ライフサイエンスコーパス: VDCC

1 VDCC involvement in the regulation of molecular rhythmic

2 VDCCs thus scale presynaptic scaffolds to maintain local

3 arboxylase), and ion channels/pumps (Kir6.2, VDCC beta, and sarcoplasmic reticulum Ca(2+)-ATPase 3).

4 for a typical CA3-CA1 synapse, there are ~70 VDCCs located 300 nm from the active zone.

5 In addition, all VDCC beta subunits enhanced the rate of current facilita

6 Tyrosine phosphorylation of alpha1 VDCC subunits is increased in neurons exposed to 4HN, an

7 ) transients that were inhibited by ANO1 and VDCC antagonists revealing the underlying asynchronous C

8 al oesophagus was also inhibited by ANO1 and VDCC antagonists, suggesting a link between type II ICC-

9 mimic SAH, cerebral artery constriction and VDCC currents were enhanced and partially resistant to L

10 cit GABA release via both NMDA receptor- and VDCC-dependent pathways.

11 wed that currents through NMDA receptors and VDCC were enhanced in hippocampal neurons lacking gelsol

12 hat involve activation of NMDA receptors and VDCC.

13 10 to >100 nm have been reported for SVs and VDCCs in different synapses.

14 DCC), and a deficit in its role as auxiliary VDCC subunit was proposed to underlie the epileptic phen

15 olish cerebral artery constriction and block VDCC currents in cerebral artery myocytes from healthy a

16 ing Ras, Erk and Src activation, or blocking VDCC or VEGF-R2 activation, but not by inhibiting P38.

17 The magnitude of whole-cell VDCC currents in freshly isolated pericytes was approxim

18 pendent on voltage-dependent Ca(2+) channel (VDCC) activity.

19 inhibited voltage-dependent Ca(2+) channel (VDCC) currents and reduced steady-state contractions to

20 to ANO1 or voltage-dependent Ca(2+) channel (VDCC) inhibition but abolished by inhibiting endoplasmic

21 the T-type voltage-dependent Ca(2+) channel (VDCC) subunit Ca(V)3.2, a key proepileptogenic protein.

22 on through voltage-dependent Ca(2+) channel (VDCC)-mediated internalization of Mn(2+), the clinical u

23 y the L-type voltage-dependent Ca2+ channel (VDCC) inhibitor, diltiazem and with P2X receptor blockad

24 including voltage-dependent calcium channel (VDCC) activation and mitogen-activated protein kinases.

25 ce from a voltage-dependent calcium channel (VDCC) cluster, and Ca2+ was buffered by calbindin.

26 (R-type) voltage-dependent calcium channel (VDCC) currents observed in the presence of EGTA or BAPTA

27 erties of voltage-dependent calcium channel (VDCC) subtypes appear mainly to be determined by the alp

28 al muscle voltage-dependent calcium channel (VDCC), and a deficit in its role as auxiliary VDCC subun

29 K induces voltage-dependent calcium channel (VDCC)-intervened calcium influx in airway epithelial cel

30 e CD4 and voltage-dependent Ca(2+) channels (VDCC) was achieved with a precision of 30 nm within neur

31 ceptors and voltage-dependent Ca2+ channels (VDCC) is a major determinant of cell injury following br

32 a2+ through voltage-dependent Ca2+ channels (VDCC) of the L-type.

33 Voltage-dependent calcium channels (VDCC) are multisubunit complexes whose expression and ta

34 tors and voltage-dependent calcium channels (VDCC) mediates an array of physiological processes in ne

35 Voltage-dependent calcium channels (VDCC), which are critical to these processes, are hetero

36 h voltage-dependent, L-type Ca(2+) channels (VDCCs) and Ca(2+) release through ryanodine receptors (R

37 he L-type voltage-dependent Ca(2+) channels (VDCCs) and require activation of the protein tyrosine ki

38 of L-type voltage-dependent Ca(2+) channels (VDCCs) block the antidepressant behavioral actions of GL

39 nals from voltage-dependent Ca(2+) channels (VDCCs) in the surface membrane and from ryanodine-sensit

40 activates voltage-dependent Ca(2+) channels (VDCCs) inducing Ca(2+) release via ryanodine receptors (

41 eptors to voltage-dependent Ca(2+) channels (VDCCs) is a relatively inefficient process and therefore

42 ), L-type voltage-dependent Ca(2+) channels (VDCCs) or TMEM16A Ca(2+)-activated Cl(-) channels signif

43 it L-type voltage-dependent Ca(2+) channels (VDCCs), resulting in reversal in [Ca(2+)]i, and this inh

44 vation of voltage-dependent Ca(2+) channels (VDCCs), which leads to the exocytosis of insulin granule

45 ANO1) and voltage-dependent Ca(2+) channels (VDCCs).

46 vation of voltage-dependent Ca(++) channels (VDCCs), but not by affecting secretory processes downstr

47 e of R-type voltage-dependent Ca2+ channels (VDCCs) encoded by the gene CaV 2.3.

