ライフサイエンスコーパス: Ca2 channel

1 inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ channel.

2 alpha1C subunit of the human cardiac L-type Ca2+ channel.

3 pore subunits of the Ca2+ release-activated Ca2+ channel.

4 e receptor (RyR1), is known to activate RyR1 Ca2+ channel.

5 relate with the functional open state of the Ca2+ channel.

6 to its physiological function as a putative Ca2+ channel.

7 e that lacks the beta3 subunit of the L-type Ca2+ channel.

8 ls and both NMDA receptors and voltage-gated Ca2+ channels.

9 rmined by the activation of voltage-operated Ca2+ channels.

10 nnels at Thr498 to facilitate cardiac L-type Ca2+ channels.

11 y sensitive to the activity of voltage-gated Ca2+ channels.

12 an inhibitory action of CO on cardiac L-type Ca2+ channels.

13 portant regulatory subunits of voltage-gated Ca2+ channels.

14 NAADP-induced activation of these lysosomal Ca2+ channels.

15 es or to the analysis of other intracellular Ca2+ channels.

16 depolarization activating voltage-dependent Ca2+ channels.

17 rization and activation of voltage-dependent Ca2+ channels.

18 Ca2+ signaling and a contribution of L-type Ca2+ channels.

19 at hard-to-release vesicles are too far from Ca2+ channels.

20 esynaptic glutamate release involving N-type Ca2+ channels.

21 1-mediated tonic inhibition of voltage-gated Ca2+ channels.

22 suggesting the presence of stretch-activated Ca2+ channels.

23 ck-regulate Ca2+ entry through voltage-gated Ca2+ channels.

24 s to regulate the activity of store-operated Ca2+ channels.

25 ence of NCX activity inactivates some L-type Ca2+ channels.

26 exclusively dependent on presynaptic N-type Ca2+ channels.

27 eta1 subunit required Ca2+ influx via L-type Ca2+ channels.

28 bited by agatoxin IVA, which blocks P/Q-type Ca2+ channels.

29 eous activation of NMDA receptors and L-type Ca2+ channels.

30 ux via channels other than voltage-dependent Ca2+ channels.

31 eta-AR subtype-specific regulation of L-type Ca2+ channels.

32 lease via inhibition of N-type voltage-gated Ca2+ channels.

33 st Ca2+ regulation eerily similar to that of Ca2+ channels.

34 re involves downregulation of store-operated Ca2+ channels.

35 ancient Ca2+ regulatory module across Na and Ca2+ channels.

36 SVs to dock in defined nanoscale relation to Ca2+ channels.

37 G(q/11)-mediated inhibition of N- or L-type Ca2+ channels.

38 ease triggered by Ca2+ influx through L-type Ca2+ channels.

39 LTP-GABAA by inhibiting L-type voltage-gated Ca2+ channels.

40 in Ca2+ influx through R-type voltage-gated Ca2+ channels.

41 depolarization and opening of voltage-gated Ca2+ channels.

42 d the resultant closure of voltage-dependent Ca2+ channels.

43 influx through dendritic, voltage-dependent Ca2+ channels.

44 olecule 1 (STIM1) and Ca2+-release-activated Ca2+ channel 1 (Orai1) within ER-plasma membrane (PM) ju

45 Cd2+, a specific blocker of voltage-operated Ca2+ channels, abolished the ability of golli to promote

46 ular Ca2+ into cells through plasma membrane Ca2+ channels activated by depletion of intracellular Ca

47 store-operated CRAC (Ca2+ release-activated Ca2+) channels activates the extracellular signal-regula

48 nt amplitude, modified voltage dependence of Ca2+ channel activation and attenuated noradrenaline-ind

49 re is the size of the overlap region between Ca2+ channel activation and inactivation, called the win

50 eterogeneity and differential sensitivity of Ca2+ channel activation by reactive oxygen species in th

51 ells or ARPKD cells with either Bay K8644, a Ca2+ channel activator, or A23187, a Ca2+ ionophore, cau

52 93]) 'AID peptide' on synaptic transmission, Ca2+ channel activity and G protein modulation in superi

53 his pathway supported the increase in L-type Ca2+ channel activity and myogenic tone in two animal mo

54 increased sAHP results from elevated L-type Ca2+ channel activity and ryanodine receptor (RyR)-media

55 or AC5 in PKA-dependent modulation of L-type Ca2+ channel activity and vascular reactivity during acu

56 These results show that skeletal muscle Ca2+ channel activity and voltage-dependent potentiation

57 had suggested that RGK proteins may regulate Ca2+ channel activity by blocking the association of CaV

58 Inactivation of Ca2+ channel activity is perturbed in a rare yet devasta

59 Whereas voltage-gated Ca2+ channel activity regulates several aspects of neuro

60 opposing hyperpolarizing influence reducing Ca2+ channel activity.

