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1 1) and D(5) receptor mRNAs and also mRNA for TRPC3 channels.
2 or-dependent I(Cat) activation that requires TRPC3 channels.
3 response to Gd3+, a competitive inhibitor of TRPC3 channels.
4 or a related G protein, phospholipase C and TRPC3 channels.
5 sed it in HEK293 cells that stably expressed TRPC3 channels.
6 xpression level on the mode of regulation of TRPC3 channels.
7 irect and involves D1 dopamine receptors and TRPC3 channels.
8 le transient receptor potential canonical-3 (TRPC3) channels.
9 pe 3 canonical transient receptor potential (TRPC3) channels.
11 ne canonical transient receptor potential 3 (TRPC3) channels activates a cation current (I(Cat)) in a
14 state 13-acetate (PMA) inhibits OAG-mediated TRPC3 channel activation, suggesting that phosphorylatio
16 of transient receptor potential canonical 3 (TRPC3) channel activity exhibited resistance to Rho-medi
19 w mechanism for the gating of the ubiquitous TRPC3 channel and identify a key role for phospholipase
20 ted as a possible mechanism of activation of TRPC3 channels and a region in the C terminus of TRPC3 h
21 ospholipase C gamma-1-mediated activation of TRPC3 channels and also B cell adhesion to vascular cell
22 tosis regulates plasma membrane insertion of TRPC3 channels and contributes to carbachol-stimulation
31 Canonical transient receptor potential 3 (TRPC3) channels are integral to the propagation of seizu
32 ansient receptor potential canonical type 3 (TRPC3) channels are involved in hypothalamic glucose det
33 These results identify the gene encoding TRPC3 channels as a MeCP2 target and suggest a potential
38 Cgamma1 (PLC-gamma1) binds to and regulates TRPC3 channels, components of agonist-induced Ca2+ entry
40 ur results are consistent with the idea that TRPC3 channels expressed by cerebral VSMCs contribute to
42 tivation that enhances constitutively active TRPC3 channels, forming an ultra-short substantia nigra
44 he Transient Receptor Potential Canonical 3 (TRPC3) channel have reduced necrosis and number of apopt
45 upling between IP(3)R1 and membrane-resident TRPC3 channels in arterial myocytes, leading to I(Cat) a
46 C-gamma (PLC-gamma) activated the expressed TRPC3 channels in both DT40w/t and DT40InsP(3)R-k/o cell
47 co-localizes SR IP(3)R1 and plasma membrane TRPC3 channels in close spatial proximity thereby enabli
48 pression systems, we examined whether native TRPC3 channels in Purkinje cells are a target for PKG or
51 of canonical transient receptor potential 3 (TRPC3) channel in allergen-induced airway disease (AIAD)
55 polar brush cells (UBCs), express functional TRPC3 channels; intriguingly, these cells are ablated in
58 nflux from the transient receptor potential (TRPC3) channel is an important determinant of NFAT activ
60 4-carboxylic acid prevents AIAD in mice, (2) TRPC3 channel KD and overexpression, respectively, block
61 at (1) intravenous or intranasal delivery of TRPC3 channel lentiviral shRNAs or blocker 1-[4-[(2,3,3-
62 thways, and lentiviral shRNA or inhibitor of TRPC3 channels may become novel and effective treatments
63 erefore, we hypothesize that cerebrovascular TRPC3 channels may contribute to seizure-induced IHR.
65 at transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced malada
68 uded (1) intravenous injection of lentiviral TRPC3 channel or nonsilencing short hairpin ribonucleic
72 r artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins
73 sient receptor potential channel (TRPC)1 and TRPC3 channel proteins by short hairpin RNA reduces the
74 current was blocked by 3 microM BTP2, single TRPC3 channel recordings revealed persistent short openi
77 both HEK293 cells and DT40 cells, TRPC5 and TRPC3 channel responses to PLC activation were highly an
78 protein-coupled M5 muscarinic receptors and TRPC3 channels resulted in successful M5 coupling to ope
81 lectrocardiography showed that inhibition of TRPC3 channel suppressed transient A(1)AR-induced conduc
82 n HEK293 cells stably transfected with human TRPC3 channels, the actions of 2-APB to block carbachol-
83 at metabotropic glutamate receptors activate TRPC3 channels through the small GTP-binding protein Rho
85 65 clonal HEK293 cell line stably expressing TRPC3 channels, TRPC3-mediated Sr2+ entry activated by m
87 a non-store-operated pathway into the cells (TRPC3 channels), we find that other Ca(2+) entry mechani
88 e and carbachol-induced Sr(2+) entry through TRPC3 channels were both reversed at high agonist levels
90 ere also inhibited when the tonically active TRPC3 channels were inhibited by intracellularly applied