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1 r an additional hyperpolarizing shift of the inactivation curve.
2 ated state and a hyperpolarized steady-state inactivation curve.
3 ctivation curve of I(A) without altering the inactivation curve.
4 nificant, negative shift of the steady-state inactivation curve.
5 ionship but produced a negative shift in the inactivation curve.
6 tion causes a dramatic positive shift of the inactivation curve.
7 erimposed after voltage shifting, as did the inactivation curves.
8 position of the activation and steady state inactivation curves.
9 ss of the sodium current, while shifting the inactivation curve ~10 mV toward more hyperpolarized pot
10 shift of the voltage-dependent steady-state inactivation curve, a slower inactivation, and a faster
11 l overlap of its activation and steady-state inactivation curves and its persistent nature suggest th
12 curves negative, decreasing the slope of the inactivation curve, and increasing the percentage of non
13 protocols (such as I-V curves, steady-state inactivation curves, and measurements of inactivation ra
14 g, shifting both steady state activation and inactivation curves, as well as accelerating channel kin
15 the midpotential of the hKv2.1 steady-state inactivation curve by approx. 15 mV in the hyperpolarizi
16 a hyperpolarizing shift in the steady-state inactivation curve completely abolished EADs in myocytes
18 current" between the voltage activation and inactivation curves, decreasing the tonically active I(A
19 s dominating and, consequently, the prepulse inactivation curves exhibit depolarizing shifts (DeltaV
20 tion in inside-out patches, the steady-state inactivation curve exhibits a hyperpolarizing shift of a
22 nt-voltage relationship and the steady-state inactivation curve for the TTX-R INa which were indistin
24 oltage-dependent activation and steady-state inactivation curves for these currents were shifted nega
25 polarizing shift in the apparent Na+ channel inactivation curves generated from Vmax and theta2, resp
26 urrents at rest and shifted the steady-state inactivation curve (h infinity) toward the hyperpolarizi
27 s altered the shape of the voltage-dependent inactivation curve indicating that the suppression of IK
29 ate constants by as much as 600%, shortening inactivation curve lag phase by up to 73% and lowering C
30 -93 shifted the midpoint of the steady-state inactivation curve leftward and markedly slowed the reco
31 In addition, we find that the steady-state inactivation curve of modified Na channels is made much
33 hat from control rats (109.4 pA/pF), and the inactivation curve of the IA current was displaced to mo
35 dings revealed a hyperpolarized shift in the inactivation curve of transient, A-type K(+) currents th
37 cantly increased at 38 h after ischemia; the inactivation curves of I(A) shifted toward the depolariz
38 ation, shifts of steady-state activation and inactivation curves of I(Na) to more depolarized potenti
40 t density, and right-shifted the V1/2 of the inactivation curve, of hindpaw innervating DRG neurons,
41 g peptides caused depolarizing shifts in the inactivation curves seen with CaM(WT) coexpression with
42 y-state channel availability relationships ("inactivation curves") shifted toward more negative membr
44 to changes in the steady-state activation or inactivation curves, the time course of current decay, t
46 in the rate of inactivation and shifted the inactivation curve to more hyperpolarized potentials, bu
47 eduction of I(Ca,L) density and shift of the inactivation curves to more depolarized potentials).
51 The midpoints of steady-state activation and inactivation curves were 1.1 mV and -61.4 mV, respective
52 ches, respectively, n = 16, P < 0.01), while inactivation curves were not significantly different.
53 ng measurements, bell-shaped Ca2+ activation/inactivation curves were obtained in media containing di
57 depolarizing shift of the steady-state fast inactivation curve, whereas EE1314,15RR produced a hyper
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