ライフサイエンスコーパス: venom

1 fe-threatening anaphylaxis (e.g. Hymenoptera venom).

2 present as a toxic chemical defence in toad venom.

3 y of these scFvs and how they neutralize the venom.

4 ection to mice against Echis carinatus snake venom.

5 fficiency in the neutralization of the whole venom.

6 om before challenge with a high dose of that venom.

7 RVV significantly enhanced resistance to the venom.

8 ly neutralize the proteases present in snake venom.

9 green mamba snake (Dendroaspis angusticeps) venom.

10 ethal effects of honeybee or Russell's viper venom.

11 gE also can enhance defense against honeybee venom.

12 x structures with peptides purified from the venom.

13 estigated due to the high complexity of this venom.

14 te anaphylaxis, predominantly to Hymenoptera venom.

15 ns a prime target for toxins found in animal venom.

16 er, possibly immune-related function outside venom.

17 hannel activation inhibitor from crab spider venom.

18 f secretion, while A. brunoi has more lethal venom.

19 i secretion is 25-fold as lethal as Bothrops venom.

20 pid venom, but not in those treated with bee venom.

21 o snakes and lizards, the fangs pre-date the venom.

22 mechanisms in acquired host defense against venoms.

23 toxins, guarantees the neutralization of the venoms.

24 tion, thus protecting against helminthes and venoms.

25 otential future anticancer drugs rather than venoms.

26 t are expressed as major components of their venoms.

27 delta-conotoxins from piscivorous cone snail venoms.

28 t frequent trigger (66%), followed by insect venom (19%).

29 ommon elicitor was drugs (41.1%) followed by venom (27.4%) and food (20.6%).

30 disulfide-rich peptide toxin from tarantula venom able to inhibit the human voltage-gated sodium cha

31 Here, we show that venoms activate human T cells via CD1a proteins.

32 gs are capable of using their skin toxins as venoms against would-be predators.

33 gical processes within each stage, including venom, aggression, olfactory recognition as well as grow

34 rom other known gating modifiers from spider venom, all of which are described from mygalomorph speci

35 o information has become available on single venom allergen sIgE reactivity and the usefulness of com

36 ty to recombinant yellow jacket and honeybee venom allergens by Immulite3 g.

37 tosis, a panel of yellow jacket and honeybee venom allergens was applied on a widely used IgE immunoa

38 s-linking or by stimulation with hymenoptera venom allergens, were significantly reduced by histamine

39 pharmaceutical grade for inhalant, food, and venom allergens.

40 icited by diverse stimuli, including toxins, venoms, allergens, and infectious agents, and play criti

41 Venom immunotherapy is indicated in venom-allergic children and adults to prevent further mo

42 es v 5-inhibitory activity of sera from wasp venom-allergic patients using the novel cell-free enzyme

43 cription of AAIs is mandatory in the case of venom-allergic patients who suffer from mast cell diseas

44 found at a similar frequency in hymenoptera venom-allergic patients with and without elevated sBT le

45 rn and diagnostic sensitivity in hymenoptera venom-allergic patients with elevated sBT levels and/or

46 ponses after stings varied in bee and vespid venom-allergic patients.

47 gs can cause severe anaphylaxis in untreated venom-allergic patients.

48 rove the diagnostic precision in Hymenoptera venom allergy (HVA), in particular in patients with doub

49 mples (P </= .002) and control subjects with venom allergy (P < .0001).

50 01) and compared with those in patients with venom allergy and healthy control subjects (21 and 23.4

51 , eczema, food allergy, rhinitis, urticaria, venom allergy and other probable allergic disorders) fro

52 therapy (AIT) in respiratory and Hymenoptera venom allergy are well established; however, clinical co

53 Hymenoptera venom allergy is a potentially life-threatening allergic

54 Anaphylaxis caused by hymenoptera venom allergy is associated with elevation of baseline s

55 of mastocytosis in patients with Hymenoptera venom allergy is high, and thus the disease should be su

56 mptions, suggested that AIT for bee and wasp venom allergy is only likely to be cost-effective for ve

57 ) in patients with yellow jacket or Polistes venom allergy of two European geographical areas.

