ArticleJournal of neurophysiology2008
IQ-motif proteins influence intracellular free Ca2+ in hippocampal neurons through their interactions with calmodulin.
Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Robust Increase in IQCK Protein Expression in Mouse Models of Alzheimer's Disease and iPSC-Derived Neurons.Journal of cellular and molecular medicine · 2025Article
- Defining hippocampal area CA2 in the fox (Vulpes vulpes) brain.Hippocampus · 2023Article
- Neurogranin Regulates Adult-Born Olfactory Granule Cell Spine Density and Odor-Reward Associative Memory in Mice.International journal of molecular sciences · 2021Article
- Neurogranin stimulates Ca2+/calmodulin-dependent kinase II by suppressing calcineurin activity at specific calcium spike frequencies.PLoS computational biology · 2020Article
- Diabetes and Exposure to Environmental Lead (Pb).Toxics · 2018Review
- Opposing Intermolecular Tuning of CaBiophysical journal · 2017Article
- Neurogranin alters the structure and calcium binding properties of calmodulin.The Journal of biological chemistry · 2014Article
- New insights into the regulation of synaptic plasticity from an unexpected place: hippocampal area CA2.Learning & memory (Cold Spring Harbor, N.Y.) · 2012Review
- Ca(2+) sensor proteins in dendritic spines: a race for Ca(2+).Frontiers in molecular neuroscience · 2012Article
- Exploring the genomic basis of pharmacoresistance in epilepsy: an integrative analysis of large-scale gene expression profiling studies on brain tissue from epilepsy surgery.Human molecular genetics · 2011Article
- Stimulation-mediated translocation of calmodulin and neurogranin from soma to dendrites of mouse hippocampal CA1 pyramidal neurons.Neuroscience · 2011Article
- Calmodulin as a direct detector of Ca2+ signals.Nature neuroscience · 2011Article
- RyRCa2+ leak limits cardiac Ca2+ window current overcoming the tonic effect of calmodulinin mice.PloS one · 2011Article
- Lobe specific Ca2+-calmodulin nano-domain in neuronal spines: a single molecule level analysis.PLoS computational biology · 2010Article
- Cellular dynamic simulator: an event driven molecular simulation environment for cellular physiology.Neuroinformatics · 2010Article
- Postsynaptic signal transduction models for long-term potentiation and depression.Frontiers in computational neuroscience · 2010Article
- Neurogranin enhances synaptic strength through its interaction with calmodulin.The EMBO journal · 2009Article
- Regional differences in hippocampal calcium handling provide a cellular mechanism for limiting plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Conservation and expression of IQ-domain-containing calpacitin gene products (neuromodulin/GAP-43, neurogranin/RC3) in the adult and developing oscine song control system.Developmental neurobiologyArticle
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4 authors.
Funding
Abstract
Calmodulin (CaM) is most recognized for its role in activating Ca(2+)-CaM-dependent enzymes following increased intracellular Ca(2+). However, CaM's high intracellular concentration indicates CaM has the potential to play a significant role as a Ca(2+) buffer. Neurogranin (Ng) is a small neuronal IQ-motif-containing protein that accelerates Ca(2+) dissociation from CaM. In cells that contain high concentrations of both Ng and CaM, like CA1 pyramidal neurons, we hypothesize that the accelerated Ca(2+) dissociation from CaM by Ng decreases the buffering capacity of CaM and thereby shapes the transient dynamics of intracellular free Ca(2+). We examined this hypothesis using a mathematical model constructed on the known biochemistry of Ng and confirmed the simulation results with Ca(2+) imaging data in the literature. In a single-compartment model that contains no Ca(2+) extrusion mechanism, Ng increased the steady-state free Ca(2+). However, in the presence of a Ca(2+) extrusion mechanism, Ng accelerated the decay rate of free Ca(2+) through its ability to increase the Ca(2+) dissociation from CaM, which in turn becomes subject to Ca(2+) extrusion. Interestingly, PEP-19, another neuronal IQ-motif protein that accelerates both Ca(2+) association and dissociation from CaM, appears to have the opposite impact than that of Ng on free Ca(2+). As such, Ng may regulate, in addition to the Ca(2+)-CaM-dependent process, Ca(2+)-sensitive enzymes by influencing the buffering capacity of CaM and subsequently free Ca(2+) levels. We examined the relative impact of these Ng-induced effects in the induction of synaptic plasticity.
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