ライフサイエンスコーパス: calcium channel

1 calcium-handling genes (eg, SERCA2a, L-type calcium channel).

2 ough the low-voltage-activated T-type CaV3.1 calcium channel.

3 es an inositol 1,4,5-triphosphate-responsive calcium channel.

4 hannels are exclusively linked to the N-type calcium channel.

5 RyR1 facilitates gating of the voltage-gated calcium channel.

6 the gating properties and trafficking of the calcium channel.

7 potential channel family, is a nonselective calcium channel.

8 TRPM7 is not a store-operated calcium channel.

9 t can bind and modulate L-type voltage-gated calcium channels.

10 kine receptors and calcium release-activated calcium channels.

11 dependent on activation of voltage-dependent calcium channels.

12 ransients due to strong expression of T-type calcium channels.

13 alpha, or by pharmacological block of L-type calcium channels.

14 osition a fraction of vesicles away from the calcium channels.

15 m entry via La(3+)- and nifedipine-sensitive calcium channels.

16 the synaptic bulk or from the entry through calcium channels.

17 ted by inhibiting cyclooxygenase-2 or L-type calcium channels.

18 ctivation of plasma membrane N-type (CaV2.2) calcium channels.

19 ion of Gbetagamma subunits and activation of calcium channels.

20 forming alpha1 subunit of CaV 2.1 (P/Q-type) calcium channels.

21 enetic and acquired, involving voltage-gated calcium channels.

22 followed by calcium entry via store-operated calcium channels.

23 ion of synaptic vesicles with respect to the calcium channels.

24 -dependent manner and binds to voltage-gated calcium channels.

25 ission showed constitutive MOR inhibition of calcium channels.

26 tor activation selectively suppresses N-type calcium channels.

27 the abundance and function of voltage-gated calcium channels.

28 llular fragment APPsalpha and involve L-type calcium channels.

29 ecreted APPsalpha-domain and involves L-type calcium channels.

30 direct G protein inhibition of voltage-gated calcium channels.

31 ubunits of GABAA receptors and voltage-gated calcium channels.

32 opening of different types of voltage-gated calcium channels.

33 rol of transcription by AT1R, integrins, and calcium channels.

34 alcin, mostly driven by N-type voltage-gated calcium channels.

35 This is the case for voltage-gated calcium channels.

36 ic reticulum with opening of plasma membrane calcium channels.

37 graded manner, due to recruitment of T-type calcium channels.

38 ting the function of pre-synaptic UNC-2/CaV2 calcium channels.

39 e Ca(2+) currents conducted by voltage-gated calcium channel 1.2 (CaV1.2) initiate excitation-contrac

40 ression is achieved by decreased presynaptic calcium channel abundance and calcium influx, changes th

41 port for the first time that BDNF slows down calcium channel activation, including P/Q-type channels,

42 glutathionylation and a concomitant loss in calcium channel activity.

43 currents are substantially increased by the calcium channel agonist Bay K 8644 and inhibited by the

44 tion potentials (APs) activate voltage-gated calcium channels, allowing calcium to enter and trigger

45 rrors of Cacna1a, the P/Q-type voltage-gated calcium channel alpha subunit gene, expressed throughout

46 c glutamate receptor 6 and voltage-dependent calcium channel alpha1.4, are not detected until fetal w

47 Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators

48 new tools to investigate the trafficking of calcium channel alpha2delta subunits.

49 molecular complex, which is an intracellular calcium channel and abundant in the brain.

50 sites, interacts with a putative trypanosome calcium channel and is required for its targeting to the

51 receptors (GABAB Rs) suppress voltage-gated calcium channels and activate G-protein coupled potassiu

52 his review summarizes the recent findings on calcium channels and associated receptors as potential t

53 ctivation and inactivation of the underlying calcium channels and correctly identified the accepted m

54 its calcium influx through voltage-dependent calcium channels and dampens adrenergic signaling, there

55 eved through the functional coupling between calcium channels and glutamate-filled synaptic vesicles.

56 teins, such as Shank3 and subunits of l-type calcium channels and NMDA receptors, and increases CaMKI

57 the optimal spatial alignment of presynaptic calcium channels and postsynaptic glutamate receptor pro

58 that the C. elegans SHN-1/Shank binds L-type calcium channels and that increased and decreased shn-1

59 We show that the coupling strength between calcium channels and the exocytosis calcium sensor at in

60 defective current densities for Ik1, l-type calcium channel, and Na(+)/Ca(2+) exchanger.