58 The diagnostic sensitivity of yellow jacket venom allergy using the combination of Ves v 1 and Ves v

59 We found one economic modelling study for venom allergy which, despite being based largely on expe

60 ing VIT efficacy was only possible in vespid venom allergy, and the sIgG4 threshold for rVes v 5 had

61 In vespid venom allergy, cross-reactivity between venoms of differ

62 allergic rhinitis, asthma, food allergy and venom allergy, respectively.

63 nd characteristics of anaphylaxis and insect venom allergy, such as suggesting that baseline platelet

64 (PLA2denat -MB) in a mouse model of honeybee venom allergy.

65 s in 847 patients with confirmed hymenoptera venom allergy.

66 tization and clinically relevant Hymenoptera venom allergy.

67 clinically relevant sensitization in vespid venom allergy.

68 lergic asthma, IgE-mediated food allergy and venom allergy.

69 nd safety of AIT in the management of insect venom allergy.

70 ithout asthma and in high-risk subgroups for venom allergy.

71 notherapy (AIT) for the management of insect venom allergy.

72 for differential sIgE diagnostics in vespid venom allergy.

73 However, components of animal venoms also can sensitize individuals to develop severe

74 e rupture was triggered with Russell's viper venom and histamine.

75 ated against MP-4 cross-react with the whole venom and provide protection to mice against Echis carin

76 gnatures of adaptive evolution in olfactory, venom and thermal-sensing genes and also functional dege

77 contribute to immunity against parasites and venoms and are the source of antigen specificity in alle

78 We screened fractions from several venoms and characterized a cystine knot toxin called JZT

79 All venoms and peptides were isolated from Black Judean Scor

80 ing responses to an initial exposure to such venoms and that acquired type 2 immune responses, IgE an

81 Here, we investigate the evolution of fangs, venom, and mimetic relationships in reef fishes from the

82 parasitic worms, noxious substances, toxins, venoms, and environmental irritants but that also trigge

83 optera, including their genomes, morphology, venoms, and parasitoid and eusocial life styles.

84 small molecules, toxins isolated from animal venoms, and the recently identified Na(v)1.7-selective a

85 was a continuous shift from food- to insect venom- and drug-induced anaphylaxis up to age 10 years,

86 found for grass and cat sensitization, while venom- and weed pollen-positive individuals were frequen

87 ic evaluation of patients with food-, insect venom-, and drug allergy and chronic urticaria.

88 gastropods characterized by a sophisticated venom apparatus responsible for the biosynthesis and del

89 iverse compartments of the Conus episcopatus venom apparatus.

90 ate determinants (CCDs) in plants and insect venoms are a common cause of irrelevant positive test re

91 Spider venoms are a rich source of ion channel modulators with

92 Spider venoms are a rich source of peptide modulators useful to

93 Venoms are complex biochemical arsenals, often containin

94 Despite their utility for prey capture, venoms are energetically expensive commodities, and cons

95 ir attractant pheromones, and larval antlion venoms are potentially important genetic leads for insec

96 Snake venoms are variable protein mixtures with a multitude of

97 s not afford direct protection against snake venom because it is actually a poor inhibitor of serine

98 that had received a second exposure to that venom before challenge with a high dose of that venom.

99 was seen in all patients treated with vespid venom, but not in those treated with bee venom.

100 ecific immunoglobulin G4 (sIgG4) to honeybee venom, but not with total IgE or sIgE.

101 mmunoCAP system for routine diagnosis of bee venom (BV) allergy.

102 re, we investigated the putative role of bee venom (Bv) in human FOXP3-expressing Treg homeostasis an

103 tropic peptide (BjIP) isolated from the full venom by chromatography increased cardiac contractility

104 ent to which type 2 immune responses against venoms can decrease pathology associated with envenomati

105 Thus, by combining the venom clotting test with the quick clotting time (prothr

106 We propose that the differences in venom complexity between centipede orders are largely a

107 es, and consequently it is hypothesized that venom complexity is inversely related to the capacity of

108 Here we describe a venom component targeting energy metabolism, a radically

109 obulins with the ability to neutralize snake venom components and to mitigate the progression of toxi

110 The vast majority of venom components identified and functionally characteriz

111 structural motifs characteristic of scorpion venom components in the form of regular expressions.

