ライフサイエンスコーパス: voltage-activated

1 vating Kv3.4 channels underlie a robust high voltage-activated A-type K(+) current (I(AHV)) in nocice

2 ll types small voltage steps at subthreshold voltages activated a substantial component of transient

3 ditional calculations performed on the KvAP (voltage-activated) and KirBac1.1 (inward rectifier) chan

4 unknown, although mPanx1 is reported to be a voltage-activated anion-selective channel.

5 e cells of Slo(-/-) mice lacked calcium- and voltage-activated BK currents, whereas local calcium tra

6 The neuronal calcium- and voltage-activated BK potassium channel is modulated by e

7 e the role of large conductance calcium- and voltage-activated (BK) channels in spontaneous and secre

8 High-voltage activated Ca channels participate in multiple ce

9 We show that high-voltage activated Ca(2+) channels are regulated by membr

10 ng Rem2, mediate profound inhibition of high-voltage activated Ca(2+) channels containing intracellul

11 induces rapid Ca(2+) signals mediated by low-voltage activated Ca(2+) channels under strict inhibitor

12 n rearing depressed multiple classes of high-voltage activated Ca(2+) current.

13 aptic mechanism of action, nor did it affect voltage-activated Ca channel currents.

14 cells might trigger Ca(2)(+) influx through voltage-activated Ca(2)(+) channels.

15 The beta subunit of high voltage-activated Ca(2+) (Ca(v)) channels targets the po

16 larly, co-assembly of the BKCa channels with voltage-activated Ca(2+) (Cav) channels, mirroring the n

17 distinct mutations in the gene encoding the voltage-activated Ca(2+) channel alpha(1A) subunit (CACN

18 ansport and physiological properties of high voltage-activated Ca(2+) channel complexes.

19 veral of its analogs directly stimulate high voltage-activated Ca(2+) channels (HVACCs) in acutely di

20 Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+)

21 Calcium influx through voltage-activated Ca(2+) channels (VACCs) plays a critic

22 e Rem is a potent negative regulator of high voltage-activated Ca(2+) channels and a known interactin

23 role of Ca(v)beta in RGK inhibition of high voltage-activated Ca(2+) channels and prompt a paradigm

24 fects of L-arginine on evoked EPSCs and high voltage-activated Ca(2+) channels expressed in HEK293 ce

25 have shown previously that NO inhibits high voltage-activated Ca(2+) channels in primary sensory neu

26 Therefore, Ca(v)3.3 is similar to high voltage-activated Ca(2+) channels in that depolarizing p

27 contrast to the well established function of voltage-activated Ca(2+) channels in the presynaptic mem

28 vated Ca(2+) channels, the inhibition of low-voltage-activated Ca(2+) channels is subtype-dependent a

29 ere, we report that the activation of L-type voltage-activated Ca(2+) channels occurs through a novel

30 ng the surface expression and gating of high voltage-activated Ca(2+) channels through their interact

31 how specific subtypes of human neuronal high-voltage-activated Ca(2+) channels were affected by acute

32 Unlike high-voltage-activated Ca(2+) channels, the inhibition of low

33 GTP-binding proteins potently inhibits high voltage-activated Ca(2+) channels.

34 fferent terminals through S-nitrosylation of voltage-activated Ca(2+) channels.

35 hyperpolarization and deinactivation of low-voltage-activated Ca(2+) channels.

36 S-nitrosylation in the NO regulation of high voltage-activated Ca(2+) channels.

37 we show that BPA acts as a potent blocker of voltage-activated Ca(2+) channels.

38 ainly regulated by subtypes of neuronal high-voltage-activated Ca(2+) channels.

39 arized level, are further boosted by the low-voltage-activated Ca(2+) conductance.

40 X) rather than presynaptic depolarization or voltage-activated Ca(2+) currents.

41 cellular excitability together with reduced voltage-activated Ca(2+) currents.

42 occur, but there is little evidence that low-voltage-activated, Ca(v)3 ("T-type"), channels take part

43 the membrane and induce Ca2+ influx via high-voltage-activated Ca2+ channels (I(HVA)).

44 tivated by Ca2+ entry through high-threshold voltage-activated Ca2+ channels (L- and N-type), and tog

45 equires proper communication of plasmalemmal voltage-activated Ca2+ channels and Ca2+ release channel

46 High-voltage-activated Ca2+ channels are essential for divers

47 High-voltage-activated Ca2+ channels regulate diverse functio

48 nd their Ca2+ sources through high-threshold voltage-activated Ca2+ channels were studied using whole

49 ts is obligatory for forming functional high-voltage-activated Ca2+ channels, yet the structural dete

50 None of these treatments alter expression of voltage-activated Ca2+ channels.

51 or a dopamine D1 receptor agonist decreased voltage-activated Ca2+ current and lowered Ca2+ influx.

