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

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

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

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

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

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

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

10 20 are not required for the interaction with alpha-latrotoxin.

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

12 uroligins, neurexophilins, dystroglycans and alpha-latrotoxins.

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

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

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

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

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

18 alpha-Latrotoxin, a potent excitatory neurotoxin, binds

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 alpha-Latrotoxin binding to the calcium-independent rece

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 The neurotoxin alpha-latrotoxin elicits spontaneous exocytosis of neuro

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

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

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

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

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

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

65 Alpha-latrotoxin induces neurotransmitter release by sti

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

67 alpha-Latrotoxin interaction with a fusion construct com

68 alpha-Latrotoxin interaction with CIRL-1 transiently exp

69 alpha-Latrotoxin interaction with CIRL-1 transiently ove

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

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

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

73 Alpha-latrotoxin is a potent neurotoxin that triggers sy

74 alpha-Latrotoxin is a potent stimulator of neurosecretio

75 Alpha-latrotoxin is thought to trigger exocytosis by bin

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

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

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

79 alpha-Latrotoxin (LTX) stimulates massive neurotransmitt

80 Alpha-latrotoxin (LTX) stimulates vesicular exocytosis b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 alpha-Latrotoxin stimulates neurotransmitter release pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Interaction of alpha-latrotoxin with these receptors stimulated secreti

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