ライフサイエンスコーパス: inward rectification

1 te probability (Po, at pH 7.4) with a strong inward rectification.

2 time-dependent, hyperpolarization-activated inward rectification.

3 ctivation that determines its characteristic inward rectification.

4 on of many of the structural requirements of inward rectification.

5 e current-voltage relationship showed marked inward rectification.

6 s, after removal of polyamine-induced strong inward rectification.

7 ng depolarizing pulses showed characteristic inward rectification.

8 e interneurons that displayed time-dependent inward rectification.

9 ative contributions of various mechanisms to inward rectification.

10 as in the relative degree of outward versus inward rectification.

11 urely potassium selective, and showed strong inward rectification.

12 nt activation but did decrease the degree of inward rectification.

13 diated) excitatory synaptic transmission and inward rectification.

14 ium relative to monovalent cations and shows inward rectification.

15 P < 0.001 versus wild type) due to a lack of inward rectification.

16 le to Ca(2+), and their currents show unique inward rectification.

17 ), eliminating polyamine inhibition and thus inward rectification.

18 n increase in single-channel conductance and inward rectification.

19 requirement for PIP(2) and Mg(2+)-dependent inward rectification.

20 reversed around -68 mV and displayed marked inward rectification.

21 go structural changes to modulate gating and inward rectification.

22 ltage (I-V) relationships, no longer showing inward rectification.

23 mutations of the G-loop disrupted gating or inward rectification.

24 f Kir2.1(L) that is important for modulating inward rectification.

25 cellular Mg(2+) (100 microm to 1 mm) causing inward rectification.

26 pression of a low-threshold spike and strong inward rectification.

27 te did not show any additional effect on the inward rectification.

28 and the beta3b subunit conferred an apparent inward rectification.

29 ellular magnesium and polyamines to generate inward rectification.

30 of multiple pore blockers to generate strong inward rectification.

31 ge relations showed similar small degrees of inward rectification, a similar apparent K(d) of approxi

32 Two processes underlie this inward rectification: an intrinsic rectification caused

33 ype channels are characterized by pronounced inward rectification and a Cl > thiocyanate > Br > NO(3)

34 acroscopic Kir7.1 conductance exhibited mild inward rectification and an inverse dependence on extrac

35 elayed rectifier current (IKr) are prominent inward rectification and an unexpected reduction in acti

36 The strong inward rectification and calcium permeability of AMPARs

37 yl)ethyl)propenamide (B-973B) showed reduced inward rectification and calcium-dependent reversal pote

38 The activating currents displayed inward rectification and deactivating current tails were

39 pha6beta4 AChR-mediated currents show strong inward rectification and dependence on extracellular Ca2

40 phasizes that measured intrinsic properties (inward rectification and external [K] dependence) and lo

41 short latency cation current that exhibited inward rectification and marked desensitization.

42 y postsynaptic currents exhibited pronounced inward rectification and marked sensitivity to 1-naphthy

43 stsynaptic to primary afferent fibres, using inward rectification and polyamine toxins for receptor i

44 h revealed a time-dependent, Cs(+)-sensitive inward rectification and rebound excitation at the termi

45 current amplitudes reflected the macroscopic inward rectification and revealed a conductance level of

46 their prominent outward rectification, peak inward rectification and robust low threshold Ca2+ poten

47 One K(+) channel showed strong inward rectification and single-channel conductance simi

48 t of postsynaptic PKC activation in both the inward rectification and UDU of EPSCs in immature rat co

49 of PA influence on synaptic AMPAR function - inward rectification and use-dependent unblock (UDU), wi

50 The outward current showed inward rectification and was blocked by the K+ channel b

51 AMPAR EPSCs in core and shell did not show inward rectification and were insensitive to 1-naphthyla

52 , lack of voltage-sensitivity of activation, inward rectification, and Ca2+ concentration dependence.

53 of glutamate receptors-calcium permeability, inward rectification, and channel block by external poly

54 exhibits alterations in sensitivity to ATP, inward rectification, and ion selectivity.

55 ited no outward rectification, only moderate inward rectification, and no high frequency firing assoc

56 n structural and chemical terms the basis of inward rectification, and they also have implications fo

57 , slower recovery from desensitization, less inward rectification, and virtually no Ca2+ permeability

58 ressed in mammalian cells and find that this inward rectification arises from a rapid and voltage-dep

59 The PP exhibits inward rectification, as evidenced by very low outward c

60 bition by Ni(2+) was accompanied by moderate inward rectification at concentrations higher than 0.1 m

61 Single-channel openings displayed inward rectification at depolarized potentials, and were

62 V) and shows rapid inactivation reflected as inward rectification at depolarized potentials.

63 ntaneously hypertensive rats (SHR) displayed inward rectification at positive holding potentials, whi

64 e current-voltage relationship showed strong inward rectification at positive membrane potential.

