ライフサイエンスコーパス: snake venom

1 n by a representative phosphodiesterase from snake venom.

2 cotinic acetylcholine receptors derived from snake venom.

3 ivated to thrombin(148) with Echis carinatus snake venom.

4 n, halysin and barbourin) were purified from snake venom.

5 was observed with the sPLA2 OS2, from Taipan snake venom.

6 response pathways, were co-opted to regulate snake venom.

7 e protection to mice against Echis carinatus snake venom.

8 entially neutralize the proteases present in snake venom.

9 ped to identify the disulfide bonds in crude snake venom.

10 ardiotoxin-I (CTX-I), from the Naja kaouthia snake venom.

11 lectin purified from Calloselasma rhodostoma snake venom.

12 rotein, Bv8, and a nontoxic protein of mamba snake venom.

13 members of this protein family occurring in snake venoms.

14 ered peptide toxin superfamily isolated from snake venoms.

15 ntegrins are cysteine-rich proteins found in snake venoms.

16 city of a broad range of medically important snake venoms.

17 s for fast adaptation and diversification of snake venoms.

18 ule and a multi-Kunitz protease inhibitor in snake venoms.

19 e original recruitment of nontoxin genes for snake venom: 1) in locus ancestral gene duplication and

20 n analogous neofunctionalization occurred in snake venom alpha-neurotoxins upon loss of another pair

21 lved first, which permitted the evolution of snake venom alpha-neurotoxins.

22 gic analysis, fibrin depletion, by using the snake venom ancrod, in Tg6074 mice also delayed the onse

23 substrate access to adsorbed enzyme for the snake venom and group X isoforms corresponding to weaken

24 lysis catalyzed by various concentrations of snake venom and human groups IIa, V, and X sPLA(2) were

25 The alignment of snake venom and mammalian MDC and MMP precursor sequence

26 a unique view of the origin and evolution of snake venom and reveal multiple genome-level adaptive re

27 Hyaluronidase is a common component of snake venoms and has been termed the "venom spreading fa

28 Varespladib was tested against several whole snake venoms and isolated PLA(2) toxins, demonstrating p

29 logy, provide insight into the regulation of snake venom, and broadly highlight the biological insigh

30 also contribute to altering the toxicity of snake venoms, and we demonstrate how this variability ca

31 M), whereas 14-kD PLA2 from pig pancreas and snake venom are inactive even at micromolar doses.

32 Snake venoms are complex protein mixtures encoded by sev

33 Snake venoms are important novel traits that are compris

34 Many snake venoms are known for their antithrombotic activity

35 Snake venoms are mixtures of toxins that vary extensivel

36 Snake venoms are rich in protein and peptide toxins that

37 Snake venoms are variable protein mixtures with a multit

38 -4 does not afford direct protection against snake venom because it is actually a poor inhibitor of s

39 Dendrotoxin proteins isolated from Mamba snake venom block potassium channels with a high degree

40 gen, collagen-related peptide (CRP), and the snake venom C-type lectin convulxin (CVX).

41 form an unbiased in vitro screen to identify snake venoms capable of activating somatosensory neurons

42 uences was designed and synthesized from the snake venom cathelicidin, batroxicidin (BatxC), with the

43 munoglobulins with the ability to neutralize snake venom components and to mitigate the progression o

44 The complexity of snake venom composition reflects adaptation to the diver

45 oxinologists to comprehensively characterize snake venom compositions, unravel the molecular mechanis

46 Snake venom consists of toxin proteins with multiple dis

47 Snake venoms contain dozens of components, including pro

48 hain and mediate functional responses to the snake venom convulxin by reconstitution of mutant forms

49 on and intracellular Ca2+ in response to the snake venom convulxin that targets GPVI.

50 e to immobilized EMS16, but not to two other snake venom-derived CLPs, echicetin and alboaggregin B.

51 belong to the heterodimeric family of these snake venom-derived proteins.

