ライフサイエンスコーパス: alpha-latrotoxin

1 uring affinity chromatography on immobilized alpha-latrotoxin.

2 han that induced either by lanthanum ions or alpha-latrotoxin.

3 tic transmission as a candidate receptor for alpha-latrotoxin.

4 muscular junction, similar to the effects of alpha-latrotoxin.

5 ding sites on neurexins for dystroglycan and alpha-latrotoxin.

6 of chromaffin cells to channel formation by alpha-latrotoxin.

7 o the cloned Ca(2+)-independent receptor for alpha-latrotoxin.

8 t as receptors for the excitatory neurotoxin alpha-latrotoxin.

9 even span transmembrane protein, which binds alpha-latrotoxin.

10 RL-2 is a functionally competent receptor of alpha-latrotoxin.

11 20 are not required for the interaction with alpha-latrotoxin.

12 of exocytosis in intact chromaffin cells by alpha-latrotoxin.

13 uroligins, neurexophilins, dystroglycans and alpha-latrotoxins.

14 CIRL (the calcium-independent receptor of alpha-latrotoxin), a neuronal cell surface receptor impl

15 on function: both proteins are receptors for alpha-latrotoxin, a component of black widow spider veno

16 alpha-Latrotoxin, a component of black widow spider veno

17 alpha-latrotoxin, a component of black widow spider veno

18 Poisoning with alpha-latrotoxin, a neurotoxic protein from black widow

19 alpha-Latrotoxin, a potent excitatory neurotoxin, binds

20 alpha-Latrotoxin, a potent neurotoxin from black widow s

21 re we report that PTPvarsigma is a target of alpha-latrotoxin, a strong stimulator of neuronal exocyt

22 We postulate that alpha-latrotoxin acts intracellularly in triggering rele

23 hanism with neurexins as receptors, in which alpha-latrotoxin acts like a Ca(2+) ionophore, and (2) a

24 e fusion complex, copurifies with CIRL on an alpha-latrotoxin affinity column and forms stable comple

25 alpha-Latrotoxin (alpha-LT) potently enhances both "spon

26 alpha-Latrotoxin (alpha-LT) potently enhances quantal re

27 alpha-Latrotoxin (alpha-LT), a potent excitatory neuroto

28 oM LaCl3 and 10 mM K+, or to 2-5 nM purified alpha-latrotoxin (alpha-LTX) were also measured.

29 alpha-Latrotoxin (alpha-Ltx), a component of black widow

30 diated extracellular Ca(2+) influx, although alpha-latrotoxin also consistently triggered mobilizatio

31 It appears that CIRL-2 can also bind alpha-latrotoxin, although its affinity to the toxin is

32 Our data show that receptor binding by alpha-latrotoxin and activation of phospholipase C do no

33 consists of the entire N-terminal domain of alpha-latrotoxin and becomes protease sensitive after ly

34 Therefore, receptor binding by alpha-latrotoxin and stimulation of phospholipase C are

35 cells was triggered by KCl depolarization or alpha-latrotoxin and was inhibited by tetanus toxin and

36 situ assay for protein kinase C reveals that alpha-latrotoxin augments the activation of protein kina

37 are also susceptible to the toxic effects of alpha-latrotoxin because of the presence of CIRL-2, a lo

38 d by depletion of neurosecretory vesicles by alpha-latrotoxin, becoming everlasting in approximately

39 ains of PTPvarsigma are not required for the alpha-latrotoxin binding and secretory response triggere

40 alpha-Latrotoxin binding to the calcium-independent rece

41 ion mutants indicates that the high affinity alpha-latrotoxin-binding site is located within residues

42 alpha-Latrotoxin binds to the cell adhesion-like extrace

43 In stimulating exocytosis, alpha-latrotoxin binds to two distinct families of neuro

44 active; therefore, neurexins and CL1 recruit alpha-latrotoxin but are not themselves involved in exoc

45 tosis caused by the black widow spider venom alpha-latrotoxin, but their endogenous ligands and funct

46 r studies reveal that the spider venom toxin alpha-latrotoxin can trigger a sustained discharge of qu

47 system is the primary target of low doses of alpha-latrotoxin, cells of other tissues are also suscep

48 The calcium-independent receptor of alpha-latrotoxin (CIRL), a neuronal cell surface recepto

49 nding to the calcium-independent receptor of alpha-latrotoxin (CIRL), an orphan neuronal G protein-co

