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1 or channels, but unlike that of any reported TRPC channel.
2 d depolarization was dependent on a putative TRPC channel.
3 ic conditions, most likely by suppression of TRPC channels.
4 of unknown function that is conserved in all TRPC channels.
5  to study the expression and localization of TRPC channels.
6 DAG sensitivity is a distinctive hallmark of TRPC channels.
7 nflicting reports from expression studies of TRPC channels.
8 pensatory changes in the expression of other TRPC channels.
9 he mechanism of action of 2APB in inhibiting TRPC channels.
10 re of the type previously envisioned for the TRPC channels.
11 dulin (CaM) contributes to the regulation of TRPC channels.
12 ectrum of regulatory phenotypes of expressed TRPC channels.
13 rved in TRPC6 and TRPC7 and in part in other TRPC channels.
14 c agonist, normalized the function of SK and TRPC channels.
15 aled the expression of all seven subtypes of TRPC channels.
16 ensitivity between homomeric and heteromeric TRPC channels.
17 expressed STIM1 and Orai1 as well as several TRPC channels.
18 ptin exert their actions in POMC neurons via TRPC channels.
19 intracellular Ca2+ wave activation of SK and TRPC channels.
20 ly affected receptor-activated WT and mutant TRPC channels.
21 here Homer1 interacts with Orai1 and various TRPC channels.
22 rent, suggesting the possible involvement of TRPC channels.
23 e for either STIM1 or Orai1 in signalling of TRPC channels.
24 ient receptor potential canonical subfamily (TRPC) channels.
25 n of canonical transient receptor potential (TRPC) channels.
26 sing canonical transient receptor potential (TRPC) channels.
27 ion with plasma membrane (PM) calcium (e.g., TRPC) channels.
28 bits transient receptor potential canonical (TRPC) channels.
29 ing the transient receptor potential cation (TRPC) channels.
30  the transient receptor potential canonical (TRPC) channels.
31 TRPC channels and specific downregulation of TRPC channels 1 and 5 resulted in suppression of CCL2-in
32  the transient receptor potential canonical (TRPC) channel 3, functioning as receptor-operated channe
33 These results suggest that immunophilins are TRPC channel accessory proteins that play an important r
34  glutamate receptors but also by heteromeric TRPC channels activated by metabotropic glutamate recept
35 3)R N-terminal region that can interact with TRPC channels activated I(Cat).
36  cardiac dysfunction that is associated with TRPC channel activation and alterations in membrane pote
37 ore depletion; however, the role of STIM1 in TRPC channel activation by receptor stimulation is not f
38 eveal similar regulation of SOC, I(crac) and TRPC channel activation by STIM1.
39       These data demonstrate a redundancy of TRPC channel activation mechanisms by widely different a
40  and canonical transient receptor potential (TRPC) channel activation, but functional signaling mecha
41 hly isolated glomeruli showed enhanced basal TRPC channel activity in the STZ-SS rats, and increased
42 vidence that Ins(1,4,5)P(3) modulates native TRPC channel activity through removal of the inhibitory
43 or-mediated intracellular Ca2+ waves, SK and TRPC channel activity.
44   Additionally, the interaction between each TRPC channel and the PDZ-containing protein, INAD (prote
45 onal link between the operation of expressed TRPC channels and endogenous SOC activity.
46                                     Blocking TRPC channels and specific downregulation of TRPC channe
47 starting point to understand the function of TRPC channels and their possible roles in pathologies.
48 a Jak2-PI3 kinase-PLCgamma pathway activates TRPC channels, and TRPC1, 4, and 5 appear to be the key
49 ngs in the absence or presence of functional TRPC channel antibodies.