61 logical and pathological processes involving calcium channels, and as a therapeutic target.

62 act upon glucose transporters, potassium and calcium channels, and G-protein-coupled receptors to mod

63 eins are auxiliary subunits of voltage-gated calcium channels, and influence their trafficking and bi

64 quired for normal function of cardiac L-type calcium channels, and its up-regulation is associated wi

65 ported to target low-voltage-activated (LVA) calcium channels, and the structural basis of toxin sens

66 ng the effect of the well-established L-type calcium channel antagonist nimodipine.

67 Using a selective T-type calcium channel antagonist, we describe a T-type compone

68 the store-operated calcium release-activated calcium channel are the Ca(2+)-sensing protein stromal i

69 Our results indicate that T-type calcium channels are critical regulators of a C. elegans

70 this study, we find that different types of calcium channels are differentially distributed, with de

71 Voltage-gated calcium channels are essential players in many physiolog

72 iliary alpha2delta subunits of voltage-gated calcium channels are extracellular membrane-associated p

73 g plasma and sarcoplasmic reticulum membrane calcium channels are important determinants of the heart

74 CaV1 L-type calcium channels are key to regulating neuronal excitabi

75 Low-threshold activated T-type calcium channels are present at the synapse, although th

76 forming subunits of voltage-gated sodium and calcium channels are structurally related and likely to

77 Drugs that block calcium channels are used in the treatment of epilepsy,

78 scillatory calcium signals via voltage-gated calcium channels as a key component.

79 We define T-type calcium channels as a target of Abeta-NgR signaling, med

80 implications, with a focus on voltage-gated calcium channels as part of the disease process and as a

81 , which organizes both synaptic vesicles and calcium channels at the active zone.

82 ma (as recognized for neuronal voltage-gated calcium channel autoantibodies).

83 e differentially distributed, with dendritic calcium channels being activated by somatic activity, bo

84 release was relatively insensitive to N-type calcium channel blockade.

85 Voltage-gated calcium-channel blockade prevents iron entry into cardio

86 econtamination following a potentially toxic calcium channel blocker ingestion (1D); 2) as first-line

87 nnel agonist Bay K 8644 and inhibited by the calcium channel blocker nifedipine in a dose-dependent m

88 rovide a management approach for adults with calcium channel blocker poisoning.

89 In this national cohort study, preadmission calcium channel blocker therapy before sepsis developmen

90 Patients who responded to calcium channel blocker therapy had metabolic profiles s

91 commendations for the stepwise management of calcium channel blocker toxicity.

92 ients with sepsis, of which, 19,742 received calcium channel blocker treatments prior to the admissio

93 The association between calcium channel blocker use and sepsis outcome was deter

94 Prior calcium channel blocker use is associated with reduced m

95 Prior calcium channel blocker use was not associated with chan

96 nsidering large baseline differences between calcium channel blocker users and nonusers, a propensity

97 hrombin levels, which were less decreased in calcium channel blocker users.

98 Use of calcium channel blocker was associated with a reduced 30

99 ial treatment of systemic corticosteroid and calcium channel blocker, remarkable improvement was noti

100 diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in albuminur

101 (-5.76 mm Hg [95% CI -10.28 to -1.23]) or a calcium-channel blocker (-5.13 mm Hg, [-9.47 to -0.79])

102 dult patients with favorable prognosis using calcium-channel blocker (CCB) therapy.

103 ccepted mechanism of action of nifedipine, a calcium-channel blocker clinically used in patients with

104 compare the effectiveness and safety of the calcium-channel blocker nifedipine and the oxytocin inhi

105 patients already receiving a beta blocker or calcium-channel blocker.

106 patients showing long-term improvement with calcium channel-blocker therapy.

107 cancer risk associated with long-term use of calcium channel blockers (CCBs) or angiotensin-convertin

108 tients with DM were more commonly prescribed calcium channel blockers and long-acting nitrates at dis

109 e reveals inverse correlation between use of calcium channel blockers and lung cancer diagnosis.