52 proenkephalin, inhibited high (but not low) voltage-activated Ca2+ current in both DRG and SCG neuro

53 The density of voltage-activated Ca2+ currents did not change between E

54 sphatidylinositol 3-kinase/Akt signaling and voltage-activated Ca2+ influx for stimulation of calmodu

55 These data identify a role of low-voltage activated calcium channels in synaptic plasticit

56 Rem2 inhibits high voltage activated calcium channels, is involved in synap

57 ble of acting as a negative modulator of low voltage activated calcium current.

58 anding of gamma(6) subunit modulation of low voltage activated calcium current.

59 Voltage-activated calcium (Cav) channels couple intracel

60 ample, gabapentin is a ligand of alpha2delta voltage-activated calcium channel subunits that are over

61 The present studies blocked voltage-activated calcium channels (CaV) using the nonse

62 High voltage-activated calcium channels (HVACCs) are essentia

63 ([Ca(2+)](o)) regulates Ca(2+) entry through voltage-activated calcium channels (VACCs) and consequen

64 CANCE STATEMENT Presynaptic Ca(2+) entry via voltage-activated calcium channels (VACCs) is the major

65 At chemical synapses, voltage-activated calcium channels (VACCs) mediate Ca(2+

66 had lower baclofen-evoked inhibition of high-voltage-activated calcium channels and a defective presy

67 with the alpha1 pore-forming subunit of high voltage-activated calcium channels and modulates several

68 ane protein related to the gamma subunits of voltage-activated calcium channels and the claudin super

69 High-voltage-activated calcium channels are hetero-oligomeric

70 L-type high-voltage-activated calcium channels are involved in the c

71 d the ability of Rem2 to modulate endogenous voltage-activated calcium channels in rat sympathetic an

72 Dihydropyridine-sensitive, voltage-activated calcium channels respond to membrane d

73 These channels are low voltage-activated calcium channels that play a key role

74 Besides opening and closing, high voltage-activated calcium channels transit to a noncondu

75 lcium currents arising from preexisting high-voltage-activated calcium channels without affecting low

76 Rather, by downregulating their voltage-activated calcium channels, vagal motoneurons ac

77 These GTPases also function as regulators of voltage-activated calcium channels, which in turn modula

78 ction site (synprint) found in synaptic high voltage-activated calcium channels.

79 y trigger glutamate release independently of voltage-activated calcium channels.

80 hether CaBP5 can modulate expressed Ca(v)1.2 voltage-activated calcium channels.

81 vated calcium channels without affecting low-voltage-activated calcium channels.

82 de of currents arising from preexisting high-voltage-activated calcium channels.

83 (I(h)), persistent Na+ current (I(NaP)), low-voltage-activated calcium current (I(L/T)) mediated by T

84 rrent flowing during the shoulder, with high voltage-activated calcium current also contributing sign

85 ardly rectifying current I(h), low-threshold voltage-activated calcium current I(t), and activity at

86 This glycine response reduced high voltage-activated calcium current.

87 further, we show that baclofen inhibits high-voltage-activated calcium currents in granule cells.

88 Ghrelin significantly increased voltage-activated calcium currents in isolated single DM

89 selective effect of gamma(6) on LVA and high voltage-activated calcium currents in vivo.

90 ly 40%), especially near threshold, and high voltage-activated calcium currents much less (approximat

91 reases in C(m), which were correlated to the voltage-activated calcium currents.

92 psulation, and does not alter the density of voltage-activated calcium or potassium channels.

93 s, it has been reported to block T-type (low-voltage activated) calcium channels.

94 on (Hv1) channels are relatives of classical voltage-activated cation channels.

95 might have been augmented by three types of voltage-activated cationic currents known to increase ne

96 Like other high voltage-activated Cav channels, Cav1.4 channels are comp

97 ted from a transcriptional downregulation of voltage-activated (Cav) calcium channels in DMV neurons,

98 n for activation of co-expressed BK and high-voltage activated CaV2.2 channels.

