IndraLab

Statements


| 8

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"Pharmacological characterization of recombinant N-type calcium channel (Cav2.2) mediated calcium mobilization using FLIPR."

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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."

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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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"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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"In neurons, Cav2.2 mediates Ca influx as a primary precursor event triggering synaptic vesicle docking [51–55]."

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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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"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."