110 termine the association between prior use of calcium channel blockers and the outcome of patients adm

111 Experimental studies suggest that calcium channel blockers can improve sepsis outcome.

112 nd burst firing, and selective triple T-type calcium channel blockers could offer a new way to treat

113 coding insect specific sodium, potassium and calcium channel blockers for their ability to improve th

114 Use of calcium channel blockers has been found to improve sepsi

115 This study determines whether the use of calcium channel blockers is associated with a decreased

116 Moreover, antiepileptics and calcium channel blockers may provide repurposing opportu

117 On subgroup analysis, calcium channel blockers tend to be more beneficial to p

118 ensity-matched cohort (20.2% vs 32.9% in non-calcium channel blockers users; p = 0.009) and in multiv

119 Prior use of calcium channel blockers was associated with improved 30

120 -reported use of statins, beta-blockers, and calcium channel blockers were all 95% or greater.

121 Statins, beta-blockers, and calcium channel blockers were each reported by over 15%

122 For the prevention of heart failure, calcium channel blockers were inferior and diuretics wer

123 Calcium channel blockers were superior to other drugs fo

124 ent for known antipsychotic drugs, selective calcium channel blockers, and antiepileptics.

125 sed by the antiseizure medication phenytoin, calcium channel blockers, and ciclosporin.

126 blockers, beta-blockers, thiazide diuretics, calcium channel blockers, and metformin.

127 rate-control treatment with beta-blockers or calcium channel blockers, and the use of beta-blockers w

128 compared with pharmacy records for statins, calcium channel blockers, beta-blockers, and bisphosphon

129 CE inhibitors, non-ophthalmic beta blockers, calcium channel blockers, diuretics, and angiotensin rec

130 e inhibitors, angiotensin-receptor blockers, calcium channel blockers, or beta blockers) was signific

131 nt for differential likelihoods of receiving calcium channel blockers.

132 potent, selective, brain-penetrating T-type calcium channel blockers.

133 brain penetrant and selective triple T-type calcium channel blockers.

134 ent, selective, and brain-penetrating T-type calcium channel blockers.

135 ement for use of statins, beta-blockers, and calcium channel blockers.

136 d with a beta-blocker or non-dihydropyridine calcium channel blockers.

137 ith sepsis were analyzed, 18.6% of whom used calcium channel blockers.

138 mpared with patients who have never received calcium channel blockers.

139 The most commonly used medication class was calcium-channel blockers (55.2%, 55.0-55.4).

140 ination with digoxin, or non-dihydropyridine calcium-channel blockers (not in heart failure) effectiv

141 ngiotensin-receptor blockers, beta blockers, calcium-channel blockers, or direct renin inhibitors (pr

142 Calcium channel blocking curtailed the enhanced insulin

143 was dependent on the activity of L-type CaV1 calcium channels but not on the activity of the calcium-

144 ing the expression levels of a voltage-gated calcium channel, cacophony.

145 el current amplitude of native voltage-gated calcium channels can be resolved accurately despite cond

146 Voltage-gated calcium channels can coassemble with auxiliary subunit a

147 The 2AG inhibits the sperm calcium channel (CatSper), and its removal leads to calc

148 d calcium modulator 1 but also voltage-gated calcium channel (Cav) 1 channels.

149 Voltage-dependent calcium channels (Cav) of the T-type family (Cav3.1, Cav

150 he present studies blocked voltage-activated calcium channels (CaV) using the nonselective CaV blocke

151 to directly interact with the voltage-gated calcium channel, Cav 2.2, and reduce its trafficking to

152 alpha1 subunit of the cardiac voltage-gated calcium channel Cav1.2 at Ser1928, suggesting enhanced p

153 alpha1C subunit of the voltage-gated L-type calcium channel Cav1.2, rank among the most consistent a

154 Here we show that the voltage-gated calcium channel CaV1.3 and the big conductance calcium-a

155 The L-type calcium channel CaV1.3 constitutes an important calcium

156 ns, only otoferlin interacts with the L-type calcium channel Cav1.3, showing a significant difference

157 influx through the voltage-dependent L-type calcium channel (CaV1.2) rapidly increases in the heart

158 d alter the properties of the cardiac L-type calcium channel (CaV1.2).