50 ssion of the calcium-independent receptor of alpha-latrotoxin (CIRL), which is a second high affinity

51 ding to the calcium-independent receptor for alpha-latrotoxin (CIRL-1), a putative G-protein-coupled

52 from PC12 cells was triggered by high K+ or alpha-latrotoxin, co-transfection of all synaptogyrins w

53 At alpha-latrotoxin concentrations below 500 pM, channel fo

54 e sensitivity of the cells to the effects of alpha-latrotoxin, demonstrating that this protein is fun

55 Profound release of glutamate with alpha-latrotoxin did cause a small, but reproducible, re

56 ith CIRL/latrophilins as receptors, in which alpha-latrotoxin directly stimulates the transmitter rel

57 a(2+)-dependent release mechanism induced by alpha-latrotoxin does not require any of these component

58 Furthermore, in the absence of Ca(2+), alpha-latrotoxin does not stimulate polyphosphoinositide

59 The neurotoxin alpha-latrotoxin elicits spontaneous exocytosis of neuro

60 Previous studies have demonstrated that alpha-latrotoxin first binds to two high-affinity recept

61 isingly, two distinct neuronal receptors for alpha-latrotoxin have been described: CIRL/latrophilin 1

62 trotoxin (LtxWT) that is as active as native alpha-latrotoxin in triggering synaptic release of gluta

63 nce of TTX and Cd2+, or after application of alpha-latrotoxin, indicated a site of action for galanin

64 Furthermore, alpha-latrotoxin induced vesicle release at adapted syna

65 mbrane segment left of seven, supported both alpha-latrotoxin-induced calcium uptake in HEK293 cells

66 Alpha-latrotoxin induces neurotransmitter release by sti

67 Our data suggest that alpha-latrotoxin inserts into the presynaptic plasma mem

68 alpha-Latrotoxin interaction with a fusion construct com

69 alpha-Latrotoxin interaction with CIRL-1 transiently exp

70 alpha-Latrotoxin interaction with CIRL-1 transiently ove

71 iguration of the patch clamp, we report that alpha-latrotoxin interaction with the CIRL receptor on t

72 The neurotoxic action of alpha-latrotoxin involves extracellular binding to its h

73 alpha-Latrotoxin is a large protein toxin (120 kDa) that

74 Alpha-latrotoxin is a potent neurotoxin that triggers sy

75 alpha-Latrotoxin is a potent stimulator of neurosecretio

76 Alpha-latrotoxin is thought to trigger exocytosis by bin

77 Thus, alpha-latrotoxin is unique among neurotoxins, because it

78 e its insertion across the membrane and that alpha-latrotoxin itself controls the conductance propert

79 previously to induce a complement-dependent alpha-latrotoxin-like effect on the murine motor endplat

80 alpha-Latrotoxin (LTX) stimulates massive neurotransmitt

81 Alpha-latrotoxin (LTX) stimulates vesicular exocytosis b

82 n (NMJ) that closely resembles the effect of alpha-latrotoxin (LTx).

83 We have now produced recombinant alpha-latrotoxin (LtxWT) that is as active as native alp

84 hat non-selective cation channels induced by alpha-latrotoxin may be a by-product of membrane inserti

85 bilization of intracellular Ca(2+) relied on alpha-latrotoxin-mediated Na(+) influx and was blocked b

86 While alpha-latrotoxin mobilizes intracellular Ca(2+) stores t

87 All four alpha-latrotoxin mutants were found to be unable to trig

88 We have also generated three alpha-latrotoxin mutants with substitutions in conserved

89 mbrane insertion of the N-terminal domain of alpha-latrotoxin occurs spontaneously, independently of

90 Here, we investigate the actions of alpha-latrotoxin on neuroendocrine nerve endings that em

91 ggering bursts of quantal events either with alpha-latrotoxin or with high-frequency trains of presyn

92 ing K(+) solution, the excitatory neurotoxin alpha-latrotoxin, or the Ca(2+)-ionophore ionomycin), th

93 s glycoprotein, and with neurexin 1alpha, an alpha-latrotoxin receptor structurally unrelated to CIRL

94 was previously described as a high affinity alpha-latrotoxin receptor that binds the toxin only in t

95 ddition, CL1 serves a specialized role as an alpha-latrotoxin receptor that does not require G-protei

96 oxin (CIRL), which is a second high affinity alpha-latrotoxin receptor that may be the major mediator

97 This suggests that as an alpha-latrotoxin receptor, CL1 recruits alpha-latrotoxin

98 n G protein-coupled receptor and presumptive alpha-latrotoxin receptor, controls the numbers of a spe

99 surprising given its presumptive role as an alpha-latrotoxin receptor.

