ライフサイエンスコーパス: voltage gated Ca2 channel

1 modipine, consistent with Zn2+ entry through voltage-gated Ca2+channels.

2 Ca2+ entry through NMDA channels or through voltage gated Ca2+ channels.

3 dent reduction in Ca2+ influx through R-type voltage-gated Ca2+ channels.

4 result from an increased Ca2+ influx through voltage-gated Ca2+ channels.

5 y removing extracellular Ca2+ or by blocking voltage-gated Ca2+ channels.

6 th muscle cell depolarization and opening of voltage-gated Ca2+ channels.

7 ux was found, mediated by both L- and T-type voltage-gated Ca2+ channels.

8 s to the unusual behavior of the hair cell's voltage-gated Ca2+ channels.

9 application of cadmium (100 microM) to block voltage-gated Ca2+ channels.

10 e-gated K+ channels and grammotoxin inhibits voltage-gated Ca2+ channels.

11 tivated in neurons by influx of Ca2+ through voltage-gated Ca2+ channels.

12 Ca2+ influx into aortic BRNs independent of voltage-gated Ca2+ channels.

13 ar Ca2+ mobilization and Ca2+ influx through voltage-gated Ca2+ channels.

14 ction potentials and both NMDA receptors and voltage-gated Ca2+ channels.

15 R-ACPD current may depend on Ca2+ influx via voltage-gated Ca2+ channels.

16 edicted from the reported La3+ dependence of voltage-gated Ca2+ channels.

17 re conserved across the different classes of voltage-gated Ca2+ channels.

18 oM) and specific for Ca2+ influx through non-voltage-gated Ca2+ channels.

19 are "stimulus-coupled" to Ba2+ entry through voltage-gated Ca2+ channels.

20 d by and highly sensitive to the activity of voltage-gated Ca2+ channels.

21 emerged as important regulatory subunits of voltage-gated Ca2+ channels.

22 suppresses CB1-mediated tonic inhibition of voltage-gated Ca2+ channels.

23 nsor to feedback-regulate Ca2+ entry through voltage-gated Ca2+ channels.

24 s glutamate release via inhibition of N-type voltage-gated Ca2+ channels.

25 ted inward rectifying potassium channels and voltage-gated Ca2+ channels.

26 c branches and increased Ca2+ influx through voltage-gated Ca2+ channels.

27 This causes Ca2+ entry through voltage-gated Ca2+ channels.

28 malities in glucose signaling or function of voltage-gated Ca2+ channels.

29 crovascular endothelial cells do not express voltage-gated Ca2+ channels.

30 A release via inhibition of Ca2+ influx from voltage-gated Ca2+ channels.

31 rcoplasmic reticulum (SR) and influx through voltage-gated Ca2+ channels.

32 h as glutamate receptor-operated channels or voltage-gated Ca2+ channels.

33 y 200 microM Cd2+, a non-specific blocker of voltage-gated Ca2+ channels.

34 e depolarization, which presumably activates voltage-gated Ca2+ channels.

35 g-term modulatory effects on the activity of voltage-gated Ca2+ channels.

36 the human homolog of the alpha1A subunit of voltage-gated Ca2+ channels.

37 ons abolishes LTP-GABAA by inhibiting L-type voltage-gated Ca2+ channels.

38 ease was mediated via the binding of Pb2+ to voltage-gated Ca2+ channels.

39 by a Gd(3+)-sensitive ion channel and not by voltage-gated Ca2+ channels; (3) the magnitude of the Ca

40 To determine if Ca2+ influx through voltage-gated Ca2+ channels, activated during this depol

41 data show that Ca2+ entering through P-type voltage-gated Ca2+ channels activates both small-conduct

42 Whereas voltage-gated Ca2+ channel activity regulates several as

43 lock by Ca2+, shows behaviour similar to the voltage-gated Ca2+ channel and the cyclic nucleotide-gat

44 data provide evidence for cross-talk between voltage-gated Ca2+ channels and 5-HT3Rs in NG108-15 cell

45 ly recognize the alpha1 subunit of class A-D voltage-gated Ca2+ channels and a monoclonal antibody (M

46 intracellular stores and Ca2+ entry through voltage-gated Ca2+ channels and a non-selective cation c

47 Activation of cannabinoid receptors inhibits voltage-gated Ca2+ channels and activates K+ channels, r

48 We report here a direct interaction between voltage-gated Ca2+ channels and endophilin, a key regula

49 the Gbeta2 C terminus induced modulation of voltage-gated Ca2+ channels and GIRK channels.

50 requires extracellular Ca2+ passing through voltage-gated Ca2+ channels and may be mediated through

51 of the gene, TRKB, via entry of Ca2+ through voltage-gated Ca2+ channels and subsequent activation of

52 se evoked by KCl depolarization, which opens voltage-gated Ca2+ channels; and (3) by enhancing Ca2+ a

53 ted by 80-95 % in the presence of the L-type voltage-gated Ca2+ channel antagonists nitrendipine (2-5

54 of Per1 expression was markedly decreased by voltage-gated Ca2+ channel antagonists.