61 were acutely sensitive to changes in L-type Ca2+ channel activity; nimodipine completely inhibited g

62 he mouth of the Abeta channel to block Abeta Ca2+ channels acutely and to block late Abeta effects on

63 d showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, w

64 The distribution of T-type Ca2+ channels along the entire somatodendritic axis of s

65 acophony (cac) locus in Drosophila encodes a Ca2+ channel alpha subunit, but little is known about pr

66 otin switch method, we identified the L-type Ca2+ channel alpha1 subunit as the predominant S-nitrosy

67 nts and S-nitrosylation levels of the L-type Ca2+ channel alpha1 subunit in heart membrane fractions.

68 e expression and gating of voltage-dependent Ca2+ channel alpha1 subunits.

69 It binds with high affinity to Ca2+ channel alpha2delta subunits that are expressed in

70 he molecular interactions between the L-type Ca2+ channel and protein kinase Calpha at only a few sub

71 The role of L-type Ca2+ channel and ryanodine receptor phosphorylation was

72 r-mediated Ca2+ influx involving both L-type Ca2+ channels and a receptor operated pathway, which dif

73 These mutants have far fewer membrane-bound Ca2+ channels and attenuated L-type activity.

74 munication of plasmalemmal voltage-activated Ca2+ channels and Ca2+ release channels on sarcoplasmic

75 to modeling localized Ca2+ influx via L-type Ca2+ channels and Ca2+-induced Ca2+ release mediated by

76 s(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection

77 probability of sarcolemmal voltage-sensitive Ca2+ channels and flux of Ca2+ into the cells.

78 riggered by the opening of voltage-dependent Ca2+ channels and followed by Ca2+ -induced Ca2+ release

79 s responsible for rapid dephosphorylation of Ca2+ channels and may contribute to regulation of synapt

80 These events are mediated by L-type Ca2+ channels and occur during early postnatal life, a t

81 Although Na+-Ca2+ exchanger, store-operated Ca2+ channels and plasma membrane Ca2+ pump were present

82 pecifying the spatial localization of L-type Ca2+ channels and ryanodine receptors.

83 s to NOX/ROS-dependent recruitment of T-type Ca2+ channels and RyRs, resulting in augmented [Ca2+]i m

84 es that enables key GPCRs to regulate L-type Ca2+ channels and the integration of glutamatergic synap

85 f voltage-gated Na+ channels but also affect Ca2+ channels and their function.

86 targets protein kinase Calpha to the L-type Ca2+ channels and thereby enables its regulatory functio

87 ed Ca2+ currents through the interplay among Ca2+ channels and various Ca(2+)-binding proteins is inc

88 upled muscarinic regulation of N- and L-type Ca2+) channels and by cAMP/protein kinase A was also stu

89 R Ca2+ cycling, ie, phospholamban and L-type Ca2+ channels (and likely others not measured in this st

90 ystin-1 (a mechanoreceptor), polycystin-2 (a Ca2+ channel), and the Ca2+-inhibitable adenylyl cyclase

91 urrent (I(L/T)) mediated by T- and/or L-type Ca2+ channels, and large-conductance Ca2+-dependent K+ c

92 tive oxygen species (ROS), the activation of Ca2+ channels, and the transcription of the MAP kinase3

93 We conclude that L-type Ca2+ channel antagonism thus exerts specific anti-arrhyt

94 Effects of specific L-type Ca2+ channel antagonism were explored in a gain-of-funct

95 in acute rat brain slices show that the P/Q Ca2+ channel antagonist agatoxin TK (250 nm) abolished G

96 cortices, which was blocked by diltiazem, a Ca2+ channel antagonist.