159 anical coupling between L-type voltage-gated calcium channels (CaV1.1) and the ryanodine receptor (Ry

160 L-type voltage-gated CaV1.2 calcium channels (CaV1.2) are key regulators of neuronal

161 lpha1A subunit of the P/Q-type voltage-gated calcium channel Cav2.1.

162 orming subunit of the neuronal voltage-gated calcium channel Cav2.1.

163 eta subunits interact with the voltage-gated calcium channel CaV2.2 on a site in the intracellular lo

164 er release is principally mediated by CaV2.1 calcium channels (CaV2.1) and is highly dependent on the

165 Neuronal voltage-gated N-type calcium channels (Cav2.2) are inhibited by activation of

166 pecific blockade of alpha1 subunit of N-type calcium channel, Cav2.2, in diabetic nephropathy, howeve

167 d drug mibefradil, which inhibits the T-type calcium channel Cav3.2.

168 ins poorly understood with respect to T-type calcium channels (Cav3).

169 P4 activates its receptor, the voltage-gated calcium channel Cavalpha2delta1 subunit (Cavalpha2delta1

170 ied Flunarizine - a well-known anti-migraine calcium channel (CC) blocker - being able to diminish in

171 he corresponding mutations affect the T-type calcium channel CCA-1 and symmetrically re-tune its volt

172 associated vesicles and reduced presynaptic calcium-channel clustering.

173 These mice also displayed N-type calcium channel compensation at descending thalamic syna

174 eckpoint allowing trafficking only of mature calcium channel complexes into neuronal processes.

175 ffect of alpha2delta subunits on trafficking calcium channel complexes remain poorly understood.

176 ve SNc neurons differ substantially in their calcium channel composition and efficacy of excitatory i

177 e, SNc neurons differ substantially in their calcium channel composition, which may contribute to the

178 Here, we recorded the voltage-gated calcium channel current in nucleated patches from layer

179 impractical because of the rapid rundown of calcium channel currents.

180 There are three main subdivisions of calcium channel, defined by the pore-forming alpha1 subu

181 The present study found that L-type calcium channel-dependent LTP in the CA3-CA1 hippocampal

182 ysical interaction between the voltage-gated calcium channel dihydropyridine receptor (DHPR) and the

183 tation-contraction coupling, a voltage-gated calcium channel directly activates opening of the calciu

184 hus, non-specific sodium influx via bonafide calcium channels disrupts unexpected signaling nodes and

185 rupts the clustering and localization of the calcium channel DmCa1A subunit (Cacophony), decreases th

186 type A receptor activation and voltage-gated calcium channels during early postnatal development.

187 CALHM1 is a cell surface calcium channel expressed in cerebral neurons.

188 uction in cacophony, a Type II voltage-gated calcium channel, expression and that genetically restori

189 to play a synaptogenic role, independent of calcium channel function.

190 uced changes in electrical driving force and calcium channel gating to cancel each other out.

191 nges in calcium driving force and changes in calcium channel gating to effectively cancel each other

192 ectrical driving force for calcium entry and calcium channel gating.

193 sion activity in a RBFOX2-target, the L-type calcium channel gene, Cacna1c.

194 several candidate genes, among others three calcium channel genes that may potentially contribute to

195 Decreased expression and activity of CaV1.2 calcium channels has been reported in pressure overload-

196 Neuronal voltage-gated calcium channels have evolved as one of the most importa

197 showing the more specific activity on L-type calcium channels, i.e. A7r5 (IC50 = 0.18 +/- 0.02 and 0.

198 vivo phosphorylation map of a voltage-gated calcium channel in a mammalian brain.

199 eaved alpha2delta subunits maintain immature calcium channels in an inhibited state.

200 ole, from fruit flies to mammals, for L-type calcium channels in augmenting motoneuron excitability.

201 al downregulation of voltage-activated (Cav) calcium channels in DMV neurons, which led to a reductio

202 ess localization and function of L-type like calcium channels in motoneurons.