100 We propose that alpha-latrotoxin receptors recruit toxin to facilitate i

101 emonstrate that neurexins indeed function as alpha-latrotoxin receptors that are at least as potent a

102 pha- and beta-neurexins represent autonomous alpha-latrotoxin receptors that are regulated by alterna

103 igma resemble two other previously described alpha-latrotoxin receptors, neurexin and CIRL.

104 protein-coupled receptors that are auxiliary alpha-latrotoxin receptors, suggesting that they may hav

105 Thus, alpha-latrotoxin represents an unusual example of the ne

106 Quantal events were elicited by high K+ or alpha-latrotoxin, required extracellular Ca2+, and were

107 Stimulation of neurotransmitter release by alpha-latrotoxin requires its binding to the calcium-ind

108 the Ca(2+)-independent release mechanism by alpha-latrotoxin requires the synaptic SNARE-proteins sy

109 Furthermore, alpha-latrotoxin reverses the inhibitory effect of injec

110 n receptor that may be the major mediator of alpha-latrotoxin's effects.

111 lyphosphoinositide-specific phospholipase C. alpha-Latrotoxin specifically enhances ATP-dependent sec

112 n-induced calcium uptake in HEK293 cells and alpha-latrotoxin-stimulated secretion when expressed in

113 Thus, alpha-latrotoxin stimulates Ca(2+)-dependent exocytosis

114 xin with neurexin I alpha cannot explain how alpha-latrotoxin stimulates neurotransmitter release in

115 alpha-Latrotoxin stimulates neurotransmitter release pro

116 We conclude that alpha-latrotoxin stimulates secretion in permeabilized c

117 cells, CIRL-2 increases their sensitivity to alpha-latrotoxin stimulation but also inhibits Ca2+-regu

118 e by K+ treatment, or application of NMDA or alpha-latrotoxin, synaptic N-cadherin dimerizes and beco

119 additional receptor-independent activity of alpha-latrotoxin that is selectively inhibited by the Lt

120 Receptor-bound alpha-latrotoxin then inserts into the presynaptic plasm

121 are receptors for the excitatory neurotoxin alpha-latrotoxin; this toxin competes with dystroglycan

122 eceptors, probably to amplify recruitment of alpha-latrotoxin to active sites.

123 To examine how binding of alpha-latrotoxin to CL1 triggers exocytosis, we used PC1

124 tussis toxin has no effect on the ability of alpha-latrotoxin to enhance secretion, suggesting that n

125 Thus receptors recruit alpha-latrotoxin to its point of action without activati

126 s an alpha-latrotoxin receptor, CL1 recruits alpha-latrotoxin to target membranes without participati

127 Binding of alpha-latrotoxin to these receptors does not in itself t

128 -signaling was as active as wild type CL1 in alpha-latrotoxin-triggered exocytosis.

129 A similar sensitization to alpha-latrotoxin was observed with different splice vari

130 ansfected into PC12 cells, their response to alpha-latrotoxin was sensitized dramatically.

131 Using affinity chromatography on immobilized alpha-latrotoxin, we have purified a novel 29 kDa protei

132 ial amplitude that was partially reversed by alpha-latrotoxin (which depletes neurosecretory vesicles

133 t manner by a direct intracellular action of alpha-latrotoxin, while exocytosis of catecholamines req

134 etry, we demonstrate that the interaction of alpha-latrotoxin with CIRL-1 produces a high conductance

135 ts, which include the 467-770 residues, bind alpha-latrotoxin with low affinity suggesting the import

136 Therefore, the interaction of alpha-latrotoxin with neurexin I alpha cannot explain ho

137 We now demonstrate that incubation of alpha-latrotoxin with synaptosomes at 0 degrees C result

138 Interaction of alpha-latrotoxin with these receptors stimulated secreti

139 Elucidation of precisely how alpha-latrotoxin works is likely to provide major insigh