97 Neither phase was affected by the L-type Ca2+ channel antagonists diltiazem (10 and 30 mum) or ni

98 n IVA at concentrations selective for P-type Ca2+ channels (approximately 85%; IC50, <1 nM) and by th

99 Recent data indicate that T-type Ca2+ channels are amplifiers of peripheral pain signals,

100 omes have shown that endosomal and lysosomal Ca2+ channels are directly modulated by endosomal lipids

101 Voltage-gated L-type Ca2+ channels are key determinants of synaptic integrati

102 L-type Ca2+ channels are macromolecular protein complexes in ne

103 T-type Ca2+ channels are reexpressed in adult ventricular myocy

104 udies establish that T-type voltage-operated Ca2+ channels are required for cell cycle progression an

105 Low voltage-activated (T-type) Ca2+ channels are responsible for generating low-thresho

106 niques such as PALM and STORM for studies of Ca2+ channels as it obviates the need for photoswitchabl

107 Junctophilins couple Ca2+ channels at the plasma membrane to those of the end

108 orylates the beta2a subunit of voltage-gated Ca2+ channels at Thr498 to facilitate cardiac L-type Ca2

109 Mibefradil, a blocker of T-type Ca2+ channels attenuated the effects of hypoxia on [Ca2+

110 To vary NP(o) alone, we altered Ca2+ channel availability by varying holding V(m) (at co

111 lly explained by dephosphorylation of L-type Ca2+ channels, because a similar degree of ICa"rundown"

112 e selectivity of the actions of CaMKII among Ca2+ channel beta subunit isoforms.

113 CT, depend on the identity of the auxiliary Ca2+ channel beta subunit.

114 A domain differs among the four subtypes of Ca2+ channel beta subunits (beta1-beta4) primarily as th

115 ng of the structure of alternatively spliced Ca2+ channel beta subunits and the cell-specific roles t

116 Ca2+ channel beta subunits regulate cell-surface express

117 the interactions of specific isoforms of the Ca2+ channel beta subunits with CaMKII.

118 Ca2+ channel beta-subunit interactions with pore-forming

119 tin inhibition occurs in the presence of the Ca2+ channel beta4a subunit but not in the presence of b

120 Anodal Ca2+ waves and resistance to Na+ and Ca2+ channel blockade suggest nonselective ion channel t

121 ghput functional screen, the atypical L-type Ca2+ channel blocker diltiazem was discovered to be an a

122 sence of GABAergic antagonists or the L-type Ca2+ channel blocker methoxyverapamil hydrochloride but

123 In muscle stimulated in the presence of a Ca2+ channel blocker or calcium-permeable Ca2+ chelator,

124 The L-type Ca2+ channel blocker verapamil reduced SS Ca2+ spark fre

125 onses, as they do in animal cells, because a Ca2+ channel blocker, a Ca2+ chelator, and calmodulin an

126 llular Ca2+ and inhibited by nitrendipine, a Ca2+ channel blocker, or 2',5'-dideoxyadenosine, a P-sit

127 eliminated by a mixture of voltage-sensitive Ca2+ channel blockers and is mimicked by a brief climbin

128 ficantly inhibited by plasma membrane L-type Ca2+ channel blockers such as verapamil, diltiazem, and

129 Gabapentin does not seem to have direct Ca2+ channel blocking properties but does affect overall

130 increase in mIPSCs depended on voltage-gated Ca2+ channels but persisted when ionotropic glutamate re

131 nigra (SN) dopamine neurons relies on L-type Ca2+ channels, but a surprising study in Nature by Chan

132 ta-adrenergic upregulation of cardiac L-type Ca2+ channels, but that phosphorylation of serine 1928 i

133 -)-(S)-Bay K8644 is known to activate L-type Ca2+ channels, but the decrease in current was not secon

134 for the in vivo modulation of native T-type Ca2+ channels by CaMKII and suggest that the disruption

135 ce of Ca2+-free solution and block of L-type Ca2+ channels by nifedipine also resulted in a cessation

136 alpha was pulled out by both N- and P/Q-type Ca2+ channel C termini.

