ArticlePLoS computational biology2018
Effect of Ca2+ on the promiscuous target-protein binding of calmodulin.
Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Functional Calmodulin States Are Selected from an Electrostatically Tuned Free Energy Landscape.Journal of chemical information and modeling · 2026Article
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Neurogranin-MYH9 interaction regulates cytoskeletal remodeling in cerebral vasculature.Fluids and barriers of the CNS · 2025Article
- Merging Natural Biopolymers with Supramolecular Chemistry: Emulating the Native Extracellular Matrix's Complexity.ACS nano · 2025Review
- Distinct intracellular spatiotemporal expression of Calmodulin genes underlies functional diversity of Calmodulin-dependent signalling in cardiac myocytes.Cardiovascular research · 2025Article
- Calmodulin enhances mTORC1 signaling by preventing TSC2-Rheb binding.The Journal of biological chemistry · 2025Article
- Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated CaActa physiologica (Oxford, England) · 2025Article
- Calcium and Non-Penetrating Traumatic Brain Injury: A Proposal for the Implementation of an Early Therapeutic Treatment for Initial Head Insults.Biomolecules · 2024Review
- Investigating the Impact of Electrostatic Interactions on Calmodulin Binding and CaInternational journal of molecular sciences · 2024Article
- Calcium mediated static and dynamic allostery in S100A12: Implications for target recognition by S100 proteins.Protein science : a publication of the Protein Society · 2024Article
- Energetic and structural insights behind calcium induced conformational transition in calmodulin.Proteins · 2024Article
- Calcium-Associated Proteins in Neuroregeneration.Biomolecules · 2024Review
- The Complex Interplay between Toxic Hallmark Proteins, Calmodulin-Binding Proteins, Ion Channels, and Receptors Involved in Calcium Dyshomeostasis in Neurodegeneration.Biomolecules · 2024Review
- Stimuli-Responsive Protein Hydrogels: Their Design, Properties, and Biomedical Applications.Polymers · 2023Review
- Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023Review
- Regulation of Cardiac Cav1.2 Channels by Calmodulin.International journal of molecular sciences · 2023Review
- Article
- Markov state modelling reveals heterogeneous drug-inhibition mechanism of Calmodulin.PLoS computational biology · 2022Article
- Calmodulin inMicroorganisms · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calmodulin (CaM) is a calcium sensing protein that regulates the function of a large number of proteins, thus playing a crucial part in many cell signaling pathways. CaM has the ability to bind more than 300 different target peptides in a Ca2+-dependent manner, mainly through the exposure of hydrophobic residues. How CaM can bind a large number of targets while retaining some selectivity is a fascinating open question. Here, we explore the mechanism of CaM selective promiscuity for selected target proteins. Analyzing enhanced sampling molecular dynamics simulations of Ca2+-bound and Ca2+-free CaM via spectral clustering has allowed us to identify distinct conformational states, characterized by interhelical angles, secondary structure determinants and the solvent exposure of specific residues. We searched for indicators of conformational selection by mapping solvent exposure of residues in these conformational states to contacts in structures of CaM/target peptide complexes. We thereby identified CaM states involved in various binding classes arranged along a depth binding gradient. Binding Ca2+ modifies the accessible hydrophobic surface of the two lobes and allows for deeper binding. Apo CaM indeed shows shallow binding involving predominantly polar and charged residues. Furthermore, binding to the C-terminal lobe of CaM appears selective and involves specific conformational states that can facilitate deep binding to target proteins, while binding to the N-terminal lobe appears to happen through a more flexible mechanism. Thus the long-ranged electrostatic interactions of the charged residues of the N-terminal lobe of CaM may initiate binding, while the short-ranged interactions of hydrophobic residues in the C-terminal lobe of CaM may account for selectivity. This work furthers our understanding of the mechanism of CaM binding and selectivity to different target proteins and paves the way towards a comprehensive model of CaM selectivity.
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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.