99 Mitral cells express low-voltage activated Cav3.3 channels on their distal apical

100 ls coimmunoprecipitate and interact with low voltage-activated Cav3.2 Ca(2+) channels at the nanodoma

101 eceptor activation was found to regulate low-voltage-activated CaV3.2 calcium channels localized to t

102 a(6) calcium channel subunit to modulate low voltage activated (Cav3.1) calcium current density.

103 The dendritic arborization and voltage-activated channel complement of rat neocortical

104 e cardiac L-type voltage-gated calcium (high voltage-activated) channel with accessory proteins beta

105 brake and its function to maintain these low voltage-activated channels closed at resting membrane po

106 R-type high voltage-activated channels inactivate fully in a few hun

107 amma-dependent inhibition of non-L-type high-voltage-activated channels of the Ca(v)2 family.

108 uring (P7-P9) type I hair cells acquired low-voltage-activated channels that shortened the rise time

109 pithelial tissues, whereas KCNQ1 function as voltage-activated channels with very slow kinetics in ca

110 r-ear mechanisms (transducer adaptation, low-voltage-activated channels, nonquantal transmission, and

111 t a fraction of channels did not gate as low voltage-activated channels, requiring stronger depolariz

112 which usually permit Ca influx through high-voltage-activated channels.

113 GTPase, between the N-cadherin JMD and these voltage-activated channels.

114 e interaction with the external potential in voltage-activated channels.

115 with a potential contribution from the high voltage-activated component at more depolarized potentia

116 pting firing pattern was mediated by the low voltage-activated component of DTX-sensitive current wit

117 As previously reported for voltage-activated conductances, none of these currents w

118 d N-type channels accounting for most of the voltage-activated current (about 40 % each); MCH attenua

119 r results suggest alteration in subthreshold voltage-activated currents might be the mechanism underl

120 v3.1b subunits, which mediate high-threshold voltage-activated currents.

121 d Rho in the opposing hormonal regulation of voltage-activated, ether-a-go-go-related potassium chann

122 Voltage-activated human ether-a-go-go-related gene (hERG

123 was attributable to calcium influx via high-voltage-activated (HVA) (N- and P/Q-type) calcium channe

124 GnRH neurons express prominent high-voltage-activated (HVA) and small low-voltage-activated

125 While both ON and OFF cells express high-voltage-activated (HVA) Ca(2+) channels, only OFF RGCs a

126 GTP-binding proteins potently inhibits high voltage-activated (HVA) Ca(2+) channels, providing a pow

127 s thought to be mediated exclusively by high-voltage-activated (HVA) Ca(2+) channels.

128 arizing steps (> or =20 ms) that evoked high-voltage-activated (HVA) Ca(2+) currents (I(Ca)) and elev

129 Mutations in several genes for high-voltage-activated (HVA) Ca2+ channel subunits are linked

130 d that the current density of high threshold voltage-activated (HVA) calcium (Ca(2+)) channels was ma

131 High-voltage-activated (HVA) calcium channels represent an im

132 ed both low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium current (I(Ca)).

133 rease in the amplitude of the high-threshold voltage-activated (HVA) calcium current.

134 ltage-gated Ca2+ channel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotr

135 on between -60 mV and -70 mV as well as high voltage-activated (HVA) current with an activation volta

136 ons, NPY application reversibly reduced high-voltage-activated (HVA) currents to 33 +/- 5 % (n = 40)

137 rolled by calcium (Ca(2)(+)) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or

138 The characteristics of voltage-activated I(Na) and I(K) in the GnRH-containing

139 itability, in part by enhancing subthreshold voltage-activated inward currents.

140 location-specific interactions of IPSPs with voltage-activated ion channels are likely to influence t

141 re simply on the selective expression of low-voltage-activated ion channels by irregular afferents.

142 The properties of the voltage-activated ion channels that regulate synaptic in

143 Cortical axons contain a diverse range of voltage-activated ion channels, including Ca(2+) current

144 data suggest that Kv3.4 and Cav1.2, two high-voltage-activated ion channels, may act together to cont

145 In voltage-activated ion channels, voltage sensor (VSD) act

146 For voltage-activated ion channels, X-ray structures suggest

147 pid bilayer are critical for the function of voltage-activated ion channels.

148 a notable example being the S1-S4 domains of voltage-activated ion channels.

149 we report a study on the characterization of voltage-activated ionic currents in GnRH-containing TN c

150 (-) conductance and the recruitment of a low-voltage activated K(+) conductance.

