ライフサイエンスコーパス: activation curve

1 mechanism consistent with a shift in the Ih activation curve.

2 induced a leftward shift of the Ca2+ channel activation curve.

3 his mutation on CaM shifts the KCNQ1 voltage-activation curve.

4 ) amplitude and a depolarizing shift in I(h) activation curve.

5 verns cellular behavior exhibits a sigmoidal activation curve.

6 actions as demonstrated by a shift in PIP(2) activation curve.

7 ve membrane effected a leftward shift in the activation curve.

8 uced a depolarized shift in the steady-state activation curve.

9 fect of mixtures of Ba(2+) and Ca(2+) on the activation curve.

10 a comparable shift in the transducer channel activation curve.

11 induced a negative shift of the steady-state activation curve.

12 d a left shift ( approximately 40 mV) of the activation curve.

13 a significantly more negative and shallower activation curve.

14 ctivation and a hyperpolarizing shift in the activation curve.

15 2 isoform is associated with a more negative activation curve.

16 esulted in a 15 mV depolarizing shift of the activation curve.

17 did not evoke a hyperpolarizing shift in the activation curve.

18 nnels, and induced a negative shift of their activation curves.

19 osition 345 rendered shifted biphasic proton activation curves.

20 proton apparent affinity and biphasic proton activation curves.

21 the nonlinear force versus displacement and activation curves.

22 mutations) or by a depolarizing shift of the activation curve (2 voltage sensor mutations) decreasing

23 ts takes place through shifts in its voltage activation curve, allowing channel opening at physiologi

24 is within the dynamic range of the synaptic activation curve and a shift in the activation curve by

25 mall negative shift in the channel's voltage-activation curve and led to an increased nonselective le

26 Voltage dependence of the If activation curve and the intracellular cAMP levels were

27 le manner but caused a depolarizing shift in activation curves and greater use-dependent block of Ca(

28 CST did not shift the Ih activation curve, and the peptide effect was unaffected

29 From activation curves approximately 2-7% of I(h)would be act

30 Second, the steady-state activation curves are either laserlike or steplike.

31 ardiac isoform showed a minimal shift in the activation curve as a function of time after whole-cell

32 We introduce "activation curves" as a useful tool to study the reperto

33 voltage curves) always preceded the channel activation curves, as expected for protein rearrangement

34 ) and one mutant subunit exhibited a shifted activation curve at low intracellular [Cl(-)].

35 me transport protein based on: (a) different activation curves, (b) different time dependencies, (c)

36 yed or improved exhibit dramatically shifted activation curves because of a change in the rate of cot

37 synaptic activation curve and a shift in the activation curve by the modulatory neuropeptide proctoli

38 hereas a leftward shift in voltage or Ca(2+) activation curves can be observed for P(o) values lower

39 Activation curves demonstrate that a significant fractio

40 Instead, the activation curve for alpha(1C) + beta(3) + alpha(2)delta

41 The activation curve for E71A KcsA is similar to that obtain

42 dies, cell permeant cAMP analogs shifted the activation curve for I(H) to depolarized potentials in C

43 d the half-point of the isochronal (7.5 sec) activation curve for IKs by -16 mV at 0.1 microM and -24

44 arizing shift (of approximately 6 mV) in the activation curve for the tetrodotoxin-resistant sodium c

45 ette resulted in a depolarizing shift in the activation curve for the transient channels of approxima

46 ective protein kinase inhibitor, shifted the activation curves for both proximal and distal Na+ chann

47 lated to the overlap of the inactivation and activation curves for I(T)), rhythmogenic properties, no

48 ng single-channel electrophysiology, and the activation curves for wild-type and E71A KcsA are indist

49 a nearly 50 mV shift in the midpoint of the activation curve in a direction consistent with stabiliz

50 a significant leftward shift of the I(Ca,L) activation curve in NF- and LVAD- but not in F-HVMs.

