IndraLab

Statements

SCN9A activates sodium(1+). 10 / 10
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"The overactive Nav1.7 potential produces sustained sodium currents, which induce high-frequency firing of nociceptive neurons and aggravate pain [43]."
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"Nav1.7 and Nav1.8 channels cannot mediate sodium influx, which hinders the formation of action potentials, and ultimately leads to insensitivity to pain [55]."
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"This t-CSM peptide inhibited CRMP2 SUMOylation, NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons."
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"By employing PF‐04856264 and KB‐R7943 to inhibit Nav1.7‐mediated sodium influx and NCX1 reverse transport (calcium influx and sodium efflux), respectively, we observed changes in calcium fluorescence intensity in small‐to‐medium diameter (diameter < 30 μm) nociceptive sensory neurons."
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"The SCN9A sodium channel, if active, allows entry of sodium into the cells and then promotes plasma membrane depolarization."
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"In contrast, the inhibition of Nav1.7 reduces sodium influx during the early phase of depolarization, as evidenced by decreased neuronal excitability in patch‐clamp recordings and the resulting analgesic effects observed in behavioral experiments.NCX1 primarily regulates intracellular calcium concentrations through sodium‐calcium exchange."
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"EGF was shown to increase metastatic potential of prostate cancer by up regulation of SCN9A; and hence, the authors have presumed that the mutations in SCN5A and SCN9A may increase the activity of sodium channels thereby increasing the invasive potential of glioblastoma [37]."
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"CeII8 functions as a blocker of Nav1.7 by inhibiting peak sodium currents, while IMe-AGAP may interact with the structural domains of Nav1.8 and Nav1.9, as shown by computer simulation studies, making it a potential analgesic candidate."
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"SCN9A belongs to the sodium channel gene family and mediates the voltage dependent sodium ion permeability of excitable membranes."
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"Endogenous sodium currents are mainly mediated by Nav1.6 and Nav1.7, but also Nav1.1, Nav1.2, Nav1.3 and Nav1.9 at low levels ( Lee et al., 2019 )."
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