137 R) in the pore-forming subunit of the L-type Ca2+ channel Ca(V)1.2.

138 nnels comprise a vital subdivision of L-type Ca2+ channels: Ca(V)1.3 channels mediate neurotransmitte

139 total dihydropyridine-sensitive (i.e. L-type Ca2+ channel) Ca2+ influx at a physiologically relevant

140 L-type, voltage-gated Ca2+ channels (CaL) play critical roles in brain and mus

141 However, these beta-less Ca2+ channels cannot be stimulated by beta-adrenergic pa

142 tantial fraction of the mworks as conductive Ca2+ channels capable of physiologically controlling the

143 For different Ca2+ channels, carboxyl-tail interactions with calmoduli

144 is autaptic action affect cone voltage-gated Ca2+ channel (CaV channel) gating through changes in pH.

145 organizes the close apposition of the L-type Ca2+ channel CaV1.2 and the ryanodine receptor 2 in the

146 nexpected roles for the L-type voltage-gated Ca2+ channel CaV1.2 in nonexcitable cells.

147 art PKA increases the activity of the L-type Ca2+ channel Cav1.2 in response to beta-adrenergic stimu

148 biophysically distinctive subtype of L-type Ca2+ channels (CaV1.3) in striatal medium spiny neurons.

149 l EGL-19 with a contribution from the T-type Ca2+ channel CCA-1.

150 Thus, the PP2calpha-Ca2+ channel complex is responsible for rapid dephosphor

151 nt gating properties of recombinant Ca(v)2.1 Ca2+ channel complexes transiently expressed in Xenopus

152 Voltage-gated Na and Ca2+ channels comprise distinct ion channel superfamilie

153 The T-type Ca2+ channels contain a regulatory alpha1 subunit, and s

154 whether IL-6 reduced Ca2+ influx via L-type Ca2+ -channel current (ICa,L).

155 We found that at P40-50, the somatic Ca2+ channel current was inhibited by omega-agatoxin IVA

156 results from loss of a direct effect on the Ca2+ channel current, as shown in a transfected cell lin

157 and an increase in the size of the atypical Ca2+ channel current.

158 ge during postnatal development, we recorded Ca2+ channel currents from Purkinje cells in cerebellar

159 ndothelial voltage-dependent alpha1G subtype Ca2+ channels, cytosolic phospholipase A2, and epoxyeico

160 Nonetheless, the dynamics of T-type Ca2+ channel-dependent dendritic Ca2+ signalling during

161 Moreover, NMDAR and L-type Ca2+ channel-dependent SC long-term potentiation (LTP) i

162 inhibitors of voltage-gated and nonspecific Ca2+ channels diminished this activity.

163 orms a signaling complex with alpha1H T-type Ca2+ channels, directly interacting with the intracellul

164 sensor dSTIM, and the Ca2+-release-activated Ca2+ channel dOrai in the same pathway that promotes cal

165 ices, it was found that antagonism of L-type Ca2+ channel effectively stopped dendritic Ca2+ oscillat

166 APs depend on Ca2+ entry through the L-type Ca2+ channel EGL-19 with a contribution from the T-type

167 However, Ca2+ channel expression is unchanged, suggesting that re

168 the sodium/calcium exchanger and the L-type Ca2+ channel expression levels were upregulated.

169 After membrane depolarization, Ca2+ channels first open but then undergo various forms

170 iated by the activation of voltage-dependent Ca2+ channels followed by Ca2+-evoked Ca2+ release from

171 ow that PP2calpha binds directly to neuronal Ca2+ channels forming a functional protein complex in vi

172 yed directionally opposite effects on L-type Ca2+ channel function and Ca2+ spark behavior.

173 We conclude that local control of L-type Ca2+ channel function is regulated by AKAP150-targeted p

174 ions to residues reported as determinants of Ca2+ channel function within the NT peptide negated inhi

175 I loop contribute molecular determinants for Ca2+ channel function; the data favour a direct interact

176 Stargazin [Cacng2 (Ca2+ channel gamma2 subunit)] is one of four closely rel

177 t it does not participate directly in Cav2.1 Ca2+ channel gating but serves as a binding site in prot

178 was further substantiated by measurements of Ca2+ channel gating currents and by analysis of another

179 s that, in the absence of Ca(v)beta, renders Ca2+ channel gating facilitated by CaM molecules other t

180 sion (syntaxin, Snap, Rop) and voltage-gated Ca2+ channel genes suppresses both the electrophysiologi

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

182 Somatodendritic L-type Ca2+ channels have long been viewed as important, if not

183 -dihydropyridine agonist specific for L-type Ca2+ channels, having no effect on gating charge movemen

184 nduce Ca2+ influx via high-voltage-activated Ca2+ channels (I(HVA)).