50                                        Thus, TRPC channels appear to be activated by mechanisms depen
51                       These data showed that TRPC channels are essential for in vitro tubulogenesis,
52  induce muscular dystrophy in vivo, and that TRPC channels are key disease initiators downstream of t
53                                      Because TRPC channels are linked to neuronal growth cone extensi
54                                        Thus, TRPC channels are necessary mediators of pathologic card
55                                              TRPC channels are postulated to be important in the func
56               These results demonstrate that TRPC channels are present in nerve terminals and provide
57                                     Although TRPC channels are thought to be tetramers, the actual su
58      Transient receptor potential canonical (TRPC) channels are a group of nonselective cation channe
59  the canonical transient receptor potential (TRPC) channels are an important pathway for Ca2+ entry d
60      Canonical transient receptor potential (TRPC) channels are Ca(2+)-permeable nonselective cation
61      Transient receptor potential canonical (TRPC) channels are Ca(2+)-permeable nonselective cation
62      Transient receptor potential canonical (TRPC) channels are G protein-coupled receptor operated c
63      Transient receptor potential canonical (TRPC) channels are highly homologous, nonselective catio
64 tive transient receptor potential canonical (TRPC) channels are impaired in CA3 pyramidal neurons of
65      Transient receptor potential canonical (TRPC) channels are important mediators of Ca(2+)-depende
66      Canonical transient receptor potential (TRPC) channels are opened by classical signal transducti
67      Canonical transient receptor potential (TRPC) channels are widely expressed in the brain and pla
68      Canonical transient receptor potential (TRPC) channels are widely expressed throughout the nervo
69                  These investigations reveal TRPC channels as critical mediators of inflammatory bone
70 ires transient receptor potential canonical (TRPC) channels as SKF-96365, but not the NMDA receptor a
71 ted that 2APB inhibits agonist activation of TRPC channels because of its ability to act as a membran
72 tant treatment of Podo-GC-A KO mice with the TRPC channel blocker SKF96365 markedly ameliorated album
73 eral transient receptor potential canonical (TRPC) channel blocker BTP2 and the selective TRPC3 inhib
74  by Na(+)-Ca(2+) exchanger (NCX) inhibitors, TRPC channel blockers and the phospholipase C inhibitor
75                                          The TRPC channel blockers SKF96365 (1-[beta-[3-(4-methoxyphe
76       The sustained component was blocked by TRPC channel blockers.
77 also transient receptor potential canonical (TRPC) channels, but it has remained unclear whether STIM
78 ore-operated channels, 2APB seems to inhibit TRPC channels by a direct mechanism not involving IP3 re
79 l mechanism involving negative regulation of TRPC channels by calcium entering through the channels.
80  the canonical transient receptor potential (TRPC) channels by developing stable human embryonic kidn
81       Together, these findings indicate that TRPC channels can function as STIM1-dependent and STIM1-
82                                   Mammalian (TRPC) channels can form hetero-oligomeric channels in vi
83                     Activation of this novel TRPC channel cascade by lysoPC, resulting in the inhibit
84                                Both types of TRPC channels colocalize with Slo1 in podocytes and in h
85  the most versatile member and forms various TRPC channel combinations but also unique channels with
86 ero-oligomeric channels in vitro, but native TRPC channel complexes have not been identified to date.
87  and the subsequent formation of heteromeric TRPC channel complexes with reduced calcium permeability
88 onal canonical transient receptor potential (TRPC) channels composed of members of the TRPC1/4/5 subg
89 ough transient receptor potential canonical (TRPC) channels contributes to post-MI structural and fun
90 These results demonstrate that expression of TRPC channels correlates with the progression of the cel
91                                              TRPC channels could be an unsuspected but critical molec
92 olvement of TRPC activation was confirmed by TRPC channel current recordings in the absence or presen
93                                        Thus, TRPC channels emerge as novel mediators of BDNF-mediated
94                          Ca2+ influx through TRPC channels expressed after MI activates pathological
95 tween two distinct vasoconstrictor-activated TRPC channels expressed in the same native VSMCs.
96 is TRPC current corresponds to the increased TRPC channel expression noted in hearts of mice subjecte
97                          Among the classical TRPC channels, expression of three N-terminal splice var
98 pids regulate TRPC3 and other members of the TRPC channel family are not well understood.
99              Based on sequence homology, the TRPC channel family can be divided into two major subgro
100  the canonical transient receptor potential (TRPC) channel family, TRPC4.
101 channels, which increases the versatility of TRPC channel function and their role in receptor-stimula
102 erning transient receptor potential channel (TRPC) channel function begun to emerge, with an essentia
103 be relevant to diseases affected by aberrant TRPC channel functions.
104 ent selective pharmacological inhibitors for TRPC channels has limited delineation of the roles of th
105 However, the influence of chronic hypoxia on TRPC channels has not been determined.
106 lian canonical transient receptor potential (TRPC) channels has been the focus of intense study.