151 KCNA10 is a cyclic nucleotide-gated, voltage-activated K channel that is detected in kidney,

152 adipose tissue expression of the Ca(2+)- and voltage-activated K(+) (BK) channel was identified in mo

153 ASIC1a and the high-conductance Ca(2+)- and voltage-activated K(+) (BK) channel.

154 Large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels are involved in a l

155 Large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels are well known for

156 muscle cells, large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels provide a critical

157 Large conductance Ca(2+)- and voltage-activated K(+) (BK) channels, composed of pore-f

158 amples from calcium-activated K(+) (BK(Ca)), voltage-activated K(+) (K(v)) and Ca(2+) channel (L-type

159 as 4-aminopyridine (4-AP) are widely used as voltage-activated K(+) (Kv) channel blockers and can imp

160 mia impairs vascular reactivity and inhibits voltage-activated K(+) (Kv) channels.

161 High-conductance Ca(2+)- and voltage-activated K(+) (Slo1 or BK) channels (KCNMA1) pl

162 The large-conductance Ca(2+)- and voltage-activated K(+) channel (BK(Ca), MaxiK), which is

163 nel, which is a large-conductance Ca(2+) and voltage-activated K(+) channel, is involved in the hypox

164 Large conductance, Ca(2+)- and voltage-activated K(+) channels (BK) respond to two dist

165 In particular, the KCNQ (Kv7) family of voltage-activated K(+) channels functions to stabilize n

166 nal with temporal precision depends on a low-voltage-activated K(+) conductance (gKL) and a hyperpola

167 nces are relatively small, in particular low-voltage-activated K(+) conductances (K(LVA)).

168 The large-conductance, calcium- and voltage-activated K(+)(BK) channel consists of the pore-

169 Large-conductance, Ca2+- and voltage-activated K+ (BK) channels are broadly expressed

170 ental question about the gating mechanism of voltage-activated K+ (Kv) channels is how five positivel

171 Reductions in voltage-activated K+ (Kv) currents may underlie arrhythm

172 Large conductance Ca(2+)- and voltage-activated K+ (maxi-K) channels modulate human my

173 Large-conductance Ca2+-voltage-activated K+ channels (BK channels) control many

174 plicating slow inactivation of low-threshold voltage-activated K+ channels as its mechanism.

175 tsynaptic sites suggests that this family of voltage-activated K+ channels may have additional roles

176 rent (I(M)), comprised of Kv7 channels, is a voltage-activated K+ conductance that plays a key role i

177 s were unchanged in TASK-1/3 KO mice as were voltage-activated K+ currents, including the non-inactiv

178 a1 subunit of BK (large conductance Ca2+ and voltage-activated K+) channels is essential for many key

179 present study tested the hypothesis that low-voltage activated Kv1 channels affect threshold dynamics

180 Low-voltage-activated Kv1-type (dendrotoxin-I sensitive) K+

181 These immature nodal structures lacked low-voltage-activated KV1.1 which was not enriched at juxtap

182 Voltage-activated Kv2.1 channels have properties commens

183 High-voltage-activated KV3.1b and KV2.2 were expressed in mut

184 us, endogenous membrane PIP(2) supports high-voltage activated L-, N-, and P/Q-type Ca(2+) channels,

185 n by SSRIs was mediated by a direct block of voltage-activated L-type Ca(2+) channels and was indepen

186 (2+) channels (Ca(v)1.3) responsible for low voltage-activated L-type Ca(2+) current.

187 cellular calcium transients mediated by high-voltage-activated L-type calcium channels.

188 herapeutic effect primarily by blocking high-voltage-activated L-type calcium channels.

189 Thus, potentiation of a low-voltage-activated L-type current by synaptically release

190 ls, we examine regulation of the Ca(2+)- and voltage-activated large conductance Ca(2+)-activated K(+

191 Molecular cloning of low-voltage activated (LVA) T-type calcium channels has enab

192 ning TN cells examined, we recorded both low-voltage-activated (LVA) and high-voltage-activated (HVA)

193 We have tested the hypothesis that low voltage-activated (LVA) and nonvoltage-gated (NVG) chann

194 2+) channels, only OFF RGCs also express low-voltage-activated (LVA) Ca(2+) channels.

195 Low-voltage-activated (LVA) Ca2+ channels are widely distrib

196 on and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca2+ channels to IGF-1, using th

197 fier toxins have been reported to target low-voltage-activated (LVA) calcium channels, and the struct

198 lcium channel gamma(6) subunit modulates low voltage-activated (LVA) calcium current in both human em

199 nsmitter release, and stimulate thalamic low-voltage-activated (LVA) currents that contribute to a co

200 tage clamp recordings revealed transient low voltage-activated (LVA) currents with activation between

201 ated via dendrotoxin-sensitive low-threshold voltage-activated (LVA) K(+) channels.