185 curtailed beta-adrenergic stimulation of WT Ca2+ channels, identifying an approach to specifically m

186 y to examine the role of the Cav1.3(alpha1D) Ca2+ channel in the atria of Cav1.3(-/-) mice.

187 n latent in adulthood, and blocking Ca(v)1.3 Ca2+ channels in adult neurons induces a reversion to th

188 iation is critical for stimulation of L-type Ca2+ channels in arterial myocytes and increased myogeni

189 Long openings and reopenings of L-type Ca2+ channels in arterial myocytes produce stuttering pe

190 inase A (PKA)-mediated stimulation of L-type Ca2+ channels in arterial myocytes resulting in increase

191 A novel finding is the role of L-type Ca2+ channels in autonomous ET cells bursting.

192 e results suggest that the downregulation of Ca2+ channels in axotomized RS neurons, and the associat

193 ular stores and influx through voltage-gated Ca2+ channels in bovine chromaffin cells and the domain

194 To determine if the properties of Ca2+ channels in cerebellar Purkinje cells change during

195 quires Munc13-mediated recruitment of L-type Ca2+ channels in close proximity to insulin granules.

196 rate increased S-nitrosylation of the L-type Ca2+ channels in female cardiomyocytes.

197 new insights into the role of voltage-gated Ca2+ channels in nonexcitable cells during development.

198 The lack of Cav1.3 Ca2+ channels in null mutant mice would result in a depo

199 r golli proteins in regulating voltage-gated Ca2+ channels in OLs during process remodeling.

200 eviously unrecognized contribution of T-type Ca2+ channels in peripheral sensory neurons to pain sens

201 appear functionally coupled to voltage-gated Ca2+ channels in SMCs of arterioles.

202 e physiological role of L-type voltage-gated Ca2+ channels in the human brain.

203 a2+ results in the opening of store-operated Ca2+ channels in the plasma membrane.

204 nt mechanism by which AngII modulates T-type Ca2+ channels in these cells.

205 inhibits trafficking of recombinant Ca(v)2.1 Ca2+ channels in X. laevis oocytes; 2) gabapentin inhibi

206 sicles with low release probability, such as Ca2+-channel inactivation, and established unexpected bo

207 o 10 micromol/L but not by voltage-dependent Ca2+ channel inhibitors, suggesting that these responses

208 sue, ER/mitochondria tethering was impaired, Ca2+ channels IP3Rs and CACNA1A were downregulated, and

209 to date is the assumption that IP3 receptor Ca2+ channels (IP3Rs) are globally coupled by a "continu

210 Modulation of presynaptic voltage-dependent Ca2+ channels is a major means of controlling neurotrans

211 d retinal activity, the expression of L-type Ca2+ channels is a requisite component in the manifestat

212 The subcellular localization of membrane Ca2+ channels is crucial for their functioning, but is d

213 ethods are shown to agree when the number of Ca2+ channels is large (i.e., physiologically realistic)

214 hydropyridines modulate L-type voltage-gated Ca2+ channels is not known.

215 racellular calcium by Ca2+ release-activated Ca2+ channels is required for lymphocyte activation.

216 ease, rather than Ca2+ influx through L-type Ca2+ channels, is the target of regulation of a novel si

217 Voltage gated Ca2+ channels, K(+)ATP channels and the alpha-gustducin

218 the CaM-binding domains of voltage-dependent Ca2+ channels, kinases, and phosphatases, which increase

219 nterplay between Ca2+ entries through L-type Ca2+ channels (LCCs) and reverse-mode Na+-Ca2+ exchange

220 tochastic molecular signaling between L-type Ca2+ channels (LCCs) and ryanodine receptors (RyR2s) tha

221 Loss-of function mutations in Orai1 Ca2+ channels lead to a form of severe combined immunode

222 actions among IP3 receptors (IP3R) and other Ca2+ channels leading to coordinated Ca2+ release from t

223 g to their association with surface membrane Ca2+ channels, leading to higher spontaneous Ca2+ spark

224 andidate modules featuring voltage-dependent Ca2+-channels link these outputs to the downstream dynam

225 inositol 1,4,5-trisphosphate receptor (IP3R) Ca2+ channel localized with Bcl-2 on the ER.

