IndraLab

Statements


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"As mentioned above, mutations in three voltage gated sodium channel subunits cause Brugada syndrome, the cardiac alpha subunit SCN5A, and accessory subunits SCN1B and SCN3B."

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"To study voltage dependent activation of SkM1 and SCN5A currents in GFP positive cMSC (n = 8/group), cells were held at -100 mV to prevent inactivation, and then pulsed to test potentials from -80 to +40 mV, with 5 mV increments (XREF_FIG)."

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"These action potentials are initiated and propagated by a single isoform of voltage gated sodium channels - SCN5A."

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"This suggests that some channel segment within, near, or interacting with the III-IV linker is involved in establishing hH1 activation voltage."

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"In addition to removing inactivation through the apparent clipping of the III-IV linker, it is quite possible that papain also cuts a second loop in hH1 and in hH1Q3 that imposes some structural (or p[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"This structure helps to set hH1 activation voltage to more depolarized potentials."

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"Voltage-dependent Nav1.5 channel activation process and associated apparent gating charge ( z m ) were unchanged between WT and Sorbs2 KO mice ( xref )."

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"While the voltage-dependent activation of Nav1.5 or Nav1.7 was not affected by mexiletine and lidocaine, the steady-state fast and slow inactivation of Nav1.5 and Nav1.7 were significantly shifted to hyperpolarized direction by either mexiletine or lidocaine in dose-dependent manner."

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"We first measured the voltage dependent activation of SkM1 and SCN5A current in GFP positive cells (XREF_FIG)."

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"Together, the data reveal a significant difference between hH1 and rSkM1 activation mechanisms.Is the shift in hH1 V a coupled to the removal of inactivation, or is the shift caused by some other phen[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"