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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       These HA vaccines were formulated with Mastoparan 7 (M7-NH(2)) mast cell degranulating peptide
12 i) expression and ATP release in response to mastoparan 7 are impaired, which is consistent with the
13                        The administration of mastoparan 7, an activator of pertussis toxin-sensitive
14 orted MC agonist was identified by screening mastoparan-7 analogs for MC degranulation activity, whic
15            Similar results were observed for mastoparan-7 but the inactive analogue mastoparan-17 had
16 1 microg/ml) exposure blocked mastoparan and mastoparan-7 vasodilation.
17 is toxin sensitive G protein, mastoparan and mastoparan-7, and the role of PKC dependent O(-)(2) gene
18 ar loop and the G protein activating peptide mastoparan-7, failed to promote uncoupling from Galpha(o
19                                              Mastoparan, a 14-residue peptide, stimulates GDP/GTP exc
20                                              Mastoparan, a hormone receptor-mimetic peptide isolated
21               We have recently reported that mastoparan, a peptide toxin isolated from wasp venom, in
22                                              Mastoparan, a tetradecapeptide component of wasp venom,
23 ed following mast cell stimulation either by mastoparan, a wasp venom secretagogue, or by the physiol
24  or indirectly, PR were chromatographed on a mastoparan affinity column.
25 (i) signaling with epinephrine or wasp venom mastoparan also inhibited invasion and migration of the
26                                              Mastoparan also stimulated PI4KIIalpha immunoprecipitate
27 tion of either activated Goalpha subunits or mastoparan) also inhibited migration in a Ca2+-dependent
28                                 Melittin and mastoparan, amphiphilic pore-forming peptides like the M
29                                              Mastoparan, an activator of G protein-coupled receptor k
30                                 We find that mastoparan, an activator of G(i) and mast cells, stimula
31 Ca2+-ionophore A23187, and when treated with mastoparan, an inducer of the MPT in rat liver mitochond
32                              Mas7, an active mastoparan analog known to stimulate Gi proteins, was fo
33 sulin release by other modulators, including mastoparan and activators of protein kinase C, is conser
34                    Stimulation of release by mastoparan and augmentation of release by glucose were u
35 om CaCl(2) plus 5 microm HgCl(2) or 1 microm mastoparan and by 200 microm CaCl(2) alone.
36 lin (1 microM), or the calmodulin inhibitors mastoparan and calmidazolium (5 microM), did not alter t
37 tion due to receptor-mimetic ligands such as mastoparan and compound 48/80.
38                                         Both mastoparan and M7, at concentrations known to invoke sec
39 rtussis toxin (1 microg/ml) exposure blocked mastoparan and mastoparan-7 vasodilation.
40 rs of a pertussis toxin sensitive G protein, mastoparan and mastoparan-7, and the role of PKC depende
41                   Previous studies examining mastoparan and related peptides and their ability to act
42 nt target of the wasp venom tetradecapeptide mastoparan and that different mechanisms of activation o
43 , and postmitochondrial phases by tamoxifen, mastoparan, and cytochrome c, respectively, allowing a f
44 toward phosphatidylcholine vesicles, but the mastoparans are more sensitive to the effect of anionic
45 ediated MAPK phosphorylation in macrophages, mastoparan blunted IL-1R-associated kinase-1 kinase acti
46 ed by the heterotrimeric G protein activator mastoparan, but not by its inactive analogue Mas-17.
47 diolabelled model peptides, somatostatin and mastoparan, by cross-linking.
48              Polybasic secretagogues such as mastoparan, compound 48/80, substance P, and somatostati
49 tivity of each membrane pool, as well as the mastoparan-dependent activities, thereby demonstrating t
50 that the GTP-dependent signal underlying the mastoparan effect acts at a "distal site" in stimulus-se
51        To identify the proteins that bind to mastoparan either directly or indirectly, PR were chroma
52   The kinetics of dye efflux induced by both mastoparans from phospholipid vesicles were also examine
53                               In contrast to mastoparan, iC5b67 failed to directly activate G protein
54                  Unsaturated fatty acids and mastoparan increased phosphorylation of ABCA1 serines.
55 ne oxidase O(-)(2) generating system blunted mastoparan induced pial artery dilation similar to FPI (
56  (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca2+]i and protect agai
57                                 However, the mastoparan-induced initial elevation of [Ca2+]i is maint
58 on in intact cells and of Ca(2+)-induced and mastoparan-induced insulin secretion in permeabilized ce
59 meabilized Syt III cells, Ca(2+)-induced and mastoparan-induced insulin secretion was also increased.
60  toxin, but not pertussis toxin, reduced the mastoparan-induced rise in [Ca2+]i.