52 sent a complementary inhibition mechanism by snake-venom-derived alpha-neurotoxins.

53 experiments included echistatin, which is a snake venom disintegrin and a partial inhibitor of FAK.

54 Barbourin, a snake venom disintegrin containing a reactive KGD sequen

55 We have employed echistatin, a 5.4 kDa snake venom disintegrin, as a model protein to investiga

56 ar models based upon the known structures of snake venom disintegrins suggested that residues contrib

57 sequence flanking the RGD tripeptide, as in snake venom disintegrins.

58 ivation of cell surface prothrombin with the snake venom enzyme Ecarin also produced PAR-1-dependent

59 graphically distinct and medically important snake venoms, even when the drug combinations are delive

60 Venom origins and contemporary snake venom evolution may therefore be driven by fundame

61 Finally, snake venom exonuclease was used to demonstrate the poly

62 of a hyperimmune human donor with extensive snake venom exposure.

63 For decades, studies of snake venoms focused on the venom-ome-specific toxins (V

64 ion in the presence of thrombin, arvin, or a snake venom from Crotalus atrox.

65 Patterns of snake venom gene enhancer conservation, in some cases sp

66 Rapid evolution of snake venom genes by positive selection has been reporte

67 aling cascades involved in the regulation of snake venom genes.

68 Snake venom gland organoids are 3D culture models that c

69 on, maintenance and selected applications of snake venom gland organoids.

70 pt designed to perform precise annotation of snake venom gland transcriptomes.

71 ally tractable model system representing the snake venom gland.

72 rlying the heterogeneous toxin production in snake venom glands, and provide an example of how constr

73 While clinical ADET related to snake venom has not yet been reported in humans, this re

74 Inhibitors against snake venoms have been explored from natural resources a

75 Snake venom hemorrhagic metalloproteinase toxins that ha

76 eins, which shows structural homology to the snake venom hemorrhagic metalloproteinases (reprolysins)

77 er the aggrecanase site or the MMP site, the snake venom hemorrhagic toxin metalloproteinase HT-d (at

78 co plant extract (in agonist assay mode) and snake venoms (in mixed antagonist-agonist assay mode).

79 as MET coreceptor, and they explain how some snake venoms induce SIRS-like conditions.

80 st, that mast cells can significantly reduce snake-venom-induced pathology in mice, at least in part

81 are a family of proteins that are related to snake venom integrin ligands and metalloproteases.

82 The origin of snake venom involved duplication and recruitment of non-

83 Snake venom is a natural substance that contains numerou

84 However, snake venom is also a rich source of bioactive molecules

85 Snake venom is well known for its ability to incapacitat

86 species polymorphism and help to explain how snake venom keeps pace with prey resistance.

87 lamp had little effect on the binding of the snake venom kistrin (M(r) 7,500) or alphaIIbbeta3-mediat

88 Snake venom L-amino acid oxidases (LAAOs) are flavoprote

89 As IL4i1 has homologs in snake venoms (L-amino acid oxidases [LAAO]), we used com

90 selectively activate GP Ib using either the snake venom lectin alboaggregin-A or mutant recombinant

91 A snake venom-like protease isolated by a differential dis

92 Despite the extensive body of research on snake venom, many facets of snake venom systems, such as

93 mmon ancestry is suggested for mammalian and snake venom MDCs; it is also possible that gene duplicat

94 nchored proteins with structural homology to snake venom metalloproteases and disintegrins.

95 hospholipase A(2)'s, serine proteinases, and snake venom metalloproteases).

