ライフサイエンスコーパス: TRPC6 channel

1 cts were partially dependent on CFTR and the TRPC6 channel.

2 d that PAR1 activation increases [Ca2+]i via TRPC6 channels.

3 t promotes externalization and activation of TRPC6 channels.

4 T1R and in the absence of angiotensinogen or TRPC6 channels.

5 hoinositide-3-kinase-dependent exocytosis of TRPC6 channels.

6 hed data, we have shown that PPZ potentiates TRPC6 channels.

7 RB) domains are present in myocyte TRPC3 and TRPC6 channels.

8 xerts a powerful inhibitory action on native TRPC6 channels.

9 nce of TRPC5 translocation on the opening of TRPC6 channels.

10 waves via a background Ca(2+) influx through TRPC6 channels.

11 ly depends on the activity of Ca2+ permeable TRPC6 channels.

12 channels, Ca(2+) -activated K(+) channels or TRPC6 channels.

13 he transient receptor potential canonical 6 (TRPC6) channel.

14 Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2+)]i concentrati

15 However, HF-induced TRPC6 channel activation stimulated nuclear translocatio

16 ectivity against muscarinic receptor-coupled TRPC6 channel activation.

17 These data show that TRPC6 channel activity at the slit diaphragm is essentia

18 ng II)-evoked whole-cell cation currents and TRPC6 channel activity by over 90%.

19 ed on the ability of Klotho to down-regulate TRPC6 channel activity confirm the importance of these r

20 inhibitor, chelerythrine, markedly increased TRPC6 channel activity evoked by 1-100 nm Ang II and blo

21 l currents but potentiated by about six-fold TRPC6 channel activity evoked by 1-100 nm Ang II in outs

22 inositol-4,5-bisphosphate (PIP(2)) on native TRPC6 channel activity in freshly dispersed rabbit mesen

23 osolic surface inhibited 10 nm Ang II-evoked TRPC6 channel activity in inside-out patches.

24 Ca(2+) (0 [Ca(2+)](o)) 100 nm Ang II induced TRPC6 channel activity in outside-out patches.

25 rs, our findings suggest that attenuation of TRPC6 channel activity in pathologic VSMCs could be a ra

26 TRPC6 channel activity is controlled by protein expressi

27 TRPC6 channel activity is enhanced via translocation to

28 an inverse relationship between TRPC1/C5 and TRPC6 channel activity suggesting that TRPC1/C5 inhibits

29 nditions (10 mm BAPTA), 10 nm Ang II-induced TRPC6 channel activity was increased by about five-fold

30 Our data demonstrate that independent of TRPC6 channel activity, the physical interaction between

31 llular epitope, also increased Ang II-evoked TRPC6 channel activity.

32 l activity suggesting that TRPC1/C5 inhibits TRPC6 channel activity.

33 cked the inhibitory action of [Ca(2+)](i) on TRPC6 channel activity.

34 on a potential drug target to interfere with TRPC6 channel activity.

35 mAChRs and remain stably associated with the TRPC6 channels after M1 mAChRs and PKC have disassociate

36 TRPC6 channels also play a role in the regulation of sur

37 study examined the effect of H(2)O(2) on the TRPC6 channel and its underlying mechanisms using a TRPC

38 BP12 binding blocks the dephosphorylation of TRPC6 channels and the disassociation of M1 mAChRs, with

39 binds alpha2-3-sialyllactose, down-regulates TRPC6 channels, and exerts protection against stress-ind

40 a multiprotein complex containing M1 mAChRs, TRPC6 channels, and protein kinase C (PKC).

41 ereas cone inner segments immunostained with TRPC6 channel antibodies.

42 families with hereditary FSGS, and TRPC5 and TRPC6 channels are now known as the Ca(2+) influx pathwa

43 on-dependent pathway not only stimulates the TRPC6 channel by itself but also sensitizes the channels

44 MTx-4 peptide also blocked the activation of TRPC6 channels by either receptor-induced PLC activation

45 Phosphorylation of the TRPC6 channels by PKC is required for the binding of FKB

46 Gain-of-function mutations in the human TRPC6 channel cause autosomal-dominant focal segmental g

47 ia canonical transient receptor potential 6 (TRPC6) channels caused increased intracellular Ca(2+) fl

48 ly, we demonstrated that upregulation of the TRPC6 channel contributes to proliferation of PASMCs iso

49 We conclude that TRPC1 and TRPC6 channels cooperate with TRPV4 channels to mediate

50 These findings suggest that TRPC6 channel-dependent [Ca(2+)]i elevation and the ensu

51 These results show that TRPC6 channels evoked by Ang II are inhibited by TRPC1/C

52 lglycerol- or receptor-activated recombinant TRPC6 channels, exhibiting approximately 12- and 5-fold

53 Here, we report that sKlotho can inhibit TRPC6 channels expressed in cells lacking endogenous FGF

54 ed transient receptor potential canonical 6 (TRPC6) channel expression and ATP-induced calcium influx

55 of canonical transient receptor potential 6 (TRPC6) channels facilitated contractile differentiation

56 Together, these results show that activated TRPC6 channels form the center of a dynamic multiprotein

57 These results suggested that TRPC6 channels have limited Ca(2+) permeability relative

58 The mechanosensing properties of TRPC6 channels highly expressed in smooth muscle cells a

59 vide strong support for a role played by the TRPC6 channel in evoking the mechanoreflex.