55 Voltage-gated Ca2+ channels are categorized as either hi

56 Beta subunits of voltage-gated Ca2+ channels are encoded in four genes an

57 Voltage-gated Ca2+ channels are targets for phosphorylat

58 CaMKII) phosphorylates the beta2a subunit of voltage-gated Ca2+ channels at Thr498 to facilitate card

59 hrough either the nicotinic receptors or the voltage-gated Ca2+ channels because the release was incr

60 reversibly inhibited by Cd2+ (200 microM), a voltage-gated Ca2+ channel blocker.

61 The increase in mIPSCs depended on voltage-gated Ca2+ channels but persisted when ionotropi

62 Hydrogen ions reduce ion flux through voltage-gated Ca2+ channels by binding to a single proto

63 rtant source of Ca2+ entry in dendrites, the voltage-gated Ca2+ channels, by applying the whole-cell

64 L-type, voltage-gated Ca2+ channels (CaL) play critical roles in

65 We tested directly whether voltage-gated Ca2+ channels can flux Zn2+ in whole-cell

66 results provide evidence that L- and N-type voltage-gated Ca2+ channels can mediate Zn2+ entry into

67 chanisms for the differential sensitivity of voltage-gated Ca2+ channels (Cav) to agonists, channel a

68 highlighted unexpected roles for the L-type voltage-gated Ca2+ channel CaV1.2 in nonexcitable cells.

69 l blocker nimodipine, indicating that L-type voltage-gated Ca2+ channels contribute to the response t

70 No measurable inward current via voltage-gated Ca2+ channels could be detected in these c

71 We hypothesized that enhanced voltage-gated Ca2+ channel current (VGCC) density in cor

72 ll patch-clamp recordings were used to study voltage-gated Ca2+ channel currents in type I carotid bo

73 esponse, suggesting that Ca2+ influx through voltage-gated Ca2+ channels does not induce refractorine

74 ing further evidence that Ca2+ entry through voltage-gated Ca2+ channels does not initiate refractori

75 ctile state of the cell, or as activators of voltage-gated Ca2+ channels due to depolarization mediat

76 flow can alter the fundamental properties of voltage-gated Ca2+ channels, even for channels which mig

77 lity that PP2calpha might be associated with voltage-gated Ca2+ channels for regulation of the Ca(2+)

78 oned a cDNA encoding the alpha1 subunit of a voltage-gated Ca2+ channel from the scyphozoan jellyfish

79 forming subunit (alpha1) of plasma membrane, voltage-gated Ca2+ channels from higher eukaryotes.

80 aptic transmission (syntaxin, Snap, Rop) and voltage-gated Ca2+ channel genes suppresses both the ele

81 euronal-specific effector molecules, such as voltage gated Ca2+ channels, has not been well studied.

82 Mammalian neuronal voltage-gated Ca2+ channels have been implicated as pote

83 Ca(v)1.3 (L-type) voltage-gated Ca2+ channels have emerged as key players

84 from intracellular stores and influx through voltage-gated Ca2+ channels in bovine chromaffin cells a

85 permeation properties of two distinct single voltage-gated Ca2+ channels in bullfrog saccular hair ce

86 We conclude that most, if not all, voltage-gated Ca2+ channels in hair cells contain an alp

87 e of Ca2+ transients following activation of voltage-gated Ca2+ channels in neurones cultured from ra

88 parent redistribution or upregulation of the voltage-gated Ca2+ channels in neurons.

89 esults provide new insights into the role of voltage-gated Ca2+ channels in nonexcitable cells during

90 a key role for golli proteins in regulating voltage-gated Ca2+ channels in OLs during process remode

91 In contrast to voltage-gated Ca2+ channels in other preparations, in th

92 hereas BK(Ca) appear functionally coupled to voltage-gated Ca2+ channels in SMCs of arterioles.

93 sights into the physiological role of L-type voltage-gated Ca2+ channels in the human brain.

94 gering action potentials, which in turn open voltage-gated Ca2+ channels in the somatic plasma membra

95 nt cations are equally effective at blocking voltage-gated Ca2+ channels in these baroreceptor neuron

96 Voltage-gated Ca2+ channels in vertebrates comprise at l

97 that Ca2+ influx through a cadmium-sensitive voltage-gated Ca2+ channel increases the cytoplasmic Ca2

98 Calcium ions entering cells through voltage-gated Ca2+ channels initiate rapid release of ne

99 Ca2+-induced inhibition of alpha1C voltage-gated Ca2+ channels is a physiologically importa

100 Calcium influx through voltage-gated Ca2+ channels is crucial in regulating syn

101 Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulat

102 How dihydropyridines modulate L-type voltage-gated Ca2+ channels is not known.

103 The pore-forming alpha1 subunit of L-type voltage-gated Ca2+ channels is pharmacologically modulat

104 Voltage gated Ca2+ channels, K(+)ATP channels and the al

105 e GK-P3 cells sufficiently to activate their voltage-gated Ca2+ channels leading to increases in intr

106 For example, L-type voltage-gated Ca2+ channels modulate SMC differentiation

107 The exclusively voltage-gated Ca2+ channel nature of the Ca2+ influx, th

108 does not require Ca2+ influx through L-type voltage-gated Ca2+ channels nor does it require protein

109 on has stimulatory and inhibitory effects on voltage-gated Ca2+ channels of basilar artery smooth mus

110 Voltage-gated Ca2+ channels of the N-, P/Q-, and R-type

111 + and is independent of synaptic activity or voltage-gated Ca2+ channel opening.

