ライフサイエンスコーパス: mastoparan

1 he rise in [Ca2+]i and cell death induced by mastoparan.

2 esponsible for the death of these neurons by mastoparan.

3 on and this response was further enhanced by mastoparan.

4 ating that PI4KIIalpha is a direct target of mastoparan.

5 s, TNF-alpha, or IL-1beta was insensitive to mastoparan.

6 ening induced by higher doses of HgCl(2) and mastoparan.

7 Mastoparan (10(-8), 10(-6) M) elicited pial artery dilat

8 d for mastoparan-7 but the inactive analogue mastoparan-17 had no effect on pial artery diameter.

9 The inactive analog mastoparan-17 had no effect on release.

10 response to incubation of erythrocytes with mastoparan 7 (10 micromol/l), an activator of G(i).

11 i) expression and ATP release in response to mastoparan 7 are impaired, which is consistent with the

12 The administration of mastoparan 7, an activator of pertussis toxin-sensitive

13 Similar results were observed for mastoparan-7 but the inactive analogue mastoparan-17 had

14 1 microg/ml) exposure blocked mastoparan and mastoparan-7 vasodilation.

15 is toxin sensitive G protein, mastoparan and mastoparan-7, and the role of PKC dependent O(-)(2) gene

16 ar loop and the G protein activating peptide mastoparan-7, failed to promote uncoupling from Galpha(o

17 Mastoparan, a 14-residue peptide, stimulates GDP/GTP exc

18 Mastoparan, a hormone receptor-mimetic peptide isolated

19 We have recently reported that mastoparan, a peptide toxin isolated from wasp venom, in

20 Mastoparan, a tetradecapeptide component of wasp venom,

21 ed following mast cell stimulation either by mastoparan, a wasp venom secretagogue, or by the physiol

22 or indirectly, PR were chromatographed on a mastoparan affinity column.

23 (i) signaling with epinephrine or wasp venom mastoparan also inhibited invasion and migration of the

24 Mastoparan also stimulated PI4KIIalpha immunoprecipitate

25 tion of either activated Goalpha subunits or mastoparan) also inhibited migration in a Ca2+-dependent

26 Melittin and mastoparan, amphiphilic pore-forming peptides like the M

27 Mastoparan, an activator of G protein-coupled receptor k

28 We find that mastoparan, an activator of G(i) and mast cells, stimula

29 Ca2+-ionophore A23187, and when treated with mastoparan, an inducer of the MPT in rat liver mitochond

30 Mas7, an active mastoparan analog known to stimulate Gi proteins, was fo

31 sulin release by other modulators, including mastoparan and activators of protein kinase C, is conser

32 Stimulation of release by mastoparan and augmentation of release by glucose were u

33 om CaCl(2) plus 5 microm HgCl(2) or 1 microm mastoparan and by 200 microm CaCl(2) alone.

34 lin (1 microM), or the calmodulin inhibitors mastoparan and calmidazolium (5 microM), did not alter t

35 tion due to receptor-mimetic ligands such as mastoparan and compound 48/80.

36 Both mastoparan and M7, at concentrations known to invoke sec

37 rtussis toxin (1 microg/ml) exposure blocked mastoparan and mastoparan-7 vasodilation.

38 rs of a pertussis toxin sensitive G protein, mastoparan and mastoparan-7, and the role of PKC depende

39 Previous studies examining mastoparan and related peptides and their ability to act

40 nt target of the wasp venom tetradecapeptide mastoparan and that different mechanisms of activation o

41 , and postmitochondrial phases by tamoxifen, mastoparan, and cytochrome c, respectively, allowing a f

42 toward phosphatidylcholine vesicles, but the mastoparans are more sensitive to the effect of anionic

43 ediated MAPK phosphorylation in macrophages, mastoparan blunted IL-1R-associated kinase-1 kinase acti

44 ed by the heterotrimeric G protein activator mastoparan, but not by its inactive analogue Mas-17.

45 diolabelled model peptides, somatostatin and mastoparan, by cross-linking.

46 Polybasic secretagogues such as mastoparan, compound 48/80, substance P, and somatostati

47 tivity of each membrane pool, as well as the mastoparan-dependent activities, thereby demonstrating t

48 that the GTP-dependent signal underlying the mastoparan effect acts at a "distal site" in stimulus-se

49 To identify the proteins that bind to mastoparan either directly or indirectly, PR were chroma

50 The kinetics of dye efflux induced by both mastoparans from phospholipid vesicles were also examine

51 In contrast to mastoparan, iC5b67 failed to directly activate G protein

52 Unsaturated fatty acids and mastoparan increased phosphorylation of ABCA1 serines.

53 ne oxidase O(-)(2) generating system blunted mastoparan induced pial artery dilation similar to FPI (

54 (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca2+]i and protect agai

55 However, the mastoparan-induced initial elevation of [Ca2+]i is maint

56 on in intact cells and of Ca(2+)-induced and mastoparan-induced insulin secretion in permeabilized ce

57 meabilized Syt III cells, Ca(2+)-induced and mastoparan-induced insulin secretion was also increased.

