ライフサイエンスコーパス: agatoxin

1 type Ca(2+) channels were blocked with omega-agatoxin.

2 The mu-agatoxins add voltage-sensitive sodium channel activity

3 ocytosis significantly in the first 60 s and Agatoxin affecting exocytosis only towards the end of 18

4 effects of omega-conotoxin (CTX) GVIA, omega-agatoxin (Aga) IVA, and the dihydropyridine nicardipine

5 (49 +/- 5%, Ctx-GVIA) or P-type (46 +/- 1%, Agatoxin) alone.

6 Our structural data show that the mu-agatoxins, although specific modifiers of sodium channel

7 toxin, heteropodatoxin-2, stromatoxin, omega-agatoxin, and isradipine.

8 r evidence for a one-to-one stoichiometry of agatoxin binding to calcium channels.

9 rescued the endocytotic activity blocked by agatoxin, but not the retrieval blocked by PAO.

10 dosomes by a mechanism that was inhibited by agatoxin, cadmium, staurosporine and FK506.

11 her omega-conotoxin GVIA (1 microM) or omega-agatoxin GIVA (200 nM).

12 While blockade with Agatoxin had no effects, Ctx-GVIA, Ctx-MVIIC and L-type

13 We report the solution structure of mu-agatoxin-I (mu-Aga-I) and model structures of the closel

14 The spider toxin omega-agatoxin IIIA (omega-Aga-IIIA) is a potent inhibitor of

15 Treatment with calcium ionophores overcame agatoxin inhibition in a calcium-dependent manner.

16 d model structures of the closely related mu-agatoxin-IV (mu-Aga-IV) which were isolated from venom o

17 Furthermore, omega-agatoxin IVA (0.1-1 microM) or omega-CTX MVIIC (0.1-1 mi

18 the amplitude of slow IPSPs, but both omega-agatoxin IVA (100 nM) and nicardipine (1-10 microM) were

19 mbination, omega-CTX GVIA (100 nM) and omega-agatoxin IVA (100 nM) inhibited the fast EPSP by 74 +/-

20 ted by either omega-CTX GVIA (100 nM), omega-agatoxin IVA (100 nM) or omega-CTX MVIIC (100 nM).

21 by omega-conotoxin GVIA (1 microM) and omega-agatoxin IVA (100 nM), respectively.

22 by the P-type calcium channel blocker omega-agatoxin IVA (100 nM).

23 rs omega-conotoxin GVIA (1 microM) and omega-agatoxin IVA (400 nM).

24 t P13-20, the current was inhibited by omega-agatoxin IVA (approximately 86%; IC50, approximately 1 n

25 ly blockable with low concentration of omega-agatoxin IVA (omega-Aga IVA) or synthetic funnel-web spi

26 The P/Q-type antagonist omega-agatoxin IVA (omega-Aga-IVA; 1-5 microM) blocked 10.4 +/

27 omega-conotoxin GVIA (omega-CgTx) and omega-agatoxin IVA (omega-AgTx) but was affected little by nif

28 e of P- and possibly Q-type VGCCs with omega-agatoxin IVA (up to 200 nM) both delayed (P < 0.05) and

29 +), or by blocking P/Q-type VGCCs with omega-agatoxin IVA also changes EPSC amplitude by reducing bot

30 a(2+) channels) but was unperturbed by omega-agatoxin IVA and omega-conotoxin GVIA (P/Q-type and N-ty

31 sed the peptides omega-conotoxin GVIA, omega-agatoxin IVA and omega-conotoxin MVIIC, singly and in co

32 Ca2+ channel current was inhibited by omega-agatoxin IVA at concentrations selective for P-type Ca2+

33 , and neither omega-conotoxin GVIA nor omega-agatoxin IVA blocked the potentiation of capsaicin-evoke

34 ry synapses was blocked by cadmium and omega-agatoxin IVA but was not affected by omega-conotoxin GVI

35 A-AM or decreasing calcium influx with omega-agatoxin IVA decreased the amount of asynchronous releas

36 ective P/Q-type Ca(2+) channel blocker omega-agatoxin IVa had no detectable effects, whereas both the

37 in GVIA and the P/Q-type Ca channel blocker -agatoxin IVA increased Ca(2+) signals in photoreceptors

38 The toxins omega-agatoxin IVa or omega-conotoxin MVIIC (after block of N-

39 blocked by the P/Q-channel antagonist omega-agatoxin IVA or the N-channel antagonist omega-conotoxin

40 nnels, nimodipine, omega-Conotoxin GVIA, and Agatoxin IVA partially suppressed DR-EPSCs, however, the

41 ng omega-conotoxins GVIA and MVIIC and omega-agatoxin IVA that block N-, Q-, and P-type channels, we

42 reversibly blocked by the spider toxin omega-Agatoxin IVA with an IC50 of 240-420 nM with no effect o

43 1 microM nifedipine) or P-type (200 nM omega-agatoxin IVA) VSCC.

