ArticleThe Journal of biological chemistry2009
An atypical role for collapsin response mediator protein 2 (CRMP-2) in neurotransmitter release via interaction with presynaptic voltage-gated calcium channels.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed.
- Changes in Dpysl2 expression are associated with prenatally stressed rat offspring and susceptibility to schizophrenia in humans.International journal of molecular medicine · 2015Trial
- Targeting CRMP2 for Chronic Pain: From Molecular Mechanisms to Therapeutic Strategies.Biomedicines · 2026Review
- Article
- Lanthionine Ketimine Ethyl Ester Induces Proliferation and Maturation and Regulates Calcium Flux in Primary Mouse Oligodendrocyte Progenitor Cells.Journal of neuroscience research · 2025Article
- Article
- SUMOylation and DeSUMOylation: Tug of War of Pain Signaling.Molecular neurobiology · 2025Review
- Genetic crosstalk of autism spectrum disorders and epilepsy: an insight into the presynapse.Frontiers in neurology · 2025Article
- Uncoupling the CRMP2-CaThe journal of pain · 2024Article
- Peptide and Peptidomimetic Inhibitors Targeting the Interaction of Collapsin Response Mediator Protein 2 with the N-Type Calcium Channel for Pain Relief.ACS pharmacology & translational science · 2024Review
- Uncoupling the CRMP2-CabioRxiv : the preprint server for biology · 2024Article
- Primary aldosteronism: molecular medicine meets public health.Nature reviews. Nephrology · 2023Review
- A peptidomimetic modulator of the CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- DPYSL2/CRMP2 isoform B knockout in human iPSC-derived glutamatergic neurons confirms its role in mTOR signaling and neurodevelopmental disorders.Molecular psychiatry · 2023Article
- The Mood Stabilizer Lithium Slows Down Synaptic Vesicle Cycling at Glutamatergic Synapses.Neuromolecular medicine · 2023Article
- Contribution of the dihydropyrimidinase-like proteins family in synaptic physiology and in neurodevelopmental disorders.Frontiers in neuroscience · 2023Review
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- Regulation of N-type calcium channels by nociceptin receptors and its possible role in neurological disorders.Molecular brain · 2022Review
- Mammalian Brain CaMembranes · 2022Article
- Targeting N-type calcium channels in young-onset of some neurological diseases.Frontiers in cell and developmental biology · 2022Review
- Implications of Phosphoinositide 3-Kinase-Akt (PI3K-Akt) Pathway in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2022Review
62 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
Collapsin response mediator proteins (CRMPs) specify axon/dendrite fate and axonal growth of neurons through protein-protein interactions. Their functions in presynaptic biology remain unknown. Here, we identify the presynaptic N-type Ca(2+) channel (CaV2.2) as a CRMP-2-interacting protein. CRMP-2 binds directly to CaV2.2 in two regions: the channel domain I-II intracellular loop and the distal C terminus. Both proteins co-localize within presynaptic sites in hippocampal neurons. Overexpression in hippocampal neurons of a CRMP-2 protein fused to enhanced green fluorescent protein caused a significant increase in Ca(2+) channel current density, whereas lentivirus-mediated CRMP-2 knockdown abolished this effect. Interestingly, the increase in Ca(2+) current density was not due to a change in channel gating. Rather, cell surface biotinylation studies showed an increased number of CaV2.2 at the cell surface in CRMP-2-overexpressing neurons. These neurons also exhibited a significant increase in vesicular release in response to a depolarizing stimulus. Depolarization of CRMP-2-enhanced green fluorescent protein-overexpressing neurons elicited a significant increase in release of glutamate compared with control neurons. Toxin block of Ca(2+) entry via CaV2.2 abolished this stimulated release. Thus, the CRMP-2-Ca(2+) channel interaction represents a novel mechanism for modulation of Ca(2+) influx into nerve terminals and, hence, of synaptic strength.
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