ライフサイエンスコーパス: TRPC6 channel

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

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

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

4 xerts a powerful inhibitory action on native TRPC6 channels.

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

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

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

8 ectivity against muscarinic receptor-coupled TRPC6 channel activation.

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

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

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

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

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

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

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

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

17 TRPC6 channel activity is controlled by protein expressi

18 TRPC6 channel activity is enhanced via translocation to

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

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

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

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

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

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

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

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

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

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

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

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

31 ereas cone inner segments immunostained with TRPC6 channel antibodies.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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