51 late Ih in primary afferents by shifting the activation curve in the depolarizing direction and incre

52 KCNC3(F448L) shifted the activation curve in the negative direction and slowed ch

53 NS additionally shifted the activation curve in the negative direction, accelerated

54 potential to a point on the I(Ca) and I(BK) activation curves in which filtering is optimized like t

55 Maximal depolarizing shift of the If activation curve induced by isoproterenol was attenuated

56 c current decay is faster, the V(1/2) of the activation curve is shifted in the depolarized direction

57 The bilayer-thickness-dependent shift in the activation curve is suggestive of a decrease in an appar

58 4 expression favored open states by shifting activation curves negative, decreasing the slope of the

59 Neither the activation curve nor the kinetics of fast inactivation w

60 The activation curve of I(A) in CA1 neurons shifted to the d

61 uced a depolarized shift in the steady-state activation curve of I(A) without altering the inactivati

62 MP-S (an activator of PKA), both shifted the activation curve of Ih to more depolarized potentials an

63 onstants and caused a rightward shift in the activation curve of KCNQ1+minK, but affected none of the

64 , whereas beta1 did not modulate the voltage-activation curve of MSSN, beta1 induced a significant le

65 Furthermore, the activation curve of somatic A-type K(+) current was depo

66 ase is caused by a depolarizing shift in the activation curve of the native HCN current, which in tur

67 the hair bundle modulate the position of the activation curve of the transducer.

68 The steady-state activation curve of the underlying conductance showed a

69 of Ih resulting from a positive shift in the activation curve of this current.

70 ttributable to a hyperpolarized shift in the activation curve of voltage-gated sodium channels (VGSCs

71 ed comparable leftward shifts in the voltage-activation curves of all three isoforms, indicating that

72 a significant leftward shift of the voltage activation curves of both the MDAL and MANG isoforms.

73 ing to L1042-T1051 alters the profile of the activation curves of full-length and C1-C2 forms of ACV

74 cytoplasmic side of excised patches shifted activation curves of MscS toward higher tensions.

75 We demonstrate that cCMP shifts the activation curves of two members of the HCN channel fami

76 o from 100 to 1 mM did not alter the voltage-activation curve or reversal potential (Vrev) but reduce

77 iated with a 4.4-mV depolarization of the Ih activation curve (P=0.0027) and an increase in mean firi

78 Its activation curve ranged from approximately -50 to -120 m

79 Tail current activation curves showed that grammotoxin shifted the st

80 We propose that the steepness of this kinase activation curve simultaneously controls the behavioral

81 By contrast, the activation curve, steady-state slow inactivation and the

82 d residue (Y75E) causes a right shift of the activation curve ("stiff" phenotype) and abolishes funct

83 The steep activation curve suggests that the channel opens when fo

84 process usually produce canonical Boltzmann activation curves that correspond to a simple two-state

85 tion was a result of a leftward shift of the activation curve to higher pH values and a slight shift

86 panied by approximately 30-mmHg shift of the activation curve to lower pressures and slower rates of

87 However, because of a shift of the activation curve to more depolarized potentials, and a c

88 uring conditions of a shift in their voltage activation curve to more depolarized potentials.

89 steps, L283F and T310M caused a shift of the activation curve to more positive potentials and F428S r

90 1 processing and shifted KCNE1/KCNQ1 channel activation curve to more positive potentials in HEK cell

91 Application of internal cAMP shifted the activation curve to more positive potentials, giving a V

92 f the maximal erg current and a shift of the activation curve to more positive potentials.

93 dentically shifted the pH-sensitivity of the activation curves to more acidic values.

94 ated temperature moved Kv11.1a/1b isochronal activation curves to more negative potentials, but shift

95 nal [Ca(2+)] or [Mg(2+)] identically shifted activation curves to the right and identically shifted t

96 The mutation p.I141V shifted the activation curve toward more negative potentials and inc

97 to mimic the prepulse effect by shifting the activation curve toward more negative potentials, leavin

98 V1 by shifting the voltage dependence of the activation curves towards more physiological membrane po

99 The midpoint of GABA activation curve was 10 nM for receptors in oocytes vers

100 some cells, the hyperpolarizing shift in the activation curve was accompanied by a decrease in peak c

101 The mean activation curve was fitted by a modified Boltzmann equa

102 tively, and a 5 mV depolarizing shift of the activation curve was observed in lh.

103 With development, the position of the activation curve was shifted in the positive direction,

104 as reduced but the shift in the Ca2+ channel activation curve was unaffected.

105 Sigmoidal activation curves were observed with Mn2+ and Mg2+ with

106 ed with a leftward shift of the Ca2+ channel activation curve which averaged -9 mV.

107 ion-activated currents could be described by activation curves with a half-maximal activation potenti

108 The slope of initial parts of activation curves, with a few channels being active, gav

109 , ICA-069673 induced a negative shift of the activation curves without significantly increasing maxim