mechanism of Aberrant PKA Deactivation.Journal of molecular biology · 2025Article
- Mitochondrial dysfunction is a key link involved in the pathogenesis of sick sinus syndrome: a review.Frontiers in cardiovascular medicine · 2024Review
- Altered cyclic nucleotide binding and pore opening in a diseased human HCN4 channel.Biophysical journal · 2022Article
- Function-Related Dynamics in Multi-Spanning Helical Membrane Proteins Revealed by Solution NMR.Membranes · 2021Review
- Allosteric Mechanisms of Nonadditive Substituent Contributions to Protein-Ligand Binding.Biophysical journal · 2020Article
- Mechanism of allosteric inhibition in theThe Journal of biological chemistry · 2020Article
- Review
- Mechanisms of Specific versus Nonspecific Interactions of Aggregation-Prone Inhibitors and Attenuators.Journal of medicinal chemistry · 2019Article
- Allostery modulates the beat rate of a cardiac pacemaker.The Journal of biological chemistry · 2017Article
- Characterizing micro-to-millisecond chemical exchange in nucleic acids using off-resonance RProgress in nuclear magnetic resonance spectroscopyReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The hyperpolarization-activated and cyclic nucleotide-modulated ion channel (HCN) drives the pacemaker activity in the heart, and its malfunction can result in heart disorders. One such disorder, familial sinus bradycardia, is caused by the S672R mutation in HCN, whose electrophysiological phenotypes include a negative shift in the channel activation voltage and an accelerated HCN deactivation. The outcomes of these changes are abnormally low resting heart rates. However, the molecular mechanism underlying these electrophysiological changes is currently not fully understood. Crystallographic investigations indicate that the S672R mutation causes limited changes in the structure of the HCN intracellular gating tetramer, but its effects on protein dynamics are unknown. Here, we utilize comparative S672R
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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.