96 ain and a domain with sequence similarity to snake venom metalloproteases, a disintegrin domain, a cy

97 unusually abundant and diverse expression of snake venom metalloproteinases (SVMP) and a broad toxin-

98 We found evidence that 1) snake venom metalloproteinases (SVMPs) and phospholipase

99 e evolutionary origin of serum inhibitors of snake venom metalloproteinases (SVMPs) in the Western Di

100 diversification of one prominent family, the snake venom metalloproteinases (SVMPs) that play key rol

101 ith fractions of C. atrox venom suggest that snake venom metalloproteinases are largely responsible f

102 ers and inhibits the proteolytic activity of snake venom metalloproteinases from five clinically rele

103 C. atrox venom contains snake venom metalloproteinases that cleave fibrinogen in

104 Elapid snake venom neurotoxins exert their effects through high

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

106 ify the protein(s) that may be important for snake venom neutralization and elucidate its mechanism o

107 hrombin-like enzyme (TLE), isolated from the snake venom of Deinagkistrodon acutus, on MRI-detected b

108 n similar in sequence to small non-enzymatic snake venom peptides that act as integrin antagonists.

109 understanding of critical factors affecting snake venom phosphodiesterase (SVP) digestion of such OD

110 The exonuclease digestion rate, with either snake venom phosphodiesterase (SVP) or bovine spleen pho

111 ied oligodeoxynucleotides was examined using snake venom phosphodiesterase (SVPD) and nuclease S1.

112 of protocols incorporating an exonucleolytic snake venom phosphodiesterase (SVPD) digestion stage to

113 in the presence of 3'-specific exonucleases, snake venom phosphodiesterase (SVPD), demonstrated signi

114 ty of O(6)-POB-dG to hinder DNA digestion by snake venom phosphodiesterase (SVPDE), a 3'-exonuclease

115 he conserved minor venom components, such as snake venom phosphodiesterase (svPDE), remain largely un

116 Second, treatment of polymers with snake venom phosphodiesterase and alkaline phosphatase y

117 sed from DNA by hydrolysis with nuclease P1, snake venom phosphodiesterase and alkaline phosphatase.

118 its 2'-deoxyribonucleosides upon exposure to snake venom phosphodiesterase and bacterial alkaline pho

119 enzyme activity such as that represented by snake venom phosphodiesterase and by that found in human

120 analogues were stable toward hydrolysis with snake venom phosphodiesterase and stimulated RNase H1 ac

121 highly resistant to enzymatic hydrolysis by snake venom phosphodiesterase and they are 4-5 times mor

122 tion was monitored in an in vitro assay with snake venom phosphodiesterase as the hydrolytic enzyme.

123 -3'dN) were corroborated by a combination of snake venom phosphodiesterase digestion in the presence

124 equence can be generated in conjunction with snake venom phosphodiesterase digestion of purified mate

125 re, we outline the steps necessary to purify snake venom phosphodiesterase I (SVP) and describe two a

126 DP saccharides based on their degradation by snake venom phosphodiesterase or hyaluronidase and by th

127 clease resistance of the oligonucleotides to snake venom phosphodiesterase or intracellular nucleases

128 le-stranded oligodeoxynucleotides (ODN) with snake venom phosphodiesterase or snake venom phosphodies

129 Enhanced stability against snake venom phosphodiesterase resulted from modification

130 The adenylyl group can be hydrolyzed by snake venom phosphodiesterase to afford the unmodified e

131 s method, alkaline phosphatase is added with snake venom phosphodiesterase to the oligonucleotide sol

132 to be completely resistant to degradation by snake venom phosphodiesterase, DNase I and HeLa cell nuc

133 ssessing phosphodiesterase activity, such as snake venom phosphodiesterase, mammalian ectonucleotide

134 exhibit moderately higher stability against snake venom phosphodiesterase, S1 nuclease and in fetal

135 phoramidates are resistant to digestion with snake venom phosphodiesterase, to nuclease activity in a

136 i Klenow fragment (KF) 3'-5' exonuclease and snake venom phosphodiesterase.

137 re very resistant to enzymatic hydrolysis by snake venom phosphodiesterase.

138 d calf spleen phosphodiesterase, but not for snake venom phosphodiesterase.