48 subunits of voltage-dependent Ca2+ channels (VDCCs) have been shown to regulate their biophysical pro

49 Voltage-dependent calcium channels (VDCCs) allow the passage of Ca(2+) ions through cellular

50 ween the voltage-dependent calcium channels (VDCCs) and the presynaptic active zone.

51 Voltage-dependent calcium channels (VDCCs) are heteromultimers composed of a pore-forming al

52 ckade of voltage-dependent calcium channels (VDCCs) by cadmium also eliminated the effect of WIN 55,2

53 vate the voltage-dependent calcium channels (VDCCs) expressed in the retinal microvasculature.

54 flux via voltage-dependent calcium channels (VDCCs) has been implicated in the regulation of gene exp

55 Two voltage-dependent calcium channels (VDCCs) have been reported in pancreatic islets: the beta

56 bunit of voltage-dependent calcium channels (VDCCs) have been shown to cause incomplete congenital st

57 ation of voltage-dependent calcium channels (VDCCs) in rat sensory neurones.

58 through voltage-dependent calcium channels (VDCCs) mediates a variety of functions in neurons and ot

59 ility of voltage-dependent calcium channels (VDCCs) modulates release probabilities (P(r)) of synapti

60 through voltage-dependent calcium channels (VDCCs) only, (iii) there was a fixed instantaneous relat

61 Voltage-dependent calcium channels (VDCCs) play a pivotal role in normal excitation-contract

62 d N-type voltage-dependent calcium channels (VDCCs) play essential roles as scaffolding proteins in t

63 Voltage-dependent calcium channels (VDCCs) show a highly non-uniform distribution in many ce

64 A and/or voltage-dependent calcium channels (VDCCs) were antagonized pharmacologically at levels that

65 ckade of voltage-dependent calcium channels (VDCCs) with Cd.

66 f R-type voltage-dependent calcium channels (VDCCs), but not by inhibition of N- or P/Q-type VDCCs, o

67 eurones, voltage-dependent calcium channels (VDCCs), including the N-type, are tonically up-regulated

68 ynaptic, voltage-dependent calcium channels (VDCCs), measured optically by using the fluorescent calc

69 P/Q-type voltage-dependent calcium channels (VDCCs), thereby converting this survival program to exci

70 through voltage-dependent calcium channels (VDCCs).

71 In the absence of coexpressed VDCC beta subunit, the G beta gamma dimers, either expre

72 Intracellular Ca(2+) chelation decreased VDCC mobility.

73 ession and circadian regulation of different VDCC alpha1 subunits.

74 polarizes the beta cell to the threshold for VDCC activation and thereby contributes to glucose-evoke

75 determine the effects of Ca(2+) signals from VDCCs and RyRs to SK and BK channels, whole cell membran

76 These data indicate that Ca(2+) signals from VDCCs, but not from RyRs, activate SK channels.

77 usive demonstration of stargazin function in VDCC regulation is still lacking.

78 ested a unique role for the beta4 isoform in VDCC maturation.

79 nting to the intrinsic role of the linker in VDCC function and suggesting that I-II linker structure

80 bladder strips, suggesting that reduction in VDCC current was sufficient to directly affect UBSM func

81 Increasing VDCC surface populations by co-expression of the alpha2d

82 Tracking individual VDCCs revealed that within hippocampal synapses, approxi

83 e inhibitors readily prevent agonist-induced VDCC internalization.

84 ition of CA1 pyramidal neurons by inhibiting VDCCs located on inhibitory nerve terminals.

85 f a cardiac macromolecular complex involving VDCC and beta-arrestin 1 (beta-Arr1) into clathrin-coate

86 also suggest that the role played by both L-VDCC and CaMKII is to promote the retrieval-dependent, s

87 L-type voltage-dependent calcium channel (L-VDCC) immunoreactivity and maintained an immature, L-VDC

88 L-type voltage-dependent calcium channel (L-VDCC) regulates calcium influx in cardiac myocytes.

89 Thus, conceivably, L-VDCC and CaMKII would enhance activity-dependent localiz

90 munoreactivity and maintained an immature, L-VDCC-dependent recycling phenotype.

91 solidation depends on the functionality of L-VDCC in dorsal CA1, that maintenance of subsequent recon

92 Targeted expression of the L-VDCC alpha(1) subunit in transgenic (Tg) mouse ventricle

93 aAR) pathway causes phosphorylation of the L-VDCC and that in turn increases Ca(2+) influx.

