IndraLab

Statements


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"It has been shown that CaMKII phosphorylation of Nav1.5 leads to an increase of late I (I ) and to a shift of voltage dependence of Nav1.5 channel inactivation to hyperpolarized potentials [27]."

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"The stimulation of SCN5A is expected to accelerate the rapid depolarization of cardiomyocytes.SGK1 up-regulates several voltage gated K+ channels including KCNE1 and KCNQ1, KCNQ4 and hERG (Lamothe and Zhang 2013, Lang and Shumilina 2013, Pakladok et al. 2013)."

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"The increased mRNA expression levels of DHPR, SCN5A and RyR2 in the aconitine group (P < 0.05) suggested that aconitine could up-regulate L-type voltage-dependent Ca channels (LVDCCs), sarcoplasmic reticulum Ca release channels and Na channels."

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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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"SCN5A mediates voltage-dependent sodium ion permeability of excitable membranes and inactivation of this channel is regulated by intracellular calcium."

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"Coexpression of hH1 with beta 1 accelerates time constants in the middle voltage range."

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

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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]"