ライフサイエンスコーパス: channel kinetics

1 transduction of the effects of the toxin on channel kinetics.

2 not appear to be secondary to changes in ion channel kinetics.

3 he fastest parts of the EPSC to be shaped by channel kinetics.

4 native KARs exhibit characteristically slow channel kinetics.

5 n activation by ACh and 4BP-TQS is in single-channel kinetics.

6 n rectification but did not alter effects on channel kinetics.

7 O neuronal model that incorporated T and P/Q channel kinetics.

8 not cell-type-specific differences in sodium channel kinetics.

9 ong the cochlea underlies the gradient of BK-channel kinetics.

10 inactivation curves, as well as accelerating channel kinetics.

11 rominent aberrations in open probability and channel kinetics.

12 ited hSlo current density but did not change channel kinetics.

13 channelrhodopsin-2, while maintaining the ms-channel kinetics.

14 protein kinase A (PKA) pathway acting on ion channel kinetics.

15 he effects of beta-adrenergic stimulation on channel kinetics.

16 of CaT but not of APD, which depends on ion-channel kinetics.

17 n the Ca(2+) dynamics, but is independent of channel kinetics.

18 -3/TASK-1) displayed nearly identical single-channel kinetics.

19 Chronos, a channelrhodopsin with ultra-fast channel kinetics.

20 n ROMK (+/+ and +/-) exhibited normal single channel kinetics.

21 f a simplified "toy" model for the potassium channel kinetics.

22 er the toxin had isoform-specific effects on channel kinetics.

23 on voltage-gated sodium channels and modify channel kinetics.

24 ndent capacitance was consistent with sodium channel kinetics.

25 es an effective approach for modeling single channel kinetics.

26 ither RGS7 or RGS9 modestly accelerated GIRK channel kinetics.

27 mic loop of MscL, and this also led to rapid channel kinetics.

28 ession of Gbeta5 alone had no effect on GIRK channel kinetics.

29 but not the phospholipid effect on the KACh channel kinetics.

30 tion with a binding site which modulates Cl- channel kinetics.

31 lpha) without altering the properties of Na+ channel kinetics.

32 single-channel conductance or the intrinsic channel kinetics.

33 uggests that the SSS-dependent regulation of channel kinetics accounts for nearly 40% of the decrease

34 that summarizes the effects of PAS on single channel kinetics, accounts for the PAS effects on macros

35 sAHP calcium sensor determines whether KCNQ channel kinetics also limit the sAHP decay.

36 corporates accurate representations of opsin channel kinetics and delivery modes, spatial distributio

37 y in Xenopus oocytes coexpressing KChAP, but channel kinetics and gating are unaffected.

38 TASK-1 and TASK-3, as judged by their single-channel kinetics and high sensitivity to pH(o).

39 tissue have evolved and include detailed ion channel kinetics and intercellular Ca(2+) handling.

40 ith notable differences in Ca2+ sensitivity, channel kinetics and modulation by DTT from the native I

41 g between gating modes with different single-channel kinetics and open probability.

42 h similar unitary conductances, but distinct channel kinetics and regulation.

43 availability in different states, as well as channel kinetics and sensitivity, have allowed us to elu

44 Side by side comparison of single-channel kinetics and steady-state ATP inhibition of huma

45 distinguished unambiguously by their single-channel kinetics and voltage-dependent rectification.

46 ntial components: two matching desensitizing channel kinetics, and a third component at least 10 time

47 comparisons of simulated and/or measured ion channel kinetics, and facilitates field-wide standardiza

48 the pore-forming alpha subunit can alter BK channel kinetics, and gating is dramatically slowed by c

49 Other mutations did not affect the single-channel kinetics, and may reduce ATP inhibition by inter

50 The unitary conductances, channel kinetics, and other characteristics of both endo

51 ransmembrane proteins alter the trafficking, channel kinetics, and pharmacology of the receptors in a

52 s in pH sensitivity, Ca(2+) permeability and channel kinetics, any change in the level of individual

53 Other schemes for varying KCa channel kinetics are examined, including one that allows

54 ther, the effects of 3alpha5alphaP on single-channel kinetics are similar for wild-type receptors and

55 This effect was separate from modulation of channel kinetics, as mutations within the extracellular

56 eling (HMM) can be applied to extract single channel kinetics at signal-to-noise ratios that are too

57 e critical to form GIRK channels with normal channel kinetics based on heterologous expression studie

58 nal deletions of Kvbeta1.2 no longer altered channel kinetics but promoted dramatic increases in Kv1.

59 d PSD-93delta had no discernible effect upon channel kinetics but resulted in cell surface Kir2.1 clu

60 e major effect of these mutations was not on channel kinetics but was largely, if not entirely, on th

61 Voltage dependence shifts affected channel kinetics by a single constant.

62 t to GABA and baclofen, Vc1.1 changes Cav2.2 channel kinetics by increasing the rate of activation an

63 to identify what specific information on ion channel kinetics, calcium handling, and dynamic changes

64 Furthermore, while subtle changes in AMPA channel kinetics could also be observed, we did not find

65 An analysis of single-channel kinetics demonstrated that Ca2+ induced the appe

66 ound additional alterations in mutant PIEZO1 channel kinetics, differences in response to osmotic str

67 with respect to their ligand preferences and channel kinetics during activation, desensitization, and

68 d replacements engineered here showed normal channel kinetics except the two aromatic substitutions,

69 extra copy of a sodium channel gene to alter channel kinetics for the electric organ discharge.