112 s as a model system, we investigated whether venoms contain CD1-presented antigens.

113 Pain-producing animal venoms contain evolutionarily honed toxins that can be e

114 Venoms contain variable mixtures of bioactive proteins.

115 Naja sputatrix (Malayan spitting cobra) venom contains 15% secretory PLA2 of its dry weight.

116 We find that fangblenny venom contains a number of toxic components that have be

117 C. atrox venom contains snake venom metalloproteinases that cleav

118 evaluate preconditioning with Crotalus atrox venom (Cv-PC) as potential preventive therapy for reduci

119 affold, we engineered a library of over 1500 venom-derived peptides and identified JNJ63955918 as a p

120 ding was explained by demonstrating that bee venom-derived phospholipase A2 (PLA2) activates T cells

121 nate host resistance to reptile or arthropod venoms during responses to an initial exposure to such v

122 enced by the type of venom, the frequency of venom exposure, and the genetic background of the host.

123 , including fatal anaphylaxis, on subsequent venom exposure.

124 ed in allergic patients and beekeepers after venom exposure.

125 4-switched memory B cells expanded after bee venom exposure.

126 patients with otherwise undetectable IgE to venom extract.

127 id otherwise undetectable IgE to hymenoptera venom extracts in about 8% of such patients.

128 Biochemical diversity of venom extracts often occurs within a small number of sha

129 re pronounced in ImmunoCAP measurements with venom extracts than in sIgE analyses with recombinant an

130 complement C3 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regeneratio

131 pletion of circulating complement with cobra venom factor eliminated, as expected, injury recorded at

132 icipated in AP activation initiated by cobra venom factor.

133 d centipedes, they appear to rely heavily on venom for prey capture.

134 ed sodium (NaV) channels, we screened spider venoms for inhibitors of human NaV1.7 (hNaV1.7) using a

135 neral utility and efficiency to mine natural venoms for KTxs.

136 Venoms frequently co-opt host immune responses, so study

137 characterization of the clotting activity of venom from Daboia russelii, distinguishing it from the b

138 433 (PhTX-433) is an active component of the venom from the Egyptian digger wasp, Philanthus triangul

139 Screening fractionated venom from the tarantula Grammostola porteri led to the

140 Here, we perform an in vitro screen of venoms from 18 cone snail species to identify toxins tar

141 the groundwork for more detailed studies of venom function and adaptation to the endoparasitic lifes

142 oxin-encoding genes that strongly influences venom function in rattlesnakes, highlighting how gene lo

143 ression in the venom gland, recent losses of venom function occur primarily among genes that show bro

144 While the majority of venom genes have specialized expression in the venom gla

145 ind that a common mode of acquisition of new venom genes in parasitoid wasps is co-option of single-c

146 Here we use the rapid turnover of venom genes in parasitoid wasps to study how new gene fu

147 Loss of venom genes is primarily due to downregulation of expres

148 quencing reveal that recruitment and loss of venom genes occur primarily by rapid cis-regulatory expr

149 isplayed distinct expression patterns in the venom gland and this was confirmed by quantitative real-

150 result of morphological restrictions of the venom gland, and consequently there is a strong correlat

151 nom genes have specialized expression in the venom gland, recent losses of venom function occur prima

152 d cis-regulatory expression evolution in the venom gland.