58 toxin, but not pertussis toxin, reduced the mastoparan-induced rise in [Ca2+]i.

59 calcium concentration ([Ca2+]i) reveal that mastoparan induces a dramatic elevation of [Ca2+]i that

60 of PLD1, results in a large increase in the mastoparan-inducible PLD activity in membrane fractions,

61 Taken together, our data suggest that mastoparan initiates cell death in cerebellar granule ne

62 Kinetic studies indicate that mastoparan interacts synergistically with phosphatidylin

63 gion of p75 that Kalirin9 binds includes its mastoparan-like fifth helix, which was shown to recruit

64 aused by direct Gialpha-protein stimulation (mastoparan M7; 10-5,000 nmol/L) was further enhanced in

65 tion in ABCA1 levels, and the PLD2 activator mastoparan markedly reduced ABCA1 protein levels, implic

66 Mastoparan (masL) and mastoparan X (masX) are two simila

67 Therefore, mastoparan may be useful for investigating the regulatio

68 dies with pertussis (PTX) toxin suggest that mastoparan may work directly to activate Cdc42 and not v

69 es with the direct G(i/o) protein activator, mastoparan, mimicked the effect of M-CSF by enhancing ch

70 rimeric G proteins were stimulated by adding mastoparan (MST) to the medium while monitoring growing

71 PDI RL90 attenuated the inhibitory effect of mastoparan on LLC activation.

72 we tested the effects of activators of G(o); mastoparan peptides induced an outward current suppressi

73 ation of eGFP-Galphai1 by the receptor-mimic mastoparan plus GTPgammaS, and constitutively active eGF

74 rine macrophages, G protein dysregulation by mastoparan resulted in significant inhibition of LPS-ind

75 a synthetic analog of the wasp venom peptide mastoparan, resulted in an approximately 2-fold increase

76 rring at the site of activation by NDPK of a mastoparan-sensitive G-protein-dependent step in exocyto

77 ndent activities, thereby demonstrating that mastoparan specifically activates this isozyme.

78 Following cell membrane fractionation mastoparan specifically stimulated a high activity Golgi

79 containing 2.8 mmol/l glucose, 20 micromol/l mastoparan stimulated insulin secretion 12- and 14-fold

80 inding protein thought to be involved in the mastoparan-stimulated GTP-dependent pathway of insulin r

81 In the control islets, alpha-KIC augmented mastoparan-stimulated insulin release by 80%.

82 cell line, resulted in a 2-fold increase in mastoparan-stimulated insulin release over vector-transf

83 In the GTP-depleted rat islets, mastoparan-stimulated insulin release was not changed, w

84 veal a striking dependence of both basal and mastoparan-stimulated PI4KIIalpha activity on endogenous

85 fect on insulin release alone, but augmented mastoparan-stimulated release by 74% in both rat and hum

86 alpha-ketoisocaproate (alpha-KIC) to augment mastoparan-stimulated release.

87 In conclusion, mastoparan stimulates insulin release by activation of a

88 rtussis toxin and other agents indicate that mastoparan stimulates PLD2 independently of G(i), ARF-1,

89 oncentrations, is a competitive inhibitor of mastoparan stimulation of PLD2.

90 The effect of cellular GTP depletion on the mastoparan stimulation of release and augmentation by al

91 Rho family GTP-binding protein Cdc42, in the mastoparan stimulus-secretion pathway, was examined.

92 Using the wasp venom-derived peptide, mastoparan, to disrupt G protein-coupled signaling, we i

93 Tp10 is more active than the mastoparans toward phosphatidylcholine vesicles, but the

94 Mastoparan treatment produced rapid growth cone collapse

95 The stimulatory effects of mastoparan were resistant to removal of extracellular Ca

96 In contrast, mastoparan (which activates GTP-binding proteins [GBPs])

97 Mastoparan, which directly activates G-proteins (and ins

98 We also demonstrate that mastoparan, which increases [Ca2+]i, also triggers DNA f

99 The wasp venom peptide mastoparan, which inhibits the chaperone activity of PDI

100 f the well studied molecular interactions of mastoparan with certain other strategic signaling protei

101 e association of melittin, mastoparan X, and mastoparan with immobilized lipodisks.

102 ed the stimulatory effects of glucose, K+ or mastoparan without altering the rise in intracellular ca

103 Mastoparan (masL) and mastoparan X (masX) are two similar peptides from the ve

104 Mastoparan X (MPX: INWKGIAAMAKKLL-NH2) belongs to a fami

105 Our results show that the association of mastoparan X with model lipid vesicles proceeds with bip

106 ters describing the association of melittin, mastoparan X, and mastoparan with immobilized lipodisks.

107 d with two well-studied AMPs, magainin 2 and mastoparan X, and two model membranes indicate that this

108 tional kinetic studies on a double mutant of mastoparan X, designed to form a nucleation site for alp

109 lpha-helical amphiphilic cell-lytic peptide, mastoparan X, was engineered to bind divalent cations.

110 lding mechanism of an antimicrobial peptide, mastoparan X.

111 We previously reported that mastoparan-X binds to alpha-subunits of Gi and Go in a p