ライフサイエンスコーパス: TRPC channel

1 or channels, but unlike that of any reported TRPC channel.

2 d depolarization was dependent on a putative TRPC channel.

3 of unknown function that is conserved in all TRPC channels.

4 to study the expression and localization of TRPC channels.

5 nflicting reports from expression studies of TRPC channels.

6 pensatory changes in the expression of other TRPC channels.

7 he mechanism of action of 2APB in inhibiting TRPC channels.

8 re of the type previously envisioned for the TRPC channels.

9 ectrum of regulatory phenotypes of expressed TRPC channels.

10 here Homer1 interacts with Orai1 and various TRPC channels.

11 c agonist, normalized the function of SK and TRPC channels.

12 aled the expression of all seven subtypes of TRPC channels.

13 ic conditions, most likely by suppression of TRPC channels.

14 expressed STIM1 and Orai1 as well as several TRPC channels.

15 ptin exert their actions in POMC neurons via TRPC channels.

16 DAG sensitivity is a distinctive hallmark of TRPC channels.

17 intracellular Ca2+ wave activation of SK and TRPC channels.

18 ly affected receptor-activated WT and mutant TRPC channels.

19 rent, suggesting the possible involvement of TRPC channels.

20 dulin (CaM) contributes to the regulation of TRPC channels.

21 e for either STIM1 or Orai1 in signalling of TRPC channels.

22 ient receptor potential canonical subfamily (TRPC) channels.

23 n of canonical transient receptor potential (TRPC) channels.

24 sing canonical transient receptor potential (TRPC) channels.

25 the transient receptor potential canonical (TRPC) channels.

26 TRPC channels and specific downregulation of TRPC channels 1 and 5 resulted in suppression of CCL2-in

27 the transient receptor potential canonical (TRPC) channel 3, functioning as receptor-operated channe

28 These results suggest that immunophilins are TRPC channel accessory proteins that play an important r

29 glutamate receptors but also by heteromeric TRPC channels activated by metabotropic glutamate recept

30 3)R N-terminal region that can interact with TRPC channels activated I(Cat).

31 ore depletion; however, the role of STIM1 in TRPC channel activation by receptor stimulation is not f

32 eveal similar regulation of SOC, I(crac) and TRPC channel activation by STIM1.

33 These data demonstrate a redundancy of TRPC channel activation mechanisms by widely different a

34 and canonical transient receptor potential (TRPC) channel activation, but functional signaling mecha

35 hly isolated glomeruli showed enhanced basal TRPC channel activity in the STZ-SS rats, and increased

36 vidence that Ins(1,4,5)P(3) modulates native TRPC channel activity through removal of the inhibitory

37 or-mediated intracellular Ca2+ waves, SK and TRPC channel activity.

38 Additionally, the interaction between each TRPC channel and the PDZ-containing protein, INAD (prote

39 onal link between the operation of expressed TRPC channels and endogenous SOC activity.

40 Blocking TRPC channels and specific downregulation of TRPC channe

41 a Jak2-PI3 kinase-PLCgamma pathway activates TRPC channels, and TRPC1, 4, and 5 appear to be the key

42 Thus, TRPC channels appear to be activated by mechanisms depen

43 These data showed that TRPC channels are essential for in vitro tubulogenesis,

44 induce muscular dystrophy in vivo, and that TRPC channels are key disease initiators downstream of t

45 Because TRPC channels are linked to neuronal growth cone extensi

46 Thus, TRPC channels are necessary mediators of pathologic card

47 TRPC channels are postulated to be important in the func

48 These results demonstrate that TRPC channels are present in nerve terminals and provide

49 Although TRPC channels are thought to be tetramers, the actual su

50 the canonical transient receptor potential (TRPC) channels are an important pathway for Ca2+ entry d

51 Canonical transient receptor potential (TRPC) channels are Ca(2+)-permeable nonselective cation

52 Transient receptor potential canonical (TRPC) channels are Ca(2+)-permeable nonselective cation

53 Transient receptor potential canonical (TRPC) channels are G protein-coupled receptor operated c

54 tive transient receptor potential canonical (TRPC) channels are impaired in CA3 pyramidal neurons of

55 Transient receptor potential canonical (TRPC) channels are important mediators of Ca(2+)-depende

56 Canonical transient receptor potential (TRPC) channels are opened by classical signal transducti

57 Canonical transient receptor potential (TRPC) channels are widely expressed in the brain and pla

58 Canonical transient receptor potential (TRPC) channels are widely expressed throughout the nervo

59 ires transient receptor potential canonical (TRPC) channels as SKF-96365, but not the NMDA receptor a

60 ted that 2APB inhibits agonist activation of TRPC channels because of its ability to act as a membran

61 tant treatment of Podo-GC-A KO mice with the TRPC channel blocker SKF96365 markedly ameliorated album

62 eral transient receptor potential canonical (TRPC) channel blocker BTP2 and the selective TRPC3 inhib

63 by Na(+)-Ca(2+) exchanger (NCX) inhibitors, TRPC channel blockers and the phospholipase C inhibitor

64 The TRPC channel blockers SKF96365 (1-[beta-[3-(4-methoxyphe

65 The sustained component was blocked by TRPC channel blockers.

66 also transient receptor potential canonical (TRPC) channels, but it has remained unclear whether STIM

67 ore-operated channels, 2APB seems to inhibit TRPC channels by a direct mechanism not involving IP3 re

68 l mechanism involving negative regulation of TRPC channels by calcium entering through the channels.