44 calcium channel antagonist, and 200 nM omega-agatoxin IVA, a P-type calcium channel blocker.

45 Application of omega-conotoxin GVIA, omega-agatoxin IVA, and nimodipine to cultured cerebellar gran

46 annels-cadmium, omega-conotoxin MVIIC, omega-agatoxin IVA, and omega-agatoxin TK-blocked membrane ret

47 e of Ca2+ channel that is inhibited by omega-agatoxin IVA, like prototypical P-type channels, and by

48 several seconds and was slowly inhibited by agatoxin IVA, which blocks P/Q-type Ca2+ channels.

49 d no effect on nifedipine- (L-type) or omega-agatoxin IVA- (P-type) sensitive ICa.

50 Win55,212-2 (100 nM) inhibited both omega-agatoxin IVA- and omega-conotoxin GVIA-sensitive current

51 ission by the P/Q-type channel blocker omega-agatoxin IVA.

52 dipine but not omega-conotoxin GVIA or omega-agatoxin IVA.

53 sitive to the alpha1A channel blocker, omega-agatoxin IVA.

54 ne, but not by omega-conotoxin GVIA or omega-agatoxin IVA.

55 blocked by CdCl2 (100 muM, n = 5) and omega-agatoxin-IVA (100 nM, n = 3), nonselective and Cav2.1 Ca

56 SCs in terms of sensitivity to TTX and omega-agatoxin-IVA (a blocker of P-type calcium channels) and

57 high and low sensitivity to the spider omega-agatoxin-IVA (omega-Aga-IVA), using whole-cell recording

58 cid enhances), P/Q-type VDCC currents (omega-agatoxin-IVA and omega-conotoxin-MVIIC inhibit, but not

59 annel toxins (omega-Conotoxin-GVIA and omega-Agatoxin-IVA) to juvenile HMs substantially inhibited th

60 h omega-conotoxin-GVIA (omega-CgTx) or omega-agatoxin-IVA, the inhibition was reduced but not abolish

61 Additionally, the omega-agatoxin-IVA-insensitive current was unaffected in homoz

62 ferentiated PC12 cells also express an omega-agatoxin-IVA-sensitive (P/Q-type) component.

63 on, but did so by acting mainly on the omega-agatoxin-IVA-sensitive Ca2+ channels.

64 Although attenuated, the omega-agatoxin-IVA-sensitive current in homozygous leaner cell

65 ells from homozygous leaner mice, this omega-agatoxin-IVA-sensitive current was 65% smaller than in c

66 HVA currents were predominantly of the omega-agatoxin-IVA-sensitive P-type.

67 ium channels were blocked by Cd(2+) or omega-agatoxin-IVA.

68 ole-cell current was blocked by 100 nM omega-agatoxin-IVA.

69 was abolished after pretreatment with omega-agatoxin-IVA.

70 ak structural/functional homology with omega-agatoxin-IVA/B, the prototypic inhibitor of vertebrate P

71 t human AGRP was homologous to that of omega-agatoxin IVB except for an additional disulfide bond, C8

72 00%) by the P/Q-type calcium channel blocker agatoxin IVB, suggesting that P/Q-type calcium channels

73 e conclude that calcium influx through omega-agatoxin-sensitive channels plays a key role in signalin

74 The agatoxin-sensitive component of CA1 pyramidal cell sIPSC

75 type, isradipine-sensitive L-type, and omega-agatoxin-sensitive P/Q-type Ca(2+)-channels.

76 The P- and Q-type Ca2+ channel blocker omega-agatoxin TK (200 nM and 1 microM) and the R- and T-type

77 es show that the P/Q Ca2+ channel antagonist agatoxin TK (250 nm) abolished GABA release from PV+ bas

78 By contrast, omega-agatoxin TK (50 nM), a P/Q-type Ca2+ channel inhibitor,

79 t was insensitive to dihydropyridines, omega-agatoxin TK and omega-conotoxin MVIIC.

80 C-terminal end as the d-amino acid in omega-agatoxin TK from a spider, an unrelated peptide.

81 notoxin MVIIC, omega-agatoxin IVA, and omega-agatoxin TK-blocked membrane retrieval; selective inhibi

82 y the P/Q-type calcium channel blocker omega-agatoxin-TK (20 nM), by 51+/-10% (n=115 cells) by the N-

83 d calcium influx was also inhibited by omega-agatoxin-TK, a calcium channel blocker specific for Ca(v

84 These studies indicate that an omega-agatoxin-TK-sensitive, Ca(v)2.1-like calcium permeabilit