ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Differential regulation of CaV2.1 channels by calcium-binding protein 1 and visinin-like protein-2 requires N-terminal myristoylation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 59 citations in OpenAlex.
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- Chronic cerebral lipocalin 2 exposure elicits hippocampal neuronal dysfunction and cognitive impairment.Brain, behavior, and immunity · 2021Article
- Neurotransmitter Release Site Replenishment and Presynaptic Plasticity.International journal of molecular sciences · 2020Review
- Cataloguing and Selection of mRNAs Localized to Dendrites in Neurons and Regulated by RNA-Binding Proteins in RNA Granules.Biomolecules · 2020Review
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Translating neuronal activity at the synapse: presynaptic calcium sensors in short-term plasticity.Frontiers in cellular neuroscience · 2014Review
- Apo states of calmodulin and CaBP1 control CaV1 voltage-gated calcium channel function through direct competition for the IQ domain.Journal of molecular biology · 2013Article
- Competitive and non-competitive regulation of calcium-dependent inactivation in CaV1.2 L-type Ca2+ channels by calmodulin and Ca2+-binding protein 1.The Journal of biological chemistry · 2013Article
- Calcium channels and short-term synaptic plasticity.The Journal of biological chemistry · 2013Review
- Calretinin regulates Ca2+-dependent inactivation and facilitation of Ca(v)2.1 Ca2+ channels through a direct interaction with the α12.1 subunit.The Journal of biological chemistry · 2012Article
- Solution NMR structure of the Ca2+-bound N-terminal domain of CaBP7: a regulator of golgi trafficking.The Journal of biological chemistry · 2012Article
- Fine-tuning synaptic plasticity by modulation of Ca(V)2.1 channels with Ca2+ sensor proteins.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Ca2+-dependent modulation of voltage-gated Ca2+ channels.Biochimica et biophysica acta · 2012Review
- Evolution and functional diversity of the Calcium Binding Proteins (CaBPs).Frontiers in molecular neuroscience · 2012Article
- The visinin-like proteins VILIP-1 and VILIP-3 in Alzheimer's disease-old wine in new bottles.Frontiers in molecular neuroscience · 2012Article
- Molecular determinants of modulation of CaV2.1 channels by visinin-like protein 2.The Journal of biological chemistry · 2012Article
- Ca(2+) sensor proteins in dendritic spines: a race for Ca(2+).Frontiers in molecular neuroscience · 2012Article
- Molecular determinants of CaV2.1 channel regulation by calcium-binding protein-1.The Journal of biological chemistry · 2011Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
P/Q-type Ca2+ currents through presynaptic CaV2.1 channels initiate neurotransmitter release, and differential modulation of these channels by neuronal calcium-binding proteins (nCaBPs) may contribute to synaptic plasticity. The nCaBPs calcium-binding protein 1 (CaBP1) and visinin-like protein-2 (VILIP-2) differ from calmodulin (CaM) in that they have an N-terminal myristoyl moiety and one EF-hand that is inactive in binding Ca2+. To determine whether myristoylation contributes to their distinctive modulatory properties, we studied the regulation of CaV2.1 channels by the myristoyl-deficient mutants CaBP1/G2A and VILIP-2/G2A. CaBP1 positively shifts the voltage dependence of CaV2.1 activation, accelerates inactivation, and prevents paired-pulse facilitation in a Ca2+-independent manner. Block of myristoylation abolished these effects, leaving regulation that is similar to endogenous CaM. CaBP1/G2A binds to CaV2.1 with reduced stability, but in situ protein cross-linking and immunocytochemical studies revealed that it binds CaV2.1 in situ and is localized to the plasma membrane by coexpression with CaV2.1, indicating that it binds effectively in intact cells. In contrast to CaBP1, coexpression of VILIP-2 slows inactivation in a Ca2+-independent manner, but this effect also requires myristoylation. These results suggest a model in which nonmyristoylated CaBP1 and VILIP-2 bind to CaV2.1 channels and regulate them like CaM, whereas myristoylation allows differential, Ca2+-independent regulation by the inactive EF-hands of CaBP1 and VILIP-2, which differ in their positions in the protein structure. Differential, myristoylation-dependent regulation of presynaptic Ca2+ channels by nCaBPs may provide a flexible mechanism for diverse forms of short-term synaptic plasticity.
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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.