Getting a handle on CaV2.2 (N-type) voltage-gated Ca2+ channels
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Summary
A mouse model expressing CaV2.2 (N-type) voltage-gated Ca2+ channels with an extracellularly accessible hemagglutinin (HA) epitope tag engineered into their pore-forming CaV 2.2 α1 subunits allowed the identification of endogenous CaV1.2 channels in the plasma membrane of peripheral somatosensory neurons and the role of accessory α2δ-1 sub units for their plasma membrane targeting.
- Type
- letter
- Published
- 2018-12-11
- Cited by
- 7
- References
- 27
- Access
- Open access
- OpenAlex
- https://openalex.org/W2905072655
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:54476181
Keywords
Neuropathic pain, Pregabalin, Duloxetine, Postherpetic neuralgia, Medicine
References
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential
- α2δ-1 Gene Deletion Affects Somatosensory Neuron Function and Delays Mechanical Hypersensitivity in Response to Peripheral Nerve Damage
- Identification of the alpha2-delta-1 subunit of voltage-dependent calcium channels as a molecular target for pain mediating the analgesic actions of pregabalin.
- Functional exofacially tagged N-type calcium channels elucidate the interaction with auxiliary α2δ-1 subunits
- Localization of N-type Ca2+ channels in the rat spinal cord following chronic constrictive nerve injury
- Targeted disruption of the voltage-dependent calcium channel alpha2/delta-1-subunit.
- Alternative Splicing Matters: N-Type Calcium Channels in Nociceptors
- Neuropathic Pain
- Regulation of CaV2 calcium channels by G protein coupled receptors
- Thrombospondin-4 divergently regulates voltage gated Ca2+ channel subtypes in sensory neurons after nerve injury
- Loss of α2δ-1 Calcium Channel Subunit Function Increases the Susceptibility for Diabetes
- Recent advances in the development of T‐type calcium channel blockers for pain intervention
- Injury‐induced maladaptation and dysregulation of calcium channel α2δ subunit proteins and its contribution to neuropathic pain development
- Calcium channel modulation as a target in chronic pain control
- Sensory profiling in animal models of neuropathic pain: a call for back-translation
- Gabapentin prevents synaptogenesis between sensory and spinal cord neurons induced by thrombospondin‐4 acting on pre‐synaptic Cavα2δ1 subunits and involving T‐type Ca2+ channels
- BK Potassium Channels Suppress Cavα2δ Subunit Function to Reduce Inflammatory and Neuropathic Pain.
- CRMP2 and voltage-gated ion channels: potential roles in neuropathic pain
- The α2δ-1-NMDA Receptor Complex Is Critically Involved in Neuropathic Pain Development and Gabapentin Therapeutic Actions
- Prevalence of Chronic Pain and High-Impact Chronic Pain Among Adults — United States, 2016
Cited by
- EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS
- Sterols lower energetic barriers of membrane bending and fission necessary for efficient clathrin-mediated endocytosis
- Voltage-Gated Ca2+-Channel α1-Subunit de novo Missense Mutations: Gain or Loss of Function – Implications for Potential Therapies
- A peptidomimetic modulator of the CaV2.2 N-type calcium channel for chronic pain
- Peptide and Peptidomimetic Inhibitors Targeting the Interaction of Collapsin Response Mediator Protein 2 with the N-Type Calcium Channel for Pain Relief.
- THC, CBD and minor cannabinoid CBDV differently modulate hippocampal neurons firing.
- Studies on the role of Terpinolene a monoterpene on neuropathic pain: an in Silico and molecular dynamic approach
- Novel Approaches to Improving Opioid Analgesic Therapy
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