65 rsal potentials near 0 mV, and showed strong inward rectification at positive potentials.

66 Melk2 channels exhibit inward rectification because of a fast C-type inactivati

67 ChRs) that, like CP-AMPARs, exhibit a strong inward rectification because of polyamine block at depol

68 Differences in the strength of inward rectification between pacemakers and nonpacemaker

69 , as well as the difference in the extent of inward rectification between the two channels.

70 M2 (AM2), which conducts protons with strong inward rectification, BM2 conducts protons both inward a

71 hwartz model, originally proposed to explain inward rectification by singly charged blocking particle

72 nward currents reversed near 0 mV and showed inward rectification common for neuronal nicotinic recep

73 entials more negative than -75 mV, there was inward rectification, consisting of a fast component lea

74 At a position critical for inward rectification (D172), the pore is sufficiently wi

75 es of quasi-instantaneous activation, strong inward rectification, depended on the external [K(+)], a

76 The results demonstrate that inward rectification depends on a single amino acid (Ala

77 s from outside-out patches demonstrated that inward rectification does not require intracellular Mg2+

78 This conduction property, called inward rectification, enables inward rectifiers to perfo

79 idue 436 are determinants of 5-HT3A receptor inward rectification, exposing an additional role for po

80 ound excitation mediated by a time-dependent inward rectification expressed intrinsically by SPNs may

81 Whole-cell current responses show stronger inward rectification for alpha4beta2-nAChR than for alph

82 tifying K+ channel, previously implicated in inward rectification gating due to cytoplasmic Mg2+ and

83 OA neurons (n=76) displayed a time-dependent inward rectification (I(h)) that was blocked by CsCl (3

84 ties of optic nerve axons, accommodation and inward rectification (I(h)), respond to temperature chan

85 ber of questions about several properties of inward rectification important to the understanding of t

86 rrent-voltage (I-V) relation showed profound inward rectification in all recording configurations.

87 matched healthy subjects, indicating greater inward rectification in iRLS.

88 e relationship of AMPAR-EPSCs from linear to inward rectification in labelled PVN neurons.

89 urrent that mediates a slower form of strong inward rectification in large pyramidal cells in neocort

90 clic nucleotide-gated (HCN) channel-mediated inward rectification in motor axons.

91 However, the impact of inward rectification in shaping action potentials (APs)

92 rrent-voltage (I-V) relations show very mild inward rectification in symmetrical solutions, are linea

93 tly, IRK1 channels display voltage-dependent inward rectification in the absence of divalent ions or

94 FK506 treatment also caused an inward rectification in the current-voltage relationship

95 This ChR2 model offers: 1) accurate inward rectification in the current-voltage response acr

96 sporadic ALS showing significantly increased inward rectification in the current-voltage threshold cu

97 SOD1/G93A mice, NET also showed an increased inward rectification in the current-voltage threshold cu

98 lded SOD1 protein levels showed an increased inward rectification in the current-voltage threshold cu

99 The observed NET pattern of increased inward rectification in the current-voltage threshold cu

100 ddition to the short QT interval, absence of inward rectification in the E299V mutation should result

101 (m) and I(thr) and allowed to quantify I(K1) inward rectification in the intact heart, identifying re

102 In the present study, we compared inward rectification in the Kir3.1/Kir3.4 channel, which

103 ur studies reveal an unexpected mechanism of inward rectification involving a linker sub-helix emergi

104 Inward rectification is caused by voltage-dependent bloc

105 by intracellular divalent ions, we find that inward rectification is in fact an intrinsic property of

106 G-protein-coupled inward rectification K(+) (GIRK) channels play an import

107 e pyramidal cells have K(+)-selective strong inward rectification like that observed in Muller cells,

108 It appears that the inward rectification mechanism by rapid inactivation has

109 ow clear that a similar mechanism results in inward rectification of alpha-amino-3-hydroxy-5-methyl-4

110 t block by internal polyamines gives rise to inward rectification of AMPA receptors lacking the GluR2

111 Moreover, an enhanced inward rectification of AMPAR current by nicotine sugges

112 1/GluA2 heteromers in the PVN and diminished inward rectification of AMPAR-EPSCs in labelled PVN neur

113 an alpha2delta-1 C terminus peptide reversed inward rectification of AMPAR-EPSCs in spinal VGluT2 neu

114 lta-1 interactions with GluA1 and GluA2, and inward rectification of AMPAR-EPSCs in spinal VGluT2 neu

115 hibition of calpain or calcineurin abolished inward rectification of AMPAR-EPSCs of PVN neurons in SH

116 However, the inward rectification of GABA-induced transport currents

117 mbrane segments TM1 and TM2 affect the steep inward rectification of GIRK1, while residues in the mai

118 In addition, the degree of inward rectification of kainate-activated currents corre

119 outside-out patch recording as the degree of inward rectification of kainate-activated currents, quan

120 Steeply voltage-dependent inward rectification of Kir (inwardly rectifying potassi

121 of DFMO may be mediated by alteration of the inward rectification of Kir4.1 channels, resulting in a

122 High external K(+) enhances the inward rectification of membrane potential, an effect me

123 e cells that lack this protein increased the inward rectification of mEPSCs.

