ライフサイエンスコーパス: TRPC3 channel

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 le transient receptor potential canonical-3 (TRPC3) channels.

8 pe 3 canonical transient receptor potential (TRPC3) channels.

9 Our data suggest the involvement of the TRPC3 channel acting together with TRPA1 to mediate CQ-i

10 ne canonical transient receptor potential 3 (TRPC3) channels activates a cation current (I(Cat)) in a

11 PKC activation totally blocked TRPC3 channel activation in response to OAG, and the act

12 state 13-acetate (PMA) inhibits OAG-mediated TRPC3 channel activation, suggesting that phosphorylatio

13 x2 also stabilizes TRPC3 proteins to enhance TRPC3 channel activity.

14 of transient receptor potential canonical 3 (TRPC3) channel activity exhibited resistance to Rho-medi

15 TRPC3 channels also provide negative feedback regulation

16 The TRPC3 channel, an intensively studied member of the wide

17 w mechanism for the gating of the ubiquitous TRPC3 channel and identify a key role for phospholipase

18 ted as a possible mechanism of activation of TRPC3 channels and a region in the C terminus of TRPC3 h

19 ospholipase C gamma-1-mediated activation of TRPC3 channels and also B cell adhesion to vascular cell

20 tosis regulates plasma membrane insertion of TRPC3 channels and contributes to carbachol-stimulation

21 ImmunoFRET indicated that cav-1, TRPC3 channels and IP(3)R1 are spatially co-localized in

22 ls were inhibited by intracellularly applied TRPC3 channel antibody.

23 We conclude that TRPC3 channels are activated independently of InsP(3)Rs

24 Because TRPC3 channels are inhibited after phosphorylation by PK

25 Last, TRPC3 channels are necessary for BDNF to increase dendri

26 How TRPC3 channels are opened is unknown, although it is wid

27 In conclusion, TRPC3 channels are present in renal fibroblasts and cont

28 Together, the results demonstrate that TRPC3 channels are required for the response to glucose

29 ansient receptor potential canonical type 3 (TRPC3) channels are involved in hypothalamic glucose det

30 These results identify the gene encoding TRPC3 channels as a MeCP2 target and suggest a potential

31 Importantly, direct activation of TRPC3 channels by diacylglycerol was also blocked by BTP

32 These data indicate that TRPC6 and TRPC3 channels can bind to Slo1, and this colocalization

33 In cerebellar Purkinje cells, TRPC3 channels cause the metabotropic glutamate receptor

34 rol replenishment re-established IP(3)R1 and TRPC3 channel close spatial proximity.

35 Cgamma1 (PLC-gamma1) binds to and regulates TRPC3 channels, components of agonist-induced Ca2+ entry

36 PKC inhibition resulted in decreased TRPC3 channel deactivation.

37 AF increases TRPC3 channel expression by causing NFAT-mediated downre

38 tivation that enhances constitutively active TRPC3 channels, forming an ultra-short substantia nigra

39 TRPC3 channel gating is independent of phospholipase C a

40 he Transient Receptor Potential Canonical 3 (TRPC3) channel have reduced necrosis and number of apopt

41 upling between IP(3)R1 and membrane-resident TRPC3 channels in arterial myocytes, leading to I(Cat) a

42 C-gamma (PLC-gamma) activated the expressed TRPC3 channels in both DT40w/t and DT40InsP(3)R-k/o cell

43 co-localizes SR IP(3)R1 and plasma membrane TRPC3 channels in close spatial proximity thereby enabli

44 pression systems, we examined whether native TRPC3 channels in Purkinje cells are a target for PKG or

45 Expression of TRPC3 channels in skeletal myocytes is up-regulated by n

46 Here, we show PMA-induced phosphorylation of TRPC3 channels in vivo.

47 of canonical transient receptor potential 3 (TRPC3) channel in allergen-induced airway disease (AIAD)

48 yl-2-acetyl-sn-glycerol (OAG) also activated TRPC3 channels independently of InsP(3)Rs.

49 Inhibition of TRPC3 channels induces hyperpolarization, decreases firi

50 Evidence indicates TRPC3 channels interact directly with intracellular inos

51 polar brush cells (UBCs), express functional TRPC3 channels; intriguingly, these cells are ablated in

52 Activation of TRPC3 channels is concurrent with inositol 1,4,5-trispho

53 hanism(s) involved in agonist-stimulation of TRPC3 channels is not yet known.

54 nflux from the transient receptor potential (TRPC3) channel is an important determinant of NFAT activ

55 Both TRPC3 channel isoforms were blocked with 2 mm Ca(2+), at

56 4-carboxylic acid prevents AIAD in mice, (2) TRPC3 channel KD and overexpression, respectively, block

57 at (1) intravenous or intranasal delivery of TRPC3 channel lentiviral shRNAs or blocker 1-[4-[(2,3,3-

58 thways, and lentiviral shRNA or inhibitor of TRPC3 channels may become novel and effective treatments

59 s resulted in successful M5 coupling to open TRPC3 channels mediated by PLC-beta.

60 at transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced malada

61 TRPC3 channels might constitute important therapeutic ta

62 In these cells TRPC3 channel opening requires stimulation of metabotrop

63 uded (1) intravenous injection of lentiviral TRPC3 channel or nonsilencing short hairpin ribonucleic

64 These data demonstrate that TRPC3 channels play important roles in ensuring the appr

65 The conclusions are that TRPC3 channels plays an essential role in AIAD via the P

66 r artery myocytes have similar properties to TRPC3 channel proteins and indicate that these proteins

67 sient receptor potential channel (TRPC)1 and TRPC3 channel proteins by short hairpin RNA reduces the

68 current was blocked by 3 microM BTP2, single TRPC3 channel recordings revealed persistent short openi

69 TRPC3 channels regulate cardiac fibroblast proliferation

70 , the receptor-induced mechanism to activate TRPC3 channels remains unclear.

71 both HEK293 cells and DT40 cells, TRPC5 and TRPC3 channel responses to PLC activation were highly an

72 protein-coupled M5 muscarinic receptors and TRPC3 channels resulted in successful M5 coupling to ope

73 IP(3)R1 and TRPC3 channel spatial localization was disrupted by Mbet

74 lectrocardiography showed that inhibition of TRPC3 channel suppressed transient A(1)AR-induced conduc

75 n HEK293 cells stably transfected with human TRPC3 channels, the actions of 2-APB to block carbachol-

76 at metabotropic glutamate receptors activate TRPC3 channels through the small GTP-binding protein Rho

77 tructural components that enable IP(3)R1 and TRPC3 channels to communicate locally are unclear.

78 65 clonal HEK293 cell line stably expressing TRPC3 channels, TRPC3-mediated Sr2+ entry activated by m

79 In the cerebellum, Purkinje cell TRPC3 channels underlie the slow excitatory postsynaptic

80 a non-store-operated pathway into the cells (TRPC3 channels), we find that other Ca(2+) entry mechani

81 e and carbachol-induced Sr(2+) entry through TRPC3 channels were both reversed at high agonist levels

82 TRPC3 channels were expressed in DT40 chicken B lymphocy

83 ere also inhibited when the tonically active TRPC3 channels were inhibited by intracellularly applied

84 2APB was specifically said to inhibit TRPC3 channels when activated through a phospholipase C-