107 n of canonical transient receptor potential (TRPC) channels have often yielded conflicting results.
108 tors (IP(3)Rs) interact with plasma membrane TRPC channels; however, at present there is no evidence
109                     However, the role of the TRPC channel in neurodegeneration is not known.
110 ss the expression and function of endogenous TRPC channels in A7r5 smooth muscle cells.
111 conferred by TRPC1 proteins to native single TRPC channels in acutely isolated mesenteric artery VSMC
112              However, the regulatory role of TRPC channels in chemoattractant receptor-mediated signa
113 tead show that M2 phototransduction requires TRPC channels in conjunction with T-type voltage-gated c
114 ines), through trafficking and activation of TrpC channels in cultured hippocampal neurons.
115      Our results suggest important roles for TRPC channels in ENS physiology and neuronal regulation
116      To determine the function of individual TRPC channels in erythropoietin modulation of calcium in
117 ay is yet to be established, the presence of TRPC channels in glomus cells and sensory nerves of the
118 ssembly mechanism increases the diversity of TRPC channels in mammalian brain and may generate novel
119 urthermore, transgene-mediated inhibition of TRPC channels in mice dramatically reduced calcium influ
120 ebral cortex and suggest a possible role for TRPC channels in mnemonic processes.
121  Study mechanisms by which IP(3)Rs stimulate TRPC channels in myocytes of resistance-size cerebral ar
122 chanical stimulation cooperatively activated TRPC channels in ommatidia.
123  PLC are essential for the activation of the TRPC channels in photoreceptor cells.
124 ally relevant endocannabinoid that activates TRPC channels in photoreceptor cells.
125      This study examines the localization of TRPC channels in polarized epithelial cells and demonstr
126    The association of immunophilins with the TRPC channels in rat brain lysates could be displaced by
127 PC channel, revealing an unexpected role for TRPC channels in regulating nicotine-dependent behavior.
128        These results define a novel role for TRPC channels in the control of cardiac growth, and sugg
129 findings clearly demonstrate a novel role of TRPC channels in the protection of neurons against Tat t
130               Mechanistically, inhibition of TRPC channels in transgenic mice or in cultured neonatal
131 ere, we report a novel mechanism for opening TRPC channels in which TRPC6 activation initiates a casc
132 t of transient receptor potential canonical (TRPC) channels in CCL2-mediated neuroprotection.
133 e of transient receptor potential canonical (TRPC) channels in PDGF-BB-mediated proliferation.
134 n our experiments, AC1903 inhibited multiple TRPC channels including TRPC3, TRPC4, TRPC5, TRPC6, TRPC
135 s of transient receptor potential canonical (TRPC) channels, including TRPC1.
136            Altogether, our findings reveal a TRPC channel-independent role of P2X4 channels as mechan
137 n of transient receptor potential canonical (TRPC) channels induces Ca(2+) entry, which is essential
138 ve of this study is to better understand how TRPC channels influence cardiomyocyte calcium signaling.
139 lcineurin inhibitor cyclosporine, and by the TRPC channel inhibitor 1-[2-(4-methoxyphenyl)-2-[3-(4-me
140 eneral TRP channel blocker), BTP2 (a general TRPC channel inhibitor), and pyrazole-3 (a selective TRP
141                             The nonselective TrpC channel inhibitors SKF96365 and 2-APB or targeted k
142 t DAG-mediated PKC-independent activation of TRPC channels is highly subtype-specific.
143 nce for a direct interaction of DAG with the TRPC channels is lacking, mutagenesis studies have ident
144 5)P(2) regulation of TRPV1-4 as well as some TRPC channels is more complex, involving both positive a
145 rmeable transient receptor potential cation (TRPC) channel is predominantly expressed in the brain, w
146                                          The TRPC channels may mediate some of these conductances sin
147 mester placentas, and that in human placenta TRPC channels may underlie this entry mechanism.