203 n our biophysical characterization of T-type calcium channels in Purkinje cells suggests that the bri

204 luR2) signaling, which acts on voltage-gated calcium channels in SACs, selectively restricts cross-se

205 timating numbers of functional voltage-gated calcium channels in the membrane and the size of channel

206 irect link to abnormal signaling of neuronal calcium channels in the SHR and that targeting cGMP can

207 Surprisingly, we observed calcium channel-independent effects on microglia, result

208 nodine receptor but not in the voltage-gated calcium channel, indicating that these phenotypes are ca

209 calcein and alexa-dextran, with or without a calcium channel inhibitor, and imaged the larvae in vivo

210 er that is caused by mutations in the CaV1.2 calcium channel-interneurons display abnormal migratory

211 ws that calcium entry through store-operated calcium channels is critical for calcium oscillations, b

212 Rem2 inhibits high voltage activated calcium channels, is involved in synaptogenesis, and reg

213 To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required for OPC developm

214 is firing activity is supported by different calcium channel landscapes.

215 harmacological blockade of the N- and L-type calcium channel lessens renal injury in kidney disease p

216 unctions of axonal and dendritic L-type like calcium channels likely operate synergistically to maxim

217 trate that Dmca1D (Cav1 homolog) L-type like calcium channels localize to both the somatodendritic an

218 und to regulate low-voltage-activated CaV3.2 calcium channels localized to the axon initial segment,

219 l-type calcium channel (LTCC) antagonists have been used in bip

220 APAs frequently have mutations of an L-type calcium channel (LTCC) CaV1.3.

221 al activity in naive rats by engaging L-type calcium channels (LTCCs) and that intra-CeA LTCC blockad

222 L-type voltage-gated calcium channels (LTCCs) are implicated in several psych

223 L-type calcium channels (LTCCs) play important roles in regulat

224 ies the developmental importance of P/Q-type calcium channel-mediated presynaptic glutamate release a

225 r findings identify endothelial TRPC6 as the calcium channel mediating the upward arrow[Ca(2+)]i requ

226 ygous tottering (tg/tg) mice with a P/Q type calcium channel mutation.

227 The calcium channel of sperm (CatSper) is essential for sper

228 was maximal (a condition achieved with an SR calcium channel opening drug) and partially when depleti

229 d with calpain-1 activation following T-type calcium channel opening, and resulted in the truncation

230 l activity and enhanced by disrupting L-type calcium channels or elevating cAMP.

231 that can be located in close vicinity to the calcium channels or more remotely from them.

232 the endoplasmic reticulum (ER) membrane, the calcium channel ORAI1 in the plasma membrane, and sites

233 In response to flow, the plasma membrane calcium channel ORAI1 mediates calcium influx in LECs an

234 T-type calcium channels play a key role in neuronal excitabilit

235 put train.SIGNIFICANCE STATEMENT CaV1 L-type calcium channels play a key role in regulating the outpu

236 d toxic injury, signaling through the plasma calcium channel PMCA4b to activate the PI3K/AKT and MAPK

237 type with or without treatment with Mn2+, a calcium channel probe) were studied using 1/T1rho MRI.

238 ntify postsynaptic density and voltage-gated calcium channel protein expression.

239 e to littermate controls, and alpha1C L-type calcium channel protein levels were significantly lower

240 s of advanced glycation end products, L-type calcium channels, protein kinase C, Rho-kinase, actin po

241 In particular, EV-associated annexin calcium channelling proteins, which form a nucleational

242 ms, including fertilization, sperm motility, calcium channel regulation, and SNARE proteins.

243 res Mid1, an endoplasmic reticulum-localized calcium channel regulatory protein implicated in the oxi

244 uences of non-specific sodium permeation via calcium channels remain unknown.

245 Calcium channels required for symbiosis signaling have b

246 triggered exocytosis was preserved by N-type calcium channel rescue, demonstrating that evoked releas

247 terpotentials after AP stimuli did not alter calcium channel responses or neurotransmitter release ap

248 els determined impact of 1 variant on T-type calcium channel responsiveness to ethosuximide.

249 us signalling, mediated via NMDAR and L-type calcium channels, results in rapid FOXP1 deSUMOylation.

250 the accumulated lipid on the skeletal muscle calcium channel ryanodine receptor 1, a negative effect

251 ated hMSC PS effects on cardiomyocyte L-type calcium channel/sarcoendoplasmic reticulum calcium-ATPas

252 D+P are endosomal trafficking, autophagy and calcium channel signaling.

253 n, localizing SNARE proteins proximal to the calcium channel so as to synchronize calcium influx with

254 and protein levels for calsequestrin, L-type calcium channel, sodium-calcium exchanger, phospholamban

255 CaV1.1e is the voltage-gated calcium channel splice variant of embryonic skeletal mus

256 t its primary sequence does not resemble any calcium channel studied to date.