124 Inward rectification of nicotine-induced responses was r

125 We conclude that inward rectification of P2X2 is due to two mechanisms: v

126 ne the in vivo role of polyamines in causing inward rectification of potassium channels.

127 Reducing [Mg2+]i to 0, which reverses inward rectification of some K+ channels, did not alter

128 ength is also associated with a shift toward inward rectification of synaptic currents and increased

129 This inward rectification of the CFTR channel was mediated by

130 dependent reduction in open probability, and inward rectification of the current-voltage relationship

131 ck by intracellular polyamines, which causes inward rectification of the current-voltage relationship

132 vation and rapid C-type inactivation produce inward rectification of the current-voltage relationship

133 oreover, the presence of CFTR prohibited the inward rectification of the gating of this renal Na+ cha

134 is decrease could quantitatively account for inward rectification of the instantaneous I-V relation.

135 174) to alanines in the central pore induced inward rectification of the ionic current and shifted re

136 exponential current relaxations and moderate inward rectification of the macroscopic currents upon ex

137 containing calcium-impermeable AMPARs by the inward rectification of their currents, which reflects v

138 currents (I(CRAC)): store dependence, strong inward rectification, positive reversal potential, limit

139 y rectifying gap junction reminiscent of the inward rectification properties of the Kir (e.g. Kir2.x)

140 ernal Ba2+ and Cs+, and no dependence of its inward rectification properties on the internal blocking

141 re domain potassium channel family with weak inward rectification properties.

142 entified unambiguously by their conductance, inward rectification, rapid gating kinetics and pharmaco

143 ke after-hyperpolarization, but greater peak inward rectification resistance, and exhibited delta osc

144 rent in LSI neurons displayed Ba2+-sensitive inward rectification, reversed polarity near EK and was

145 is thought to help extrude chloride because inward rectification should, in principle, allow ClC-2 t

146 In addition, extinction training increased inward rectification, suggesting that extinction induces

147 suggests that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1 because of the differen

148 nstrating that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1.

149 he faster rate of activation results in less inward rectification than that observed in HERG channels

150 he current-to-voltage relations (i-V) showed inward rectification that disappeared at 1000 mM K(+).

151 sidue F168 generates channels with intrinsic inward rectification that does not require blockade by i

152 can account for the anomalous time-dependent inward rectification that has previously been described

153 in a voltage-dependent fashion and displayed inward rectification that was intermediate between that

154 I-V relationship of I5-HT,outward showed an inward rectification; the 5-HT-induced current, which re

155 en a slow after-hyperpolarization (sAHP) and inward rectification through hyperpolarization-activated

156 CRAC current from being Ca2+-selective with inward rectification to being selective for monovalent c

157 Xenopus oocytes, the channel displays strong inward rectification typical of inward rectifiers.

158 veral biophysical characteristics, including inward rectification, voltage sensitivity of open probab

159 the spatial segregation of glial cells with inward rectification was addressed in slices that were b

160 PK/PCl = 0.3) 1.5-nS channel displaying mild inward rectification was noted.

161 Marked inward rectification was observed for depolarizations po

162 Inward rectification was present only in caecum-projecti

163 e intracellular Mg2+ or polyamines, and that inward rectification was present when the same solution

164 the potassium equilibrium potential, showed inward rectification, was blocked by extracellular bariu

165 dependent on K+ driving force, and the weak inward rectification were indistinguishable for both cha

166 ased GIRK currents ( I(K,ACh)) and a reduced inward rectification which was not compensated by intrac

167 ium currents through SK channels demonstrate inward rectification, which further reduces their small

168 PSCs in immature pyramidal neurons displayed inward rectification, which was enhanced by intracellula

169 ypes, AMPA-mediated synaptic currents showed inward rectification, which was more pronounced in OT ne

170 In symmetrical KCl solutions GBa showed inward rectification, while Gquin demonstrated outward r

171 mm K(+)-containing solutions exhibited weak inward rectification with a mean conductance of 66.2 +/-

172 ng depolarising ramps, the current underwent inward rectification with a negative slope region that b

173 ogress in research on the molecular basis of inward rectification, with significant implications for

174 mM) blocked the hyperpolarization-activated inward rectification without affecting the expression of

175 t GluK2(Q) kainate receptors greatly reduced inward rectification without altering calcium permeabili