70 activations and adaptations, irrespective of channel kinetics, from the requirement that the free ene

71 a recent study, examination of these single-channel kinetics has revealed that NMDA receptors can en

72 ctural bases of their ligand preferences and channel kinetics have been incompletely characterized.

73 e shows that truncation of the N2 CTD alters channel kinetics; however, the mechanism by which this o

74 parable effects of SUR on ATP inhibition and channel kinetics implies that the cytoplasmic C terminus

75 d to analyse effects of alcohols on receptor-channel kinetics in detail.

76 he cell surface and those that cause altered channel kinetics in proteins that reach the cell surface

77 n exhibit striking inter-cell variability in channel kinetics in response to the agonists kainate and

78 he roles of glutamate diffusion, uptake, and channel kinetics in shaping the AMPA receptor EPSC were

79 idly equilibrating steps are eliminated, the channel kinetics in these models are represented by a si

80 Each mutation alters channel kinetics in ways that can explain the clinical p

81 Single-R50P channel kinetics (in the absence of ATP) did not differ

82 Channel kinetics include a single, invariant, open durat

83 Analysis of the single channel kinetics indicated that Ca2+ and ATP modulate th

84 , ATP dose-response relationships and single-channel kinetics, indicating that DeltaF508-CFTR is not

85 c acid and alkaline pH(i), and showed single-channel kinetics indistinguishable from those of TRAAK.

86 ell data indicated that although one type of channel kinetics is preferentially activated in each Thl

87 site 2 neurotoxins often irreversibly modify channel kinetics, lappaconitine irreversibly blocks the

88 neurons is feasible, but opsins with faster channel kinetics may be necessary to convey information

89 myocyte contraction and relaxation and Ca2+ channel kinetics more in TG than in WT.

90 synaptic network activity through their slow channel kinetics, most prominently at mossy fiber (MF)-C

91 bona-fide AMPAR modulatory protein affecting channel kinetics of AMPARs, necessary for synaptic hippo

92 Interestingly, we observe that the single channel kinetics of Ca(2+) inactivation influences the t

93 Single channel kinetics of mutants revealed no long open state,

94 atergic synapses is determined by the single-channel kinetics of postsynaptic NMDA receptor channels.

95 sion is compromised by AChR deficiency, fast channel kinetics of the epsilonN346del-AChR and incomple

96 based on molecular mechanisms, e.g., single channel kinetics of the inositol 1,4,5-trisphosphate (IP

97 mutations in the Cys-Cys loop on the single-channel kinetics of the rho1 subunit.

98 epsy and neuropathic pain because changes in channel kinetics or axonal properties can change the rat

99 s, which when deleted or substituted, affect channel kinetics or mechanosensitivity.

100 synaptic potentials, acetylcholine receptor channel kinetics, or endplate ultrastructure, but endpla

101 ytoskeletal disruption in vitro alters Na(+) channel kinetics, producing a late Na(+) current that ca

102 These changes of single-channel kinetics result in a significant decrease in the

103 duced modification of nicotinic ACh receptor channel kinetics results in an increase in the open-chan

104 Analysis of KATP single channel kinetics showed that spermine inhibited the chan

105 For random-channel kinetics, the stability of the total rate coeffi

106 ding to both declustering and alterations in channel kinetics, thus normalizing activity.

107 oring of Nav channel kinetics with potassium channel kinetics to enhance energy savings.

108 ny cellular processes, ranging from membrane channel kinetics to transcriptional regulation, and link

109 ould not be attributed to a change in Ca(2+) channel kinetics, voltage dependence, prepulse inactivat

110 ither RGS7 or RGS9, the acceleration of GIRK channel kinetics was strongly increased over that produc

111 lular loop of IRK, including the "P-region." Channel kinetics were essentially unaffected by the N- a

112 Activation gating and channel kinetics were measured for 47 single mutants and

113 acetylcholine; acetylcholine receptor (AChR) channel kinetics were normal.

114 Channel kinetics were similar across different transfect

115 The channel kinetics were solved using complex stimulus wave

116 Channel kinetics were well described by assuming two ope

117 Channel kinetics were well modeled by fitting dwell time

118 idal neurons is critically dependent on KCNQ channel kinetics whereas the identity of the sAHP calciu

119 t position 56 to histidine led to changes in channel kinetics which were dependent upon the pH on the

120 n either the cell-attached or excised single-channel kinetics which, in this channel, argues against

121 munication is a consequence of rapid calcium-channel kinetics, which allow significant calcium entry

122 ated neural computation and tailoring of Nav channel kinetics with potassium channel kinetics to enha