94 acting voltage-dependent calcium channels (L-VDCCs), but not of glutamatergic NMDA receptors, in the

95 r of L-voltage-dependent calcium channels (L-VDCCs), nifedipine.

96 naptic territory through the regulation of L-VDCCs.

97 ses than hitherto thought: NMDA receptors, L-VDCCs, CaMKII, and synaptic protein turnover.

98 ropose that dynamic coupling based on mobile VDCCs supports calcium domain cooperativity and tunes ne

99 ynaptotagmins and Rabs, or blockade of nAChR/VDCC-mediated Ca(2+) influx significantly suppresses NNK

100 -dependent inhibitory modulation of neuronal VDCCs occurs primarily by activation of G-proteins and e

101 vitro and in vivo using glucose, nifedipine (VDCC blocker), the sulfonylureas tolbutamide and glibenc

102 is involved in modulating the confinement of VDCC within sarcolemmal membrane nanodomains in response

103 rosine phosphorylation in the enhancement of VDCC activity in response to 4HN.

104 transition zone pericytes and independent of VDCC activity in distal pericytes.

105 Relative levels of VDCC expression in the rat SCN and SCN2.2 cells were gre

106 llectively, these results indicate a loss of VDCC involvement in pressure-induced constriction along

107 possibility that the circadian regulation of VDCC activity may play an important role in maintaining

108 bited mRNA expression for all major types of VDCC alpha1 subunits.

109 n hippocampal synapses, approximately 60% of VDCCs are mobile while confined to presynaptic membrane

110 F through exocytosis caused by activation of VDCCs and subsequent TrkB-Rac1 signaling is required for

111 increases [Ca(2+)](i) through activation of VDCCs, leading to increased P-CREB and c-fos, and that R

112 id peroxidation can modulate the activity of VDCCs.

113 lta receptors reduced neither the density of VDCCs nor their inhibition by either the GABA(B) recepto

114 e increased Ca(2+) sparks are independent of VDCCs and the associated extracellular Ca(2+) influx.

115 ta receptors exhibited reduced inhibition of VDCCs by morphine and [D-Ala(2),Phe(4),Gly(5)-ol]-enkeph

116 BK current was reduced 95 % by inhibition of VDCCs, suggesting that this process depends largely on C

117 Nisoldipine, an inhibitor of VDCCs, reversed the effects of depolarization and ryanod

118 tussis toxin prevents the internalization of VDCCs, suggesting that G(i/o) mediates this response.

119 and suggests that differential modulation of VDCCs by EGTA and BAPTA offers an alternative or complem

120 MEK inhibition suggests direct modulation of VDCCs via the Ras-MAPK pathway rather than gene expressi

121 lar mechanisms that govern the regulation of VDCCs and their cell surface localization remain unknown

122 istent with this idea, all known subtypes of VDCCs except R-type were calcium sources for the apamin-

123 o dentify which of the four beta subunits of VDCCs participates in the formation of this channel at t

124 hout each of the four known beta subunits of VDCCs were generated by gene targeting and transgenic re

125 e neurons are weakly coupled to a variety of VDCCs.

126 actile responses were partially dependent on VDCC activity in transition zone pericytes and independe

127 nergic Ca2+ transients were not dependent on VDCC activity.

128 ion stimulator) had no significant effect on VDCC current.

129 is likely to be from non-specific effects on VDCCs and K(V) 2 channels.

130 +) transients that were inhibited by ANO1 or VDCC antagonists revealing the underlying asynchronous C

131 hes the effects of modulators for TMEM16A or VDCCs on a RyR-mediated rise in global [Ca(2+)]i and imp

132 Pancreatic VDCC uptake of (52)Mn(2+) was successfully manipulated p

133 active zones caused by a loss of presynaptic VDCCs resembled the pathological conditions observed in

134 These results suggest that presynaptic VDCCs link the target-derived synapse organizer laminin

135 this, we used IgG antibodies to presynaptic VDCCs at motor nerve terminals that underlie muscle weak

136 type, P/Q-type, and unidentified presynaptic VDCCs.

137 in required its interaction with presynaptic VDCCs.

138 different combinations of human recombinant VDCC subunits.

139 elies on calcium influx through Cd-sensitive VDCCs.