112 It is not mediated by inhibition of voltage-gated Ca2+ channels, opening of K+ channels, pro

113 Ca2+ entry through ligand-gated channels or voltage-gated Ca2+ channels, or through release from int

114 Voltage-gated Ca2+ channels participate in dendritic int

115 of Ca2+, through L-, N- and possibly R-type voltage-gated Ca2+ channels, participates in the pathoph

116 teraction between the endoplasmic reticulum, voltage-gated Ca2+ channels, PMCAs and mitochondrial Ca2

117 ith and distinctly modulates Cav1.2 (L-type) voltage-gated Ca2+ channels relative to other Ca2+-bindi

118 Recessive mutations in genes encoding voltage-gated Ca2+ channel subunits alter high-voltage-a

119 d that the inorganic and organic blockers of voltage-gated Ca2+ channels suppressed the hypercapnic r

120 We propose that CatSper1 functions as a voltage-gated Ca2+ channel that controls Ca2+ entry to m

121 We show this is caused by dendritic L-type voltage-gated Ca2+ channels that are prominently activat

122 The L-type voltage-gated Ca2+ channels that control tonic release o

123 The voltage-gated Ca2+ channels that effect tonic release of

124 CREB and NFAT through both voltage- and non-voltage-gated Ca2+ channels that lead to expression of s

125 s in sensory neurons, including increases in voltage-gated Ca2+ channels that likely underlie the mec

126 n which autoantibodies apparently target the voltage-gated Ca2+ channels that regulate acetylcholine

127 As a second test for the role of voltage-gated Ca2+ channels, these channels were blocked

128 To examine the potential contribution of voltage-gated Ca2+ channels to anoxic injury of spinal c

129 onse was consistent with Ca2+ influx through voltage-gated Ca2+ channels triggering release from ryan

130 xonal glutamate receptors, and activation of voltage-gated Ca2+ channels, ultimately leading to exces

131 Voltage-gated Ca2+ channels undergo a negative feedback

132 increase caused by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought

133 The L-type voltage-gated Ca2+ channel (VGCC) blockers verapamil and

134 des, significantly reduced endogenous oocyte voltage-gated Ca2+ channel (VGCC) currents and obliterat

135 ted in part by calcium influx through L-type voltage-gated Ca2+ channels (VGCC) and activation of the

136 Voltage-gated Ca2+ channels (VGCC) are well-characterize

137 Several classes of voltage-gated Ca2+ channels (VGCCs) are inhibited by G p

138 methyl-D-aspartate (NMDA) receptor-gated and voltage-gated Ca2+ channels (VGCCs) contributed to the i

139 hysiologically relevant ES does not activate voltage-gated Ca2+ channels (VGCCs) directly, but rather

140 investigated the coupling of mu receptors to voltage-gated Ca2+ channels (VGCCs) in beta arr2+/+ and

141 The role of voltage-gated Ca2+ channels (VGCCs) in spontaneous minia

142 Voltage-gated Ca2+ channels (VGCCs) of the P/Q-type, whi

143 d mediated by influx through both NMDARs and voltage-gated Ca2+ channels (VGCCs).

144 Modulation of voltage-gated Ca2+ channels via G-protein-coupled recept

145 pic glutamate receptor (mGluR) modulation of voltage-gated Ca2+ channels was examined in isolated dee

146 carotid chemosensory activity is mediated by voltage-gated Ca2+ channels was investigated by measurin

147 state-dependent pharmacological blockade of voltage-gated Ca2+ channels, we systematically character

148 tral cell secondary dendrites persisted when voltage-gated Ca2+ channels were blocked by cadmium (Cd2

149 ed by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked.

150 Perfusion solutions containing blockers of voltage-gated Ca2+ channels were introduced 60 min prior

151 t positive membrane potentials (e.g. +40 mV) voltage-gated Ca2+ channels were largely responsible.

152 ig and, within 10 h, inward currents through voltage-gated Ca2+ channels were recorded using the amph

153 lial cells express a Cav3.1 (alpha1G) T-type voltage-gated Ca2+ channel, whereas lung macrovascular e

154 es resting inactivation of T-type and N-type voltage-gated Ca2+ channels, which contribute to the Ca2

155 ited 65 +/- 3% by blockade of high-threshold voltage-gated Ca2+ channels with omega-grammotoxin SIA (

156 lease is initiated by influx of Ca2+ through voltage-gated Ca2+ channels, within 200 microseconds of