202 t high-voltage-activated (HVA) and small low-voltage-activated (LVA) macroscopic (whole-cell) Ca curr

203 Ca(v)3.x gene family members, encoding low voltage-activated (LVA) or T-type channels, were first i

204 Low-voltage-activated (LVA) T-type calcium channels have a w

205 Low voltage-activated (LVA), T-type, calcium channels mediat

206 In contrast, voltage-activated M-type K(+) current (I(M)) improved sp

207 A voltage-activated molecular-plasmonics device was create

208 tor (nAChR) subtype and an inhibitor of high-voltage-activated N-type calcium channel currents.

209 al output reflects a progressive decrease in voltage-activated Na(+) and K(+) currents, which occurs

210 The roles of oligodendroglial voltage-activated Na(+) channels (Nav) and electrical ex

211 try via noninactivating AMPA/KA receptors or voltage-activated Na(+) channels compromises mitochondri

212 receptors, l-calcium channels, nitric oxide, voltage-activated Na(+) channels, or intracellular calci

213 of the fast inactivation phase of mammalian voltage-activated Na(+) channels.

214 SCs generated a TTX (1 microm)-resistant voltage-activated Na(+) current (I(Na)) that had a peak

215 Voltage-activated Na+ channels in the primary sensory ne

216 The peak of transient component (NaT) of the voltage-activated Na+ current is also filtered more than

217 The opening and closing of voltage-activated Na+, Ca2+ and K+ (Kv) channels underli

218 ltage ramps revealed a non-inactivating, low-voltage-activated, nimodipine-sensitive current that was

219 itude and that they display distinct linear, voltage-activated or rectified current-voltage character

220 d inhibitory because of this increase in low-voltage activated outward currents.

221 type I hair cells is the expression of a low-voltage-activated outward rectifying K(+) current, IK,L

222 ed the calyx, and by the expression of a low-voltage-activated outward rectifying K(+) current, IK,L

223 In spinal motoneurons, dendrites have voltage-activated persistent inward currents that are fa

224 The large conductance Ca(2+)-and-voltage activated potassium channel (BK) is well-suited

225 elegans slo-1 large-conductance calcium and voltage-activated potassium (BK) channel gene, which con

226 Large-conductance Ca(2+)- and voltage-activated potassium (BK) channels are important

227 Large conductance calcium- and voltage-activated potassium (BK) channels are widely exp

228 e the role of large conductance calcium- and voltage-activated potassium (BK) channels in spontaneous

229 a-subunits of large conductance calcium- and voltage-activated potassium (BK) channels play an import

230 Here we use four-fold symmetric voltage-activated potassium (K(v)) channels as reporters

231 Voltage-activated potassium (K(v)) channels contain a ce

232 end of pore, as it has been established for voltage-activated potassium (K(V)) channels.

233 In voltage-activated potassium (Kv) channels, basic residue

234 rly understood when compared to those of the voltage-activated potassium (Kv) channels.

235 ssion of the large-conductance, calcium- and voltage-activated potassium (MaxiK) channel in the corti

236 The large conductance calcium- and voltage-activated potassium channel (BK channel) and its

237 The large conductance calcium- and voltage-activated potassium channel (BK(Ca)) is widely e

238 The large-conductance calcium- and voltage-activated potassium channel (BK) is a well-estab

239 in, the human large-conductance calcium- and voltage-activated potassium channel (BK), in a lipid env

240 on when transplanted from an archaebacterial voltage-activated potassium channel (KvAP) or voltage-se

241 rminus of the large conductance calcium- and voltage-activated potassium channel is an important dete

242 ifically in this area, including a number of voltage-activated potassium channel subunits.

243 Calcium- and voltage-activated potassium channels (BK) are regulated

244 Large conductance Ca(2+)- and voltage-activated potassium channels (BKCa) shape neuron

245 unanticipated action of COX-2 inhibitors on voltage-activated potassium channels and their physiolog

246 calcium-activated potassium channels and Kv2 voltage-activated potassium channels both regulate actio

247 Opposing regulation of these calcium- and voltage-activated potassium channels by cAMP- and cGMP-d

248 amplitudes were mediated extensively by low voltage-activated potassium channels containing the Kv1.