257 chi et al. (2016) describe the voltage-gated calcium channel subunit alpha2delta2 as a developmental

258 n subjects as well as aberrant voltage-gated calcium channel subunit protein expression linked to spi

259 The effect of increased voltage-gated calcium channel subunit protein expression on spine dens

260 s (R192Q and S218L) in the CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the speed of

261 ome-wide association study risk genes (e.g., calcium channel subunits [Cacna1c and Cacnb2], cholinerg

262 odynia by regulating auxiliary voltage-gated calcium channel subunits alpha2delta-1 and alpha2delta-2

263 ominent role of low-voltage-activated T-type calcium channels (T-channels) in the firing activity of

264 3 alpha1 subunit, a subtype of voltage-gated calcium channel that contributes to T-type currents.

265 example, the SZ risk gene CACNA1I encodes a calcium channel that is abundantly expressed in the thal

266 Inner hair cells possess calcium channels that are essential for transmitting sou

267 For all the subtypes of voltage-gated calcium channel, their gating properties are key for the

268 d for symbiotic Ca(2+) oscillations, but the calcium channels themselves have been unknown until now.

269 own of KHARON mRNA results in failure of the calcium channel to enter the flagellar membrane, detachm

270 (2017) show that alpha2delta4 subunits link calcium channels to a trans-synaptic complex with glutam

271 als leverage distinct types of voltage-gated calcium channels to mediate short-term facilitation rema

272 ssays in cells coexpressing transporters and calcium channels to study the effects of increasing N-al

273 2delta binding to gabapentin, and influences calcium channel trafficking and function.

274 n interacts with alpha2delta-1, and inhibits calcium channel trafficking.

275 proper lysosomal calcium release through the calcium channel TRPML1 is required for mTORC1 activation

276 vity and prevented cleavage of the lysosomal calcium channel TRPML1.

277 st nephrolithiasis by upregulating the renal calcium channel TRPV5.

278 ells and potently activate the intracellular calcium channel type 1 ryanodine receptor (RyR1).

279 esynaptic Ca(2+) entry via voltage-activated calcium channels (VACCs) is the major trigger of action

280 At chemical synapses, voltage-activated calcium channels (VACCs) mediate Ca(2+) influx to trigge

281 r, by downregulating their voltage-activated calcium channels, vagal motoneurons acquire a stressless

282 INTERPRETATION: Four T-type calcium channel variants and 1 ABCB1 transporter variant

283 ulation of CaV2.3 (R-type) voltage-dependent calcium channel (VDCC) currents observed in the presence

284 NNK induces voltage-dependent calcium channel (VDCC)-intervened calcium influx in airw

285 receptors (nmdaLTP) or L-type voltage-gated calcium channels (vdccLTP).

286 be how surface mobility of voltage-dependent calcium channels (VDCCs) modulates release probabilities

287 g exon (exon 47) of the Cav2.1 voltage-gated calcium channel (VGCC) gene produces two major isoforms

288 P/Q-type voltage-gated calcium channel (VGCC) puncta colocalized with Bassoon p

289 intronic region of the L-type voltage-gated calcium channel (VGCC) subunit gene CACNA1C (peak associ

290 e importance of the T-type low-voltage-gated calcium channels (VGCC) in different cancer types, inclu

291 tagamma-mediated modulation of voltage-gated calcium channels (VGCC), inhibition can also be mediated

292 lity to activate L- and N-type voltage-gated calcium channels (VGCCs) and delineated their crucial ro

293 nt potentiation of presynaptic voltage-gated calcium channels (VGCCs) underlies 3,4-diaminopyridine (

294 y, and the spatial location of voltage-gated calcium channels (VGCCs).

295 Elucidating the mechanisms that modulate calcium channels via opioid receptor activation is funda

296 Voltage-gated L-type calcium channels (VLCC) are distributed widely throughou

297 This calcium channel was highly expressed in human GBM specim

298 ore subunit of the calcium release-activated calcium channel, was identified to induce the shear stre

299 because GABAB Rs selectively suppress N-type calcium channels, which in turn are specifically linked

300 the plasma membrane, Cch1p, and the vacuolar calcium channel, Yvc1p.