148                  These results indicate that TRPC channels mediate the muscarinic receptor-induced sl
149 hile classical transient receptor potential (TRPC) channel mediate receptor-operated Ca(2+) entry (RO
150 ned, transient receptor potential canonical (TRPC) channels mediate a significant portion of the rece
151 the putative transient receptor potential C (TRPC) channels mediate the activation of a subpopulation
152 SKF96365, an inhibitor of store-operated and TRPC channel-mediated Ca(2+) entry.
153 ar Ca2+ concentration ([Ca2+]i), whereas the TRPC channel-mediated depolarization required both a sma
154 its regulation of cAMP, modulates I-SK and I-TRPC channel-mediated ionic currents that we have shown
155 ion of intraocular pressure, suggesting that TRPC channels might play a neuroprotective role during m
156  to address the impact of the absence of all TRPC channels on gene expression.
157                        However, postsynaptic TRPC channel opening by the PI3K-PLC signalling pathway
158  and canonical transient receptor potential (TRPC) channel opening.
159 support the hypothesis that OA-NO2 activates TRPC channels other than the TRPV1 and TRPA1 channels al
160                                              TRPC channel overexpression may be partially responsible
161 To determine subunit arrangement, individual TRPC channel pairs were heterologously expressed in Sf9
162 l (TRP) channels indicate the involvement of TRPC channels, possibly TRPC5 and TRPC1.
163  the canonical transient receptor potential (TRPC) channel protein TRPC5, in addition to STIM1 and Or
164  if mammalian FKBP12 or FKBP52 interact with TRPC channel proteins.
165 ide in this region is conserved in mammalian TRPC channel proteins.
166  the canonical transient receptor potential (TRPC) channel proteins.
167 s to canonical transient receptor potential (TRPC) channel proteins.
168 ever, how intracellular pH affects mammalian TRPC channels remains obscure.
169          The subunit composition of neuronal TRPC channels remains uncertain because of conflicting d
170                         We also propose that TRPC channels represent appealing targets for epilepsy t
171 dependence and independence of WT and mutant TRPC channels, respectively.
172                                  Blockage of TRPC channels resulted in suppression of both CCL2-media
173 that such a defect can be rescued by a human TRPC channel, revealing an unexpected role for TRPC chan
174 vered about physiological roles of mammalian TRPC channels since the time of their discovery.
175 a nonselective cation current reminiscent of TRPC channels subjected to pressure overload.
176 n granule cells from mice deficient for both TRPC channel subtypes 1 and 4, whereas the deletion of e
177  control by PKC and DAG of the activation of TRPC channel subtypes is likely the basis of a spectrum
178              Here, we established mutants of TRPC channels that could not be activated by STIM1 but w
179          TRP and TRPL are the canonical TRP (TRPC) channels that are regulated by light stimulation o
180                     In contrast to all other TRPC channels, the PLC product diacylglycerol (DAG) is n
181 lamp electrophysiology that Ang II activates TRPC channels; then using confocal calcium imaging we de
182 he activation of neuronal FcgammaRI triggers TRPC channels through the Syk-PLC-IP(3) pathway and that
183 e findings demonstrate a novel mechanism for TRPC channels to mediate NF-kappaB activation in endothe
184                          The contribution of TRPC channels to osteoclastogenesis was examined using B
185 e to immunoreceptor activation that utilizes TRPC channels to specify the initiation site of the Ca(2
186 late transient receptor potential canonical (TRPCs) channels to control cytosolic calcium equilibria
187  leads to the opening of the light-sensitive TRPC channels (TRP and TRPL) remains unresolved.
188                             A sperm-specific TRPC channel, TRP-3, is required for fertilization.
189 e of transient receptor potential canonical (TRPC) channels TRPC3 and TRPC6 and their modulation by p
190                                    Two other TRPC channels, TRPL and TRPgamma, are expressed in photo
191 n situ hybridization, and modulation of both TrpC channels was reconstituted in HEK293 (human embryon
192  Ca(2+) signaling, including STIM1 and other TRPC channels, was not altered.
193 eas most studies have examined overexpressed TRPC channels, we used molecular, biochemical, and elect
194             Significantly, WT but not mutant TRPC channels were inhibited by scavenging STIM1 with Or
195                          Importantly, mutant TRPC channels were robustly activated by receptor stimul
196  the transient receptor potential canonical (TRPC) channels, which are activated by the endoplasmic r
197 alcium flux was decreased upon inhibition of TRPC channels with SAR7334, SKF 96365, clemizole hydroch
198 HEK) 293T cells transiently coexpressing the TRPC channels with Slo1.

 
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