226 ctivity causes internalization of the L-type Ca2+ channel (LTC) CaV1.2 and that this is mediated by b

227 sgenic mice with enhanced sarcolemmal L-type Ca2+ channel (LTCC) activity showed progressive myocyte

228 The priming by prior Ca2+ influx in P/Q-type Ca2+ channels may determine the path of mGluR1 signallin

229 nel modulation rather than the activation of Ca2+ channel mediated PICs, despite phrenic motoneurones

230 f the mature form (BFA insensitive, P/Q type Ca2+ channel mediated) of vesicle cycling at the termina

231 immature form (Brefeldin A sensitive, L-type Ca2+ channel mediated) of vesicle cycling.

232 erstanding how therapeutics targeting L-type Ca2+ channels might protect dopaminergic neurons in Park

233 For example, L-type voltage-gated Ca2+ channels modulate SMC differentiation marker gene e

234 gether these data suggest that Rem-dependent Ca2+ channel modulation involves formation of a Rem x Ca

235 IH upregulated Cav3.1 and Cav3.2 T-type Ca2+ channel mRNAs via NOX/ROS signaling and augmented T

236 y the Na+ channel blocker tetrodotoxin and a Ca2+ channel mutation but could be mimicked by raising c

237 in the type 1 ryanodine receptor, RyR1, the Ca2+ channel of the sarcoplasmic reticulum (SR) of skele

238 incubation of neurons in a blocker of N-type Ca2+ channels (omega-conotoxin GVIA; 30 nM).

239 inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ channels on the ER, regulating their opening in res

240 depends on lower NP(o) and reduced redundant Ca2+ channel openings (per junction) and a consequently

241 ed by Ca2+ influx through clusters of L-type Ca2+ channels operating in this persistently active mode

242 SOCE by forming punctate structures with the Ca2+ channel Orai1 and the inositol trisphosphate recept

243 inherited mutations in the gene encoding the Ca2+ channel ORAI1 or its activator stromal interaction

244 influx via activation of the plasma membrane Ca2+ channel Orai1.

245 ng evidence that the store-operated calcium (Ca2+) channel Orai1 sustains Th17-driven inflammatory re

246 TIM1, and the plasma membrane (PM)-localized Ca2+ channel, Orai1/CRACM1.

247 ns that abolish the short-term inhibition of Ca2+ channels, PDC and PDCL require prolonged agonist ex

248 lizes the transient receptor potential (TRP) Ca2+ channel, phospholipase Cbeta, and eye protein kinas

249 Furthermore, T-type Ca2+ channels play an integral role in low frequency osc

250 insic membrane properties, especially T-type Ca2+ channels, play a key role in the genesis of burst d

251 between subpopulations of AC5 and the L-type Ca2+ channel pore-forming subunit CaV1.2.

252 ntagonist and calcicludine binding to L-type Ca2+ channels promote similar structural changes in the

253 hrough store-operated Ca2+ release-activated Ca2+ channels, promoting nuclear translocation of the tr

254 sensor, Stim1, and calcium release-activated Ca2+ channel protein, Orai1, and provide further support

255 receptors, which can be triggered by L-type Ca2+ channels, provides a common source of dysregulated

256 d transplanting the NaV1.4 carboxy tail onto Ca2+ channels recapitulates Ca2+ regulation.

257 TRP channel 1 (TRPML1) as the key lysosomal Ca2+ channel regulating focal exocytosis and phagosome b

258 ctly modulates Cav1.2 (L-type) voltage-gated Ca2+ channels relative to other Ca2+-binding proteins.

259 nal SH3 domain tandem binds RIM, Munc13, and Ca2+ channels release machinery collectively.

260 gion of RyR1, which activate and inhibit the Ca2+ channel, respectively.