153 We show that the venom glands are large and well developed in both scutig

154 Moreover, we reveal that scolopendrid venom glands have evolved to accommodate a much larger n

155 mes are highly expressed specifically in the venom glands of predatory cone snails, animals that synt

156 ssed in a spatially homogenous manner within venom glands, and they suggest that the link between eco

157 ns (KTxs) from the cDNA library of M. eupeus venom glands, and we compare the deduced KTx structures

158 liced spidroin, a spidroin expressed only in venom glands, evolutionary mechanisms for spidroin diver

159 Additionally, hymenoptera venom has for a long time been claimed to modulate immun

160 The evolution of fangblenny venom has seemingly led to phenotypic convergence via th

161 Spiked virus-like particles (VLPs) in wasp venom have clearly been linked to wasps' successful para

162 Microproteins isolated from animal venoms have been identified as promising therapeutic lea

163 distinct sensitization profiles in honey bee venom (HBV) allergy, some of which were dominated by spe

164 panel of the EAACI Interest Group of Insect Venom Hypersensitivity.

165 in volume and in quality, but suggested that venom immunotherapy (VIT) could substantially reduce the

166 A reliable serological marker to monitor venom immunotherapy (VIT) does also not exist.

167 d Clinical Immunology's (EAACI) Taskforce on Venom Immunotherapy as part of the EAACI Guidelines on A

168 Venom immunotherapy is also recommended in adults with o

169 Venom immunotherapy is efficient to desensitize people s

170 Venom immunotherapy is indicated in venom-allergic child

171 ver general considerations before initiating venom immunotherapy, evidence-based clinical recommendat

172 vidence-based recommendations for the use of venom immunotherapy, has been informed by a formal syste

173 The observed B-cell responses in both venom immunotherapy-treated patients and naturally expos

174 ituations before, during, and after stopping venom immunotherapy.

175 aims to give practical advice on performing venom immunotherapy.

176 ual and subcutaneous AIT for respiratory and venom immunotherapy.

177 prevent further systemic sting reactions is venom immunotherapy.

178 ent effects on resistance to RVV or honeybee venom in BALB/c versus C57BL/6 mice that had received a

179 eveals the evolutionary origins of fangs and venom in the Nemophini blennies and shows that, in contr

180 nt extract (in agonist assay mode) and snake venoms (in mixed antagonist-agonist assay mode).

181 The full scorpion venom increased left ventricular function in sedated mic

182 dentifies SM among patients with hymenoptera venom-induced anaphylaxis in whom the diagnosis would mo

183 rteen SM patients presented with Hymenoptera venom-induced anaphylaxis, no skin lesions, and baseline

184 reted phospholipases A2 (sPLA2s) from animal venoms inhibit the in vitro development of Plasmodium fa

185 , a peptide from predatory marine cone snail venom, inhibits Cav2.2 channels by activating pertussis

186 When injected into fish, the venom insulin elicits hypoglycemic shock, a condition ch

187 young, both ecto- and endoparasitoids inject venoms into the host to modulate host immunity, metaboli

188 Snake venom is a natural substance that contains numerous bioa

189 sed species of the Mesobuthus genus, and its venom is actively studied.

190 The venom is now known to act by directly activating factor

191 The lethal factor in stonefish venom is stonustoxin (SNTX), a heterodimeric cytolytic p

192 Characterization of teratocyte-secreted venom-like protein 8 (TSVP-8) indicated it inhibits mela

193 lated endoparasitoids but have no detectable venom matches in Nasonia.

194 actions of C. atrox venom suggest that snake venom metalloproteinases are largely responsible for the

195 C. atrox venom contains snake venom metalloproteinases that cleave fibrinogen into fib

196 Spider venom neurotoxins and cytolytic peptides are expressed a

197 M protease, essential for maturing of spider venom neurotoxins.

198 MP-4 contributes significantly to the snake venom neutralization activity of M. pruriens seeds throu

199 e protein(s) that may be important for snake venom neutralization and elucidate its mechanism of acti

200 tn), a cathelicidin-related peptide from the venom of a South American rattlesnake, possesses potent

201 ly acts on vertebrate sodium channels in the venom of a worm-hunting cone snail suggests that a close

202 The acetylcholinesterase found in the venom of Bungarus fasciatus (BfAChE) is produced as a so

203 Through bioassay-guided fractionation of the venom of Conus brunneus, we found BruIB, an alpha-conoto

204 is delta-conotoxin TsVIA, a peptide from the venom of Conus tessulatus that delays inactivation of ve

205 onopeptide of only four amino acids from the venom of Conus textile that strongly potentiated current

206 on of a novel anticoagulant protein from the venom of Hemachatus haemachatus (African Ringhals cobra)

207 In addition, peptides found in the venom of poisonous animals, along with the lipids phosph

208 uced currents of TRPA1 was isolated from the venom of sea anemone Metridium senile.

