ライフサイエンスコーパス: Maxi-K channel

1 K(Ca)1.1 gene is a likely candidate for the maxi-K channel.

2 usly reported values for the skeletal muscle maxi-K channel.

3 s: intermediate conductance IK1 channels and maxi-K channels.

4 the alpha- and beta-subunits of human brain maxi-K channels.

5 ants, all of these chimeras inhibited single maxi-K channels.

6 Kv1.3 channels and on current through single maxi-K channels.

7 ctive and uniquely Ca++-sensitive openers of maxi-K channels.

8 chanism for PKG-Ialpha-induced activation of maxi-K channels.

9 rge-conductance, Ca(2+)-activated potassium (maxi-K) channel.

10 corresponding increase in prevalence of the maxi-K+ channel.

11 de-out patches by Ca 2+(i) and is the type I maxi-K+ channel.

12 may explain why PiTX-K alpha does not block maxi-K+ channels.

13 le dysfunction by a direct oxidant effect on maxi K(+) channels.

14 Large conductance, Ca(2+)-activated K(+) (maxi-K ) channel activity was recorded in excised, insid

15 st, these same NxTX mutants had no effect on maxi-K channel activity with estimated Kd values exceedi

16 functional, cell-based assay for identifying Maxi-K channel agonists was established and used to scre

17 ge conductance, calcium-activated potassium (maxi-K) channel (alpha and beta subunits) and beta2-adre

18 To confirm the genetic identity of the maxi-K channel and to probe its specific roles, we studi

19 r studies demonstrate that estrogen binds to maxi-K channels and may directly regulate channel expres

20 al and pharmacological footprints of IK1 and maxi-K channels and their molecular identities were conf

21 ge conductance, calcium-activated potassium (maxi-K) channels and voltage-gated potassium (Kv1.3) cha

22 changes in cGKI isoforms immunoisolated with Maxi-K channels; and (4) a large increase in cGKIbeta mR

23 Although Maxi-K channels appear to indirectly mediate the relaxan

24 uctance Ca(2+)-dependent potassium (K(Ca) or maxi K) channels are composed of a pore-forming alpha su

25 indings verify that multiple isoforms of the maxi-K channel are present in the mouse myometrium and a

26 Our findings show that the maxi-K channels are critical for the regulatory volume d

27 igh-conductance calcium-activated potassium (Maxi-K) channels are present in smooth muscle where they

28 conductance Ca(2+)-activated K(+) channels (maxi-K channels) are known to modulate uterine activity

29 est that the large extracellular loop of the maxi-K channel beta subunit has a restricted conformatio

30 ect low affinity binding of estradiol to the maxi-K channel but not to its accessory beta1-subunit, a

31 e association of beta 1 subunits with native maxi-K channels by monitoring the kinetics of ChTX block

32 gh-conductance, calcium-activated potassium (Maxi-K) channel C-terminal domain in channel tetrameriza

33 Activation of Maxi-K channels causes smooth muscle hyperpolarization a

34 used a decrease in ChTX-S10A block times for maxi-K channel complexes of alpha+beta 1 subunits but no

35 rotid acinar cells from these animals lacked maxi-K channels, confirming their genetic identity.

36 Whole-cell maxi-K channel currents and protein expression were atte

37 large-conductance, Ca2+-activated potassium (maxi-K) channel, demonstrated efficacy in in vivo stroke

38 of the large-conductance, calcium-activated (maxi-K) channel, exhibits a unique, asymmetric distribut

39 The maxi-K channel from bovine aortic smooth muscle consists

40 nder low external ionic strength conditions, maxi-K channels from smooth muscle showed ChTX-S10A bloc

41 vel insight into cell-specific regulation of maxi-K channel function.

42 channel, and could play an important role in maxi-K channel function.

43 Here we demonstrate that the maxi-K channel functions as an estrogen-binding protein

44 s of the high-conductance Ca2+-activated K+ (maxi-K) channel has been achieved in COS-1 cells.

45 l properties of Ca(2+)-activated K(+) (BK or Maxi-K) channels have been investigated in presynaptic m

46 ctance calcium-activated potassium channels (maxi-K channels) have an essential role in the control o

47 pared and evaluated as openers of the cloned maxi-K channel hSlo expressed in Xenopus laevis oocytes

48 These were used to reconstitute Maxi K channels in the 100- and 200-microm diameter pore

49 Membrane expression of endogenous maxi-K channels in cultured vascular smooth muscle cells

50 We have recently shown that the IK1 and maxi-K channels in parotid salivary gland acinar cells a

51 xamine ChTX-S10A blocking kinetics of single maxi-K channels in planar lipid bilayers from smooth mus

52 de of single channels, and they suggest that maxi-K channels in skeletal muscle do not contain a beta

53 Ca2+-activated K+ (Maxi-K) channels in VSMCs from AHR showed reduced activa

54 n-blocked and -unblocked durations of single maxi-K channels incorporated into planar lipid bilayers.

55 regulation was observed in excised patches, maxi-K channel inhibition by hypoxia does not require so

56 at key microscopic interactions at the toxin-maxi-K channel interface may be absent.

57 ar coupling of beta2-adrenergic receptors to maxi-K channels involves endogenous cAMP-PK.

58 aordinary specificity of NxTX for Kv1.3 over maxi-K channels is controlled, in part, by the toxin alp

59 ctance Ca(2+)-activated K(+) channels (BK or maxi-K channels) is controlled by a Ca(2+)-sensor, forme

60 viously shown that the transcript of a human maxi-K channel isoform (mK44) is expressed predominantly

61 hannel protein or differential expression of maxi-K channel isoforms that vary in their Ca(2+) and vo

62 s of the high conductance Ca2+-activated K+ (maxi-K) channel leads to a 50-fold increase in the affin

63 Maxi-K channel-mediated current evoked by depolarization

64 ion of iberiotoxin or paxilline, blockers of Maxi-K channels, mimicked NGF treatment and sensitized n

65 onductance Ca(2+)- and voltage-activated K+ (maxi-K) channels modulate human myometrial smooth muscle

66 ed and evaluated as activators of the cloned maxi-K channel mSlo expressed in Xenopus laevis oocytes

67 e data demonstrate that the domain(s) in the Maxi-K channel necessary for formation of tetramers, coa

68 logical coupling between beta2 receptors and maxi-K channels occurs by the cAMP-PK mediated phosphory

69 maxi-K = 158%) was identified as the optimal maxi-K channel opener.

70 We found that NGF reduces Maxi-K channel opening by decreasing the activity of nif

71 Its maxi-K channel opening properties were consistent with i

72 iomers of (+/-)-8c were synthesized, and the maxi-K channel-opening properties were shown to depend o

73 K current suppression is due to reduction of maxi-K channel protein or differential expression of max

74 Immunoblot analyses show an increase of maxi-K channel protein throughout gestation.

75 suggest that studies of ChTX block of single maxi-K channels provide an approach for characterizing s

76 condarily, the calcium-sensitive activity of Maxi-K channels, rendering sympathetic neurons electrica

77 together, suggest that direct activation of Maxi-K channels represents a mechanism to be explored fo

78 An insert that increases the maxi-K channel sensitivity to voltage and Ca(2+) is pres

79 data indicate that functional coassembly of maxi-K channel subunits can be obtained in a transient e

80 Only one gene Slo is known to encode maxi-K channels, which are sensitive to both membrane po