249 The Kv7 family (Kv7.1-7.5) of voltage-activated potassium channels contributes to the

250 ch residues are involved in this process for voltage-activated potassium channels, several different

251 Using available structures of TRPV1 and voltage-activated potassium channels, we engineered chim

252 smooth muscle cells express Kv7.4 and Kv7.5 voltage-activated potassium channels, which contribute t

253 ion is associated with altered physiology of voltage-activated potassium channels.

254 lancing the suppression of EPSP peaks by low voltage-activated potassium channels.

255 in proteins (Hv1 and Ci-VSP) into eukaryotic voltage-activated potassium channels.

256 A strong, low-voltage-activated potassium conductance (g(KL)) at the c

257 Interestingly, we also found a low-voltage-activated potassium conductance present at E18,

258 low input resistance and activation of a low-voltage-activated potassium conductance that are charact

259 uronal excitability is governed primarily by voltage-activated potassium conductances (K(VA)).

260 ing subthreshold synaptic integration: a low-voltage-activated potassium current (I(K-LVA)) and a hyp

261 A low voltage-activated potassium current, IKL, is found in au

262 rpolarization-activated cation current (Ih), voltage-activated potassium current, large-conductance c

263 SP (1 to 25 microM) also suppressed voltage-activated potassium currents (IK+) and calcium c

264 ligand for 30 min increased the amplitude of voltage-activated potassium currents 2-fold on average.

265 was accompanied by consistent reductions in voltage-activated potassium currents near the action pot

266 re associated with increased inactivation of voltage-activated potassium currents.

267 Voltage-activated proton (Hv1) channels are relatives of

268 The voltage-activated rGO was highly sensitive to NO2 with a

269 e development of chemiresistive sensors with voltage-activated sensitivity for the detection of CO co

270 Voltage-activated sodium (Na(v)) channels are crucial fo

271 s and is a vital step in the biosynthesis of voltage-activated sodium (Nav) channels.

272 precipitous, and complete internalization of voltage-activated sodium channel proteins from the plasm

273 ations of the SCN1A gene encoding a neuronal voltage-activated sodium channel.

274 high-frequency action potentials by blocking voltage-activated sodium channels in a use-dependent fas

275 te the action potential is conducted through voltage-activated sodium channels, and mutations of thes

276 cologically, revealing all of the major high-voltage activated subtypes: L-, N-, P/Q-, and R-type Ca(

277 indicated that T-type calcium channels (low-voltage activated T-channels) are potently inhibited by

278 molecule that has been shown to inhibit low-voltage activated T-type Ca(2+) channels (TCCs).

279 All three forms of recombinant low voltage-activated T-type Ca(2)(+) channels (Ca(v)3.1, Ca

280 has been considered electrically silent, low voltage-activated T-type Ca(2+) channels are assumed to

281 ent evidence that H2 S is a modulator of low voltage-activated T-type Ca(2+) channels, and discrimina

282 Low voltage-activated T-type Ca(v)3.2 calcium channels are e

283 enetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) i

284 nd in mice, secondarily elevate neuronal low-voltage-activated T-type calcium currents.

285 r calcium entry into T cells-through the low-voltage-activated T-type CaV3.1 calcium channel.

286 Calcium currents via low-voltage-activated T-type channels mediate burst firing,

287 between P/Q channels and Gem-insensitive low voltage-activated T-type channels, we identify a region

288 depolarized from -100 mV, inactivating, low voltage-activated (T-type channel-mediated) Ca2+ current

289 Although the presence of low-voltage-activated (T-type) Ca channels in nuclear neuron

290 (2+) channel subunit Ca(V)3.2 mediates a low voltage-activated (T-type) Ca(2+) current (I(CaT)) that

291 Low voltage-activated (T-type) Ca2+ channels are responsible

292 Low-voltage-activated (T-type) calcium channels are responsi

293 s oxide's selective inhibition of CaV3.2 low-voltage-activated (T-type) calcium channels in pain path

294 ACNA1H is a human gene encoding Ca(v)3.2 low-voltage-activated, T-type calcium channels associated wi

295 s wherein redox active recognition units are voltage-activated to give enhanced and highly specific r

296 After 24 h in NA, additional low-voltage activated transient Ca(2+) current developed who

297 ytes in noradrenaline for 24 h induced a low-voltage activated transient Ca(2+) current whose pharmac

298 In cac neurons, unexpectedly, voltage-activated transient K+ current I(A) is upregulat

299 -driven action potentials, because they lack voltage-activated transient Na(+) currents.

300 at 23 A resolution, for a member of the low voltage-activated voltage-gated calcium channel family,