209 Among the toxic polypeptides secreted in the venom of sea anemones, actinoporins are the pore-forming

210 a cystine knot toxin called JZTx-27 from the venom of tarantula Chilobrachys jingzhao as a high-affin

211 isolated an insecticidal peptide (Ae1a) from venom of the African spider Augacephalus ezendami (famil

212 Ts3 is an alpha scorpion toxin from the venom of the Brazilian scorpion Tityus serrulatus.

213 itor, mu-TRTX-Tp1a (Tp1a), isolated from the venom of the Peruvian green-velvet tarantula Thrixopelma

214 pacity to neutralize the Cn2 toxin and whole venom of the scorpion Centruroides noxius.

215 toxin precursor processing protease from the venom of the spider Cupiennius salei The chymotrypsin-li

216 eptide, mu-theraphotoxin-Pn3a, isolated from venom of the tarantula Pamphobeteus nigricolor, potently

217 arasphenodon brunoi) are more toxic than the venoms of deadly venomous Brazilian pitvipers, genus Bot

218 spid venom allergy, cross-reactivity between venoms of different species can be a diagnostic challeng

219 n addition, 13 venom proteins are similar to venoms of distantly related endoparasitoids but have no

220 Like the venoms of other animals, the skin secretions of these fr

221 Venoms of the sicariid spiders contain phospholipase D e

222 novel Kv1.3 channel blockers from a natural venom peptide library that was formatted for autocrine-b

223 The venom peptide maurocalcin (MCa) is atypical among toxins

224 the first crystal structure of an ICK spider venom peptide not bound to a substrate.

225 Venom peptide toxins such as conotoxins play a critical

226 monstrate that Hi1a, a disulfide-rich spider venom peptide, is highly neuroprotective in a focal mode

227 Using the tarantula venom-peptide ProTX-II as a scaffold, we engineered a li

228 In particular, a class of spider-venom peptides (NaSpTx1) has been found to potently inhi

229 gs remains because of the slow pace at which venom peptides are discovered and refined.

230 Many spider-venom peptides are known to modulate the activity of the

231 Insecticidal spider-venom peptides are promising candidates for bioinsectici

232 lso able to depict the largest population of venom peptides containing the pharmacologically active C

233 system was developed to discover and refine venom peptides that target ion channels.

234 ze the pharmacophore region of this class of venom peptides.

235 outline the steps necessary to purify snake venom phosphodiesterase I (SVP) and describe two alterna

236 Enhanced stability against snake venom phosphodiesterase resulted from modification of th

237 rporation increases resistance against snake venom phosphodiesterase.

238 ospholipid as a novel substrate of honey bee venom phospholipase A2.

239 nzymatic activity of membrane-associated bee venom PLA2, covering a pressure range up to 2 kbar.

240 We investigated if Naja sputatrix venom preconditioning (VPC) reduces surgical brain injur

241 tion, development of axis pattern formation, venom production, haplo-diploid sex determination, and h

242 s is co-option of single-copy genes from non-venom progenitors.

243 In addition, 13 venom proteins are similar to venoms of distantly relate

244 Most of them show higher similarity to venom proteins from the related ectoparasitoid Nasonia v

245 c approaches, we have identified 70 putative venom proteins in P. puparum.

246 ng their specific physiological functions as venom proteins in suppressing host immune responses.

247 These venom proteins may have a role in adaptation to endopara

248 Levels of sIgE and sIgG4 to bee and vespid venom, rApi m 1, and rVes v 5 were measured immediately

249 stigated whether the changes observed during venom-related anaphylaxis also occur during allergic rea

250 s most common in children aged 0 to 9 years, venom-related anaphylaxis was most common in those 20 to

251 Animal venoms represent a rich source of pharmacologically acti

252 Venom represents one of the most extreme manifestations

253 were detected from tobacco extract and snake venoms, respectively.

