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CACNA1B activates calcium(2+). 12 / 12
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"The Cav2.2 gene in the Cav2 subfamily mainly distributed in the presynaptic ends of nerve-muscle encodes N-type calcium channels; the opening of the Cav2.2 channels enables calcium ions to flow into the ganglion, resulting in the release of neurotransmitters [25]."
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"Among those 31 genes, 29 genes such as TSK3 [65] show no change of their mRNA level suggesting an altered translation.The apparent decrease of Cav2.2 at the plasma membrane (Fig. 2b) of SNI DRGs would reduce the influx of calcium thus leading to neuronal hyperexcitability."
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"ERK modulation of several channel types has been documented including Kv4.2 [4, 91], a K channel subtype contributing to transient outward or A-type K currents, and Cav2.2 channels [68] mediating N-type Ca current and the target of the analgesic ziconotide."
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"The greater impairment of CaV2.2 recycling was accompanied with a superior ability to block depolarization-triggered calcium influx (Fig. 5); a significantly higher extent of inhibition (~50%) of calcium influx in DRG neurons was concomitant with a >4-fold change in IC value compared with tat-CBD3."
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"In neurones, Cav2.2 mediates Ca influx as a primary precursor event triggering synaptic vesicle docking [51–55]."
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"To verify whether N-type Cav2.2 channels mediated the Ca influx, motor neurons were treated with ω-Conotoxin MVIIA (CTX), together with nifedipine, over the entire culture period."
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"A study of 20 ASD patients identified a duplication of the chromosomal region 9q43.3, which contains the gene CACNA1B, which produces Ca currents in Ca 2.2 channels [222]."
| PMC
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"Transient expression in cultured skeletal muscle myotubes derived from muscular dysgenic mice demonstrates that the BIII channel mediates an omega-conotoxin-sensitive calcium current with kinetics and voltage dependence like those previously reported for whole-cell N-type current."
8386525
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"In Wallerian degeneration of DRG or SCG neurons, various calcium channels have been implicated in this calcium influx (40, 58, 59), where our data indicate that in primary hippocampal neurons the SARM1-dependent calcium influx is mediated by Cav2.2 as cilnidipine, but not nifedipine, blunted SARM1-dependent calcium influx (Figs."
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"Cav2.2 mediates the rapid influx of calcium ions into synaptic terminals, thus triggering synaptic vesicle exocytosis as well as neurotransmitter release [12, 13]."
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"In contrast, voltage-dependent N-type calcium channel subunit alpha-1B (CACNA1B) mediates the ingress of calcium ions (Ca2 ) into excitable cells, thus controlling the neurotransmitter release from the presynaptic compartment ."
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"It is known that increased intracellular calcium activates the reactive oxygen species (ROS) production pathways, so that the Cav2.2 blockade reduces the influx of calcium into the cells, having the p[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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