261 ACNA1A gene, which encodes a neuronal Cav2.1 Ca2+ channel, resulting in increased Ca2+ flow into dend

262 onents of BiMPTs activates voltage-dependent Ca2+ channels, resulting in an increase in global [Ca2+]

263 ponse dependent on dihydropyridine-sensitive Ca2+ channels, resulting in greater susceptibility of SN

264 k due to PKA-dependent phosphorylation of SR Ca2+ channels (RyR2s), fewer RyR2s, and smaller RyR2 clu

265 dependent regulation of voltage-gated CaV1-2 Ca2+ channels shows extraordinary modes of spatial Ca2+

266 ssociated with increased mRNA levels for the Ca2+ channel subunit alpha2delta1 and TRPV1 receptor.

267 demonstrated, to be a constitutive Ca(V)1.2 Ca2+ channel subunit.

268 Functional assays of intracellular Ca2+ channels, such as the inositol 1,4,5-trisphosphate

269 versely affect currents through both Na+ and Ca2+ channels, suggesting that FHFs may be arrhythmogeni

270 properties but does affect overall levels of Ca2+channel surface expression in some circumstances.

271 T-type Ca2+ channels (T-channels) are involved in the control o

272 ve demonstrated an important role for T-type Ca2+ channels (T-channels) in controlling the excitabili

273 ns express a previously unrecognized type of Ca2+ channel that is inhibited by omega-agatoxin IVA, li

274 B-1 regulate the signaling properties of two Ca2+ channels that are encoded by the NMR-1 N-methyl D-a

275 is caused by dendritic L-type voltage-gated Ca2+ channels that are prominently activated during acti

276 eurons, including increases in voltage-gated Ca2+ channels that likely underlie the mechanical hypera

277 From the Ca2+ channels that mediate this influx, to the K+ , Cl-

278 reliance of these neurons on L-type Ca(v)1.3 Ca2+ channels to drive their maintained, rhythmic pacema

279 ng beta cells, and opening voltage-dependent Ca2+ channels to elicit insulin exocytosis.

280 and subsequent opening of voltage-dependent Ca2+ channels to elicit insulin granule exocytosis.

281 favour a direct interaction of peptides with Ca2+ channels to inhibit synaptic transmission and atten

282 KCalpha) coerces discrete clusters of L-type Ca2+ channels to operate in a high open probability mode

283 The N-type Ca2+ channel toxin omega-conotoxin GVIA inhibited both t

284 Ca2+ entry through voltage-gated L-type Ca2+ channels triggers exocytosis of insulin-containing

285 ith genetics, we here identify the lysosomal Ca2+ channel Trpml as an essential player in the couplin

286 e receptors, and activation of voltage-gated Ca2+ channels, ultimately leading to excessive stimulati

287 Voltage-gated Ca2+ channels undergo a negative feedback regulation by

288 re inhibited by the L-type voltage-dependent Ca2+ channel (VDCC) inhibitor, diltiazem and with P2X re

289 d by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought to determine

290 The L-type voltage-gated Ca2+ channel (VGCC) blockers verapamil and (+)-cis-dilti

291 he coupling of mu receptors to voltage-gated Ca2+ channels (VGCCs) in beta arr2+/+ and beta arr2-/- d

292 The role of voltage-gated Ca2+ channels (VGCCs) in spontaneous miniature neurotran

293 Voltage-gated Ca2+ channels (VGCCs) of the P/Q-type, which are express

294 influx through both NMDARs and voltage-gated Ca2+ channels (VGCCs).

295 emonstrate that the membrane distribution of Ca2+ channels was not reduced at a time when channel act

296 In conclusion, Ca2+ flux through L-type Ca2+ channels was tightly coupled to changes in OCR and

297 a2+ was removed from the bath or when N-type Ca2+ channels were inhibited with omega-conotoxin GVIA,

298 that CaBP4 directly regulates Ca(v)1 L-type Ca2+ channels, which are essential for normal photorecep

299 ctivation of T-type and N-type voltage-gated Ca2+ channels, which contribute to the Ca2+ spikes.

300 direct peptide interaction with presynaptic Ca2+ channels, with effects on current amplitude and gat

301 tion of NMDARs followed by voltage-sensitive Ca2+ channels within dendritic spines.