254 Using bee and wasp venom responses as a model system, we investigated wheth

255 en can enhance defense against Russell viper venom (RVV) and determined whether such responses can be

256 apaport and colleagues demonstrated that the venom's clotting activity does not require factor VII, b

257 28-kDa heterodimer with optimum activity at venom's pH of 6.0.

258 m the plasma of animals immunised with whole venom(s) and contain antibodies against snake venom toxi

259 the proteins and whole protein content in a venom sample.

260 deep anterior grooves and their coupling to venom secretory tissue provide Meiacanthus spp. with tox

261 to follow Kv1.1 pore binding activity during venom separation.

262 gest that it may show efficacy as an in vivo venom sequestrant and may serve as a generalized lipid-m

263 en independently recruited into other animal venoms, some of which cause toxicity via interactions wi

264 tive carbohydrate determinants from plant or venom sources (nCup a 1, nArt v 1, and MUXF3).

265 Venom-specific immunotherapy (VIT) is well recognized by

266 the family of three-finger toxins from snake venoms, specifically stained the alpha1beta3gamma2 recep

267 Naja sputatrix venom sublethal dose was injected subcutaneously for 3 c

268 contain a high diversity of toxins in their venom such as conotoxins, which are short polypeptides s

269 Cv-PC studies with fractions of C. atrox venom suggest that snake venom metalloproteinases are la

270 al and biochemical complexity of this unique venom system.

271 Venom systems have evolved on multiple occasions across

272 utigeromorph centipedes produce less complex venom than those secreted by scolopendrid centipedes, th

273 We identified a peptide from green mamba venom that exhibits nanomolar affinity for the V2R witho

274 Mambalgins are peptides isolated from mamba venom that specifically inhibit a set of acid-sensing io

275 y tissue provide Meiacanthus spp. with toxic venom that they effectively employ for defense.

276 wo toxins present in Costa Rican coral snake venom that tightly bind to GABAA receptors at subnanomol

277 d peptides present in predatory marine snail venoms that function as allosteric antagonists of ion ch

278 Nature is replete with predator venoms that immobilize prey by targeting ion channels.

279 nirvana cabal, a toxin combination in these venoms that is released into the water to disorient scho

280 mation seems to be influenced by the type of venom, the frequency of venom exposure, and the genetic

281 rom moth) with residues 2-9 of melittin (bee venom)], three fluorescence signals report oxidative str

282 In this study, we subjected snake venom to enzymatic hydrolysis to identify previously unr

283 lergen-specific B cells before and after bee venom tolerance induction.

284 ogical processes, including immune defenses, venom toxicity, and sperm maturation.

285 New work shows that parasitoid wasp venom toxins evolve by the co-option of genes rather tha

286 n antivenom antibodies and epitopes on snake venom toxins, a high-throughput immuno-profiling study o

287 enom(s) and contain antibodies against snake venom toxins, but also against other antigens.

288 Spider venom toxins, such as Protoxin-II (ProTx-II), have recen

289 peptides, adapted to the maturing of spider venom toxins.

290 olecular mechanisms underlying T. serrulatus venom (TsV) activity remain unknown.

291 resent lipids, chromatographic separation of venoms unexpectedly showed that stimulatory factors part

292 M. eupeus venom was then separated to individual components by mul

293 Melittin, the main component of dry bee venom, was used as a model amphipathic alpha-helical pep

294 Reactions to insect venom were seen more in young adulthood.

295 level and systemic reactions to hymenoptera venoms were analyzed for their IgE reactivity to recombi

296 ttin, the active molecule of apitoxin or bee venom, were investigated on human red blood cells (RBCs)

297 ied from the rattlesnake Crotalus adamanteus venom, which is contaminated with proteases detrimental

298 hesis was that preconditioning with C. atrox venom will produce fibrinogen spilt products, thereby up

299 who may be exposed to multiple exposures to venom/year (eg bee keepers).

300 on to both honey bee (HBV) and yellow jacket venom (YJV).