60 C7 subunits, while OAG activates a homomeric TRPC6 channel in mesenteric artery myocytes.

61 GsMTx-4, in particular, inhibits TRPC6 channels in addition to Piezo 2.

62 mmary, this paper defines a specific role of TRPC6 channels in CXCR2-induced intermediary chemotaxis.

63 nels can associate with endogenous TRPC3 and TRPC6 channels in differentiated cells of a podocyte cel

64 ctivity as a red light-operated activator of TRPC6 channels in HEK293 cells.

65 The knockout of TRPC6 channels in murine neutrophils led to a strongly i

66 demonstrate functional localization of TRPC3/TRPC6 channels in the apical region of polarized epithel

67 normal mice is mediated by downregulation of TRPC6 channels in the heart.

68 ted both 2 pS TRPC1/C5 channels and 15-45 pS TRPC6 channels in the same outside-out patches.

69 he transient receptor potential canonical 6 (TRPC6) channel in evoking the mechanical component of th

70 receptor potential canonical type isoform 6 (TRPC6) channels in cardiomyocytes and glomerular podocyt

71 le canonical transient receptor potential-6 (TRPC6) channels in podocytes.

72 ent receptor potential-canonical, subtype 6 (TRPC6), channels in neuronal PC12D cells.

73 the effects of GsMTx-4 are mediated through TRPC6 channel inhibition and that the role played by Pie

74 sarcolemmal background Ca(2+) influx via the TRPC6 channel is responsible for SR Ca(2+) overload and

75 ng of FKBP12, calcineurin, and calmodulin to TRPC6 channels is blocked by the following: 1) inhibitio

76 Activation of TRPC6 channels is correlated with the formation of a mul

77 ise mechanism through which lysoPC activates TRPC6 channels is not known, but calmodulin (CaM) contri

78 and IP(3)-induced vasoconstriction, whereas TRPC6 channel knockdown had no effect.

79 BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 channel knockdown.

80 te canonical transient receptor potential 6 (TRPC6) channels leading to inhibition of endothelial cel

81 es canonical transient receptor potential 6 (TRPC6) channels, leading to a prolonged increase in intr

82 disease conditions may modify intracellular TRPC6 channel localization and activity, which further c

83 Current evidence also suggests that blocking TRPC6 channels may be of therapeutic benefit in idiopath

84 cytes, a rise in extracellular zinc promotes TRPC6 channel-mediated calcium entry but not altered int

85 showed that H(2)O(2) significantly increased TRPC6 channel open probability and whole-cell currents.

86 gen, transient receptor potential channel 6 (TRPC6) channels, or several subtypes of the voltage-gate

87 In this study, we demonstrate that the TRPC6 channels play a pronounced role in CXCR2-mediated

88 We propose that TRPC6 channels play an essential role in regulation of m

89 Evidence suggests that Piezo 2 and TRPC6 channels play important roles in evoking the mecha

90 ow that enhancing vesicular insertion of the TRPC6 channel to the plasma membrane may represent a gen

91 hat stimulation of ASM causes recruitment of TRPC6 channels to caveolae, thus allowing for Ca(2+) inf

92 ound that overexpression of gain-of-function TRPC6 channel variants is cytotoxic in cultured cells.

93 tan on PASMCs involves the downregulation of TRPC6 channels via a mechanism possibly independent of e

94 These data indicate that H(2)O(2) activates TRPC6 channels via modification of thiol groups of intra

95 The human TRPC6 channel was expressed in human embryonic kidney (H

96 NMDA mobilization of TRPC6 channels was blocked by concurrent treatment with

97 TRPC6 channels were identified by quadruple-labelled (Di

98 PAF increased the caveolar abundance of TRPC6 channels, which was similarly blocked by ASM inhib

99 he transient receptor potential canonical 6 (TRPC6) channel, which is activated by mechanical stimuli

100 ) with that of TRPC3, resulted in a chimeric TRPC6 channel with Epo responsiveness similar to TRPC3.

101 tes the intriguing possibility that blocking TRPC6 channels within the podocyte may translate into lo

102 sponse to PAF, in that they directly blocked TRPC6 channels without interfering with their PAF-induce

103 lculations reveal that even 90% reduction of TRPC6 channels would allow depolarization sufficient to