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

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

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

10 hat involve activation of NMDA receptors and VDCC.

11 10 to >100 nm have been reported for SVs and VDCCs in different synapses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 through voltage-dependent calcium channels (VDCCs).

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

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

64 ession and circadian regulation of different VDCC alpha1 subunits.

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

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

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

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

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

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

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

72 Tracking individual VDCCs revealed that within hippocampal synapses, approxi

73 e inhibitors readily prevent agonist-induced VDCC internalization.

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

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

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

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

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

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

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

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

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

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

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

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

86 naptic territory through the regulation of L-VDCCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

100 id peroxidation can modulate the activity of VDCCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 in required its interaction with presynaptic VDCCs.

123 different combinations of human recombinant VDCC subunits.

124 elies on calcium influx through Cd-sensitive VDCCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 -4-phosphonobutyric acid enhances), P/Q-type VDCC currents (omega-agatoxin-IVA and omega-conotoxin-MV

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

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

164 200 microM CdCl2, a potent blocker of L-type VDCCs.

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

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

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

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

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

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

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

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

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

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