61 ne asthma exacerbation model as well as in a mastoparan-induced skin challenge PK/PD model and was pr
62  calcium concentration ([Ca2+]i) reveal that mastoparan induces a dramatic elevation of [Ca2+]i that
63  of PLD1, results in a large increase in the mastoparan-inducible PLD activity in membrane fractions,
64        Taken together, our data suggest that mastoparan initiates cell death in cerebellar granule ne
65                Kinetic studies indicate that mastoparan interacts synergistically with phosphatidylin
66                                              Mastoparan-L (parent/control), R1, and R4 inhibited susc
67               Moreover, the toxic effects of mastoparan-L toward mammalian cells were drastically red
68 e mastoparan variants were designed based on mastoparan-L, among which two (R1 and R4) were selected
69                           Here we repurposed mastoparan-L, the toxic active principle derived from th
70 gion of p75 that Kalirin9 binds includes its mastoparan-like fifth helix, which was shown to recruit
71 optimized the therapeutic potential of these mastoparan-like peptides both in vitro and in vivo.
72 aused by direct Gialpha-protein stimulation (mastoparan M7; 10-5,000 nmol/L) was further enhanced in
73 tion in ABCA1 levels, and the PLD2 activator mastoparan markedly reduced ABCA1 protein levels, implic
74                                              Mastoparan (masL) and mastoparan X (masX) are two simila
75                                   Therefore, mastoparan may be useful for investigating the regulatio
76 dies with pertussis (PTX) toxin suggest that mastoparan may work directly to activate Cdc42 and not v
77 es with the direct G(i/o) protein activator, mastoparan, mimicked the effect of M-CSF by enhancing ch
78 rimeric G proteins were stimulated by adding mastoparan (MST) to the medium while monitoring growing
79 PDI RL90 attenuated the inhibitory effect of mastoparan on LLC activation.
80 we tested the effects of activators of G(o); mastoparan peptides induced an outward current suppressi
81 ation of eGFP-Galphai1 by the receptor-mimic mastoparan plus GTPgammaS, and constitutively active eGF
82 rine macrophages, G protein dysregulation by mastoparan resulted in significant inhibition of LPS-ind
83 a synthetic analog of the wasp venom peptide mastoparan, resulted in an approximately 2-fold increase
84 rring at the site of activation by NDPK of a mastoparan-sensitive G-protein-dependent step in exocyto
85 ndent activities, thereby demonstrating that mastoparan specifically activates this isozyme.
86        Following cell membrane fractionation mastoparan specifically stimulated a high activity Golgi
87 containing 2.8 mmol/l glucose, 20 micromol/l mastoparan stimulated insulin secretion 12- and 14-fold
88 inding protein thought to be involved in the mastoparan-stimulated GTP-dependent pathway of insulin r
89   In the control islets, alpha-KIC augmented mastoparan-stimulated insulin release by 80%.
90  cell line, resulted in a 2-fold increase in mastoparan-stimulated insulin release over vector-transf
91              In the GTP-depleted rat islets, mastoparan-stimulated insulin release was not changed, w
92 veal a striking dependence of both basal and mastoparan-stimulated PI4KIIalpha activity on endogenous
93 fect on insulin release alone, but augmented mastoparan-stimulated release by 74% in both rat and hum
94 alpha-ketoisocaproate (alpha-KIC) to augment mastoparan-stimulated release.
95                               In conclusion, mastoparan stimulates insulin release by activation of a
96 rtussis toxin and other agents indicate that mastoparan stimulates PLD2 independently of G(i), ARF-1,
97 oncentrations, is a competitive inhibitor of mastoparan stimulation of PLD2.
98  The effect of cellular GTP depletion on the mastoparan stimulation of release and augmentation by al
99 Rho family GTP-binding protein Cdc42, in the mastoparan stimulus-secretion pathway, was examined.
100        Using the wasp venom-derived peptide, mastoparan, to disrupt G protein-coupled signaling, we i
101                 Tp10 is more active than the mastoparans toward phosphatidylcholine vesicles, but the
102                                              Mastoparan treatment produced rapid growth cone collapse
103                                   Here, five mastoparan variants were designed based on mastoparan-L,
104                   The stimulatory effects of mastoparan were resistant to removal of extracellular Ca
105                                 In contrast, mastoparan (which activates GTP-binding proteins [GBPs])
106                                              Mastoparan, which directly activates G-proteins (and ins
107                     We also demonstrate that mastoparan, which increases [Ca2+]i, also triggers DNA f
108                       The wasp venom peptide mastoparan, which inhibits the chaperone activity of PDI
109 f the well studied molecular interactions of mastoparan with certain other strategic signaling protei
110 e association of melittin, mastoparan X, and mastoparan with immobilized lipodisks.
111 ed the stimulatory effects of glucose, K+ or mastoparan without altering the rise in intracellular ca
112                        Mastoparan (masL) and mastoparan X (masX) are two similar peptides from the ve
113                                              Mastoparan X (MPX: INWKGIAAMAKKLL-NH2) belongs to a fami
114     Our results show that the association of mastoparan X with model lipid vesicles proceeds with bip
115 ters describing the association of melittin, mastoparan X, and mastoparan with immobilized lipodisks.
116 d with two well-studied AMPs, magainin 2 and mastoparan X, and two model membranes indicate that this
117 tional kinetic studies on a double mutant of mastoparan X, designed to form a nucleation site for alp
118 lpha-helical amphiphilic cell-lytic peptide, mastoparan X, was engineered to bind divalent cations.
119 lding mechanism of an antimicrobial peptide, mastoparan X.
120                  We previously reported that mastoparan-X binds to alpha-subunits of Gi and Go in a p

 
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