69 the canonical transient receptor potential (TRPC) channels by developing stable human embryonic kidn

70 Together, these findings indicate that TRPC channels can function as STIM1-dependent and STIM1-

71 Mammalian (TRPC) channels can form hetero-oligomeric channels in vi

72 Activation of this novel TRPC channel cascade by lysoPC, resulting in the inhibit

73 Both types of TRPC channels colocalize with Slo1 in podocytes and in h

74 the most versatile member and forms various TRPC channel combinations but also unique channels with

75 ero-oligomeric channels in vitro, but native TRPC channel complexes have not been identified to date.

76 and the subsequent formation of heteromeric TRPC channel complexes with reduced calcium permeability

77 onal canonical transient receptor potential (TRPC) channels composed of members of the TRPC1/4/5 subg

78 ough transient receptor potential canonical (TRPC) channels contributes to post-MI structural and fun

79 These results demonstrate that expression of TRPC channels correlates with the progression of the cel

80 TRPC channels could be an unsuspected but critical molec

81 Thus, TRPC channels emerge as novel mediators of BDNF-mediated

82 Ca2+ influx through TRPC channels expressed after MI activates pathological

83 tween two distinct vasoconstrictor-activated TRPC channels expressed in the same native VSMCs.

84 is TRPC current corresponds to the increased TRPC channel expression noted in hearts of mice subjecte

85 Among the classical TRPC channels, expression of three N-terminal splice var

86 Based on sequence homology, the TRPC channel family can be divided into two major subgro

87 the canonical transient receptor potential (TRPC) channel family, TRPC4.

88 channels, which increases the versatility of TRPC channel function and their role in receptor-stimula

89 erning transient receptor potential channel (TRPC) channel function begun to emerge, with an essentia

90 ent selective pharmacological inhibitors for TRPC channels has limited delineation of the roles of th

91 However, the influence of chronic hypoxia on TRPC channels has not been determined.

92 lian canonical transient receptor potential (TRPC) channels has been the focus of intense study.

93 n of canonical transient receptor potential (TRPC) channels have often yielded conflicting results.

94 tors (IP(3)Rs) interact with plasma membrane TRPC channels; however, at present there is no evidence

95 However, the role of the TRPC channel in neurodegeneration is not known.

96 ss the expression and function of endogenous TRPC channels in A7r5 smooth muscle cells.

97 conferred by TRPC1 proteins to native single TRPC channels in acutely isolated mesenteric artery VSMC

98 However, the regulatory role of TRPC channels in chemoattractant receptor-mediated signa

99 ines), through trafficking and activation of TrpC channels in cultured hippocampal neurons.

100 Our results suggest important roles for TRPC channels in ENS physiology and neuronal regulation

101 To determine the function of individual TRPC channels in erythropoietin modulation of calcium in

102 ay is yet to be established, the presence of TRPC channels in glomus cells and sensory nerves of the

103 ssembly mechanism increases the diversity of TRPC channels in mammalian brain and may generate novel

104 urthermore, transgene-mediated inhibition of TRPC channels in mice dramatically reduced calcium influ

105 ebral cortex and suggest a possible role for TRPC channels in mnemonic processes.

106 Study mechanisms by which IP(3)Rs stimulate TRPC channels in myocytes of resistance-size cerebral ar

107 This study examines the localization of TRPC channels in polarized epithelial cells and demonstr

108 The association of immunophilins with the TRPC channels in rat brain lysates could be displaced by

109 PC channel, revealing an unexpected role for TRPC channels in regulating nicotine-dependent behavior.

110 These results define a novel role for TRPC channels in the control of cardiac growth, and sugg

111 findings clearly demonstrate a novel role of TRPC channels in the protection of neurons against Tat t

112 Mechanistically, inhibition of TRPC channels in transgenic mice or in cultured neonatal

113 ere, we report a novel mechanism for opening TRPC channels in which TRPC6 activation initiates a casc

114 t of transient receptor potential canonical (TRPC) channels in CCL2-mediated neuroprotection.

115 e of transient receptor potential canonical (TRPC) channels in PDGF-BB-mediated proliferation.

116 s of transient receptor potential canonical (TRPC) channels, including TRPC1.