140 These observations suggest that VDCC trafficking is mediated by G protein switching to G

141 ng antagonism of G protein inhibition by the VDCC beta subunit, we found a significantly larger G bet

142 In conclusion, the VDCC alpha1 subunit appears to be the primary determinan

143 beta subunits function to direct the VDCC complex to the plasma membrane as well as regulate

144 We expressed the VDCC alpha1A, alpha1B or alpha1C subunits either alone o

145 h this phenotype, direct interactions of the VDCC beta1b or beta4 subunits and the active zone-specif

146 We found Egr1 to drive the expression of the VDCC subunit alpha2delta4, which was augmented early and

147 nclusion, Egr1 controls the abundance of the VDCC subunits Ca(V)3.2 and alpha2delta4, which act syner

148 be the primary determinant for targeting the VDCC complex, but the beta subunit can modify this desti

149 These results suggest that the VDCC beta subunit must be present for G beta gamma to in

150 ion of alpha 1 B channel activation when the VDCC alpha 1 B and beta subunits were coexpressed.

151 distribution of the alpha(1F) subunit of the VDCCs in the OPL is dependent on the expression of the b

152 nt with influx of extracellular Ca2+ through VDCCs according to the membrane potential model.

153 onclusion, when Ca2+ enters the cell through VDCCs, the time course of the consequent Ca2+ signal in

154 e results indicate that Ca(2+) entry through VDCCs activates both BK and SK channels, but Ca(2+) rele

155 cess depends largely on Ca(2+) entry through VDCCs and not Ca(2+) release through RyRs.

156 y indirectly regulating Ca(2+) entry through VDCCs.

157 + flashes that represent Ca2+ influx through VDCCs during action potentials, and local, purinergic Ca

158 ese events are caused by Ca2+ influx through VDCCs during action potentials.

159 a global rise in [Ca(2+)]i via a RyR-TMEM16A-VDCC signalling module sets the basal tone.

160 We examined micro-receptor coupling to VDCCs in dorsal root ganglion neurons of delta(+/+), del

161 electrophysiology, we have found that L-type VDCC antagonists abolish cerebral artery constriction an

162 Nimodipine, an L-type VDCC blocker, inhibited M3G-induced Ca(2+) influx, while

163 On the other hand, L-type VDCC blockers are not protective.

164 e enhanced and partially resistant to L-type VDCC blockers.

165 Silencing nAChR, alpha1 subunit of L-type VDCC, or various vesicular trafficking curators, includi

166 rate that clustering of NCAM2 induces L-type VDCC- and c-Src-dependent activation of CaMKII.

167 neurite branching and outgrowth in an L-type VDCC-, c-Src-, and CaMKII-dependent manner.

168 As the beta component of N-type VDCC changed during postnatal development, we were able

169 beta3, and beta4) in the assembly of N-type VDCC during rat brain development.

170 sociated with decreased expression of N-type VDCC in forebrain and cerebellum.

171 immature rat brain, the population of N-type VDCC present in adult lh/lh mice is characterized by the

172 iking similarity to the population of N-type VDCC present in immature rat brain, the population of N-

173 orms with the alpha1B subunit to form N-type VDCC suggested a unique role for the beta4 isoform in VD

174 pression of an immature population of N-type VDCC throughout neuronal development.

175 ssembled with the rat alpha1B to form N-type VDCC with a time course that paralleled its level of exp

176 d beta1b expression and assembly into N-type VDCC.

177 ify both immature and mature forms of N-type VDCC.

178 in the assembly and maturation of the N-type VDCC.

179 -4-phosphonobutyric acid enhances), P/Q-type VDCC currents (omega-agatoxin-IVA and omega-conotoxin-MV

180 hy animals were found to express only L-type VDCCs (CaV 1.2), whereas after SAH, cerebral arteries we

181 +)]i at rest while blocking activated L-type VDCCs to induce bronchodilation of contracted ASM.

182 e voltage-dependent calcium channels (L-type VDCCs) and Ca(2+) release from the endoplasmic reticulum

183 on by promoting Ca(2+) influx through L-type VDCCs, facilitating Ca(2+) release from the ER, and upre

184 200 microM CdCl2, a potent blocker of L-type VDCCs.

185 of double knock-out mice for P/Q- and N-type VDCCs displayed a normal size but had significantly redu

186 , an extracellular ligand of P/Q- and N-type VDCCs.

187 re-forming subunit but, whether P-and Q-type VDCCs are encoded by the same alpha1 gene presently is u

188 Cs), but not by inhibition of N- or P/Q-type VDCCs, or block of calcium release from intracellular st

189 re-forming subunit of both P-type and Q-type VDCCs.

190 We propose that R-type VDCCs may contribute to enhanced cerebral artery constri

191 nt manner, and are tightly coupled to R-type VDCCs.

192 uce pericytes to contract, calcium entry via VDCCs serves to enhance the contractile response of thes

193 1, causing depolarization, Ca(2+) influx via VDCCs and contraction.

194 olarization and subsequent Ca(2+) influx via VDCCs.

195 To determine whether VDCC beta subunit is involved in this process, the role

196 activation and prepulse facilitation, while VDCC beta subunit coexpression restored all of the hallm