117 Altogether, our findings reveal a TRPC channel-independent role of P2X4 channels as mechan

118 n of transient receptor potential canonical (TRPC) channels induces Ca(2+) entry, which is essential

119 ve of this study is to better understand how TRPC channels influence cardiomyocyte calcium signaling.

120 lcineurin inhibitor cyclosporine, and by the TRPC channel inhibitor 1-[2-(4-methoxyphenyl)-2-[3-(4-me

121 eneral TRP channel blocker), BTP2 (a general TRPC channel inhibitor), and pyrazole-3 (a selective TRP

122 The nonselective TrpC channel inhibitors SKF96365 and 2-APB or targeted k

123 t DAG-mediated PKC-independent activation of TRPC channels is highly subtype-specific.

124 nce for a direct interaction of DAG with the TRPC channels is lacking, mutagenesis studies have ident

125 rmeable transient receptor potential cation (TRPC) channel is predominantly expressed in the brain, w

126 The TRPC channels may mediate some of these conductances sin

127 mester placentas, and that in human placenta TRPC channels may underlie this entry mechanism.

128 These results indicate that TRPC channels mediate the muscarinic receptor-induced sl

129 ned, transient receptor potential canonical (TRPC) channels mediate a significant portion of the rece

130 the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation

131 ar Ca2+ concentration ([Ca2+]i), whereas the TRPC channel-mediated depolarization required both a sma

132 its regulation of cAMP, modulates I-SK and I-TRPC channel-mediated ionic currents that we have shown

133 ion of intraocular pressure, suggesting that TRPC channels might play a neuroprotective role during m

134 However, postsynaptic TRPC channel opening by the PI3K-PLC signalling pathway

135 support the hypothesis that OA-NO2 activates TRPC channels other than the TRPV1 and TRPA1 channels al

136 TRPC channel overexpression may be partially responsible

137 To determine subunit arrangement, individual TRPC channel pairs were heterologously expressed in Sf9

138 l (TRP) channels indicate the involvement of TRPC channels, possibly TRPC5 and TRPC1.

139 the canonical transient receptor potential (TRPC) channel protein TRPC5, in addition to STIM1 and Or

140 if mammalian FKBP12 or FKBP52 interact with TRPC channel proteins.

141 ide in this region is conserved in mammalian TRPC channel proteins.

142 the canonical transient receptor potential (TRPC) channel proteins.

143 s to canonical transient receptor potential (TRPC) channel proteins.

144 The subunit composition of neuronal TRPC channels remains uncertain because of conflicting d

145 dependence and independence of WT and mutant TRPC channels, respectively.

146 Blockage of TRPC channels resulted in suppression of both CCL2-media

147 that such a defect can be rescued by a human TRPC channel, revealing an unexpected role for TRPC chan

148 vered about physiological roles of mammalian TRPC channels since the time of their discovery.

149 a nonselective cation current reminiscent of TRPC channels subjected to pressure overload.

150 n granule cells from mice deficient for both TRPC channel subtypes 1 and 4, whereas the deletion of e

151 control by PKC and DAG of the activation of TRPC channel subtypes is likely the basis of a spectrum

152 Here, we established mutants of TRPC channels that could not be activated by STIM1 but w

153 In contrast to all other TRPC channels, the PLC product diacylglycerol (DAG) is n

154 lamp electrophysiology that Ang II activates TRPC channels; then using confocal calcium imaging we de

155 he activation of neuronal FcgammaRI triggers TRPC channels through the Syk-PLC-IP(3) pathway and that

156 e findings demonstrate a novel mechanism for TRPC channels to mediate NF-kappaB activation in endothe

157 e to immunoreceptor activation that utilizes TRPC channels to specify the initiation site of the Ca(2

158 late transient receptor potential canonical (TRPCs) channels to control cytosolic calcium equilibria

159 leads to the opening of the light-sensitive TRPC channels (TRP and TRPL) remains unresolved.

160 A sperm-specific TRPC channel, TRP-3, is required for fertilization.

161 e of transient receptor potential canonical (TRPC) channels TRPC3 and TRPC6 and their modulation by p

162 Two other TRPC channels, TRPL and TRPgamma, are expressed in photo

163 n situ hybridization, and modulation of both TrpC channels was reconstituted in HEK293 (human embryon

164 Ca(2+) signaling, including STIM1 and other TRPC channels, was not altered.

165 eas most studies have examined overexpressed TRPC channels, we used molecular, biochemical, and elect

166 Significantly, WT but not mutant TRPC channels were inhibited by scavenging STIM1 with Or

167 Importantly, mutant TRPC channels were robustly activated by receptor stimul

168 the transient receptor potential canonical (TRPC) channels, which are activated by the endoplasmic r

169 alcium flux was decreased upon inhibition of TRPC channels with SAR7334, SKF 96365, clemizole hydroch

170 HEK) 293T cells transiently coexpressing the TRPC channels with Slo1.