139 ine phosphatase and sensitive to cleavage by snake venom phosphodiesterase.

140 e incorporation increases resistance against snake venom phosphodiesterase.

141 y (ESI-MS), and is resistant to digestion by snake venom phosphodiesterase.

142 (ODN) with snake venom phosphodiesterase or snake venom phosphodiesterase/DNase I was used to measur

143 gnificantly more stable against digestion by snake venom phosphodiesterases (SVPD) as compared to unm

144 A snake-venom PLA(2) was completely inhibited by covalent

145 endent platelet activity can be inhibited by snake venom polypeptides.

146 arative analysis of 102 species we show that snake venom potency is generally prey-specific.

147 These findings reveal a mechanism whereby snake venoms produce pain, and highlight an unexpected c

148 evented by a pretreatment with mocarhagin, a snake venom protease that cleaves human GPIbalpha.

149 to type I fibrillar collagen or convulxin, a snake venom protein and known platelet agonist of GP VI.

150 ariety of RGD-containing peptides and by the snake venom protein echistatin, whereas an RGE-containin

151 The snake venom protein rhodocytin and the endogenous protei

152 sive and signaling responses to convulxin (a snake venom protein that directly binds GPVI) and weak r

153 In this context, snake venom proteins have demonstrated antiviral activit

154 re well documented as causes of variation in snake venom proteins, whereas the importance of gene reg

155 oding for proteins with sequence homology to snake venom prothrombin activator, trypsin-like enzymes,

156 Snake venoms provide a model system for studying the phe

157 oxins were detected from tobacco extract and snake venoms, respectively.

158 and intraspecies complexity and diversity of snake venoms, revealed by modern venomics, demands a rad

159 ic bioactives from mixtures of standards and snake venoms, revealing active peptides and coagulopathi

160 asis and thrombosis that is activated by the snake venom rhodocytin.

161 Snake venom-secreted phospholipase A(2) (svPLA(2)) enzym

162 In one large venom gene family (snake venom serine proteases), this co-option was likely

163 n with homology to integrin ligands found in snake venoms; several of these snake proteins have an RG

164 ng to the family of three-finger toxins from snake venoms, specifically stained the alpha1beta3gamma2

165 usceptible to the noxious effects of bee and snake venoms, suggesting that a caspase-1-dependent immu

166 Snake venom systems represent a valuable and tractable m

167 y of research on snake venom, many facets of snake venom systems, such as the physiology and regulati

168 TX2, two toxins present in Costa Rican coral snake venom that tightly bind to GABAA receptors at subn

169 (3FTx) are highly toxic components of elapid snake venoms that can cause diverse pathologies, includi

170 In this study, we subjected snake venom to enzymatic hydrolysis to identify previous

171 utics (SMTs) against the principal toxins of snake venoms to inhibit their lethality and/or obnoxious

172 omplex between Varespladib and a PLA(2)-like snake venom toxin (MjTX-II).

173 One subclass of AChRs that binds the snake venom toxin alpha-bungarotoxin (alpha-Bgt-AChRs) h

174 induced by the glycoprotein (GP)VI-selective snake venom toxin convulxin and by collagen.

175 flow cytometry and ligand blotting using the snake venom toxin convulxin.

176 The platelet receptor CLEC-2 binds to the snake venom toxin rhodocytin and the tumor cell surface

177 ified through interaction with a presynaptic snake venom toxin taipoxin.

178 The snake venom toxin trimucytin-stimulated a similar patter

179 d by affinity chromatography on columns of a snake venom toxin, taipoxin, and columns of the taipoxin

180 ake of synaptic material and the presynaptic snake venom toxin, taipoxin.

181 In a case study of snake venom toxin-protein interactions, our model accura

182 with MT7, a subtype-selective anti-M(1)AChR snake venom toxin.

183 The analysis and detection of snake venom toxins are a matter of great importance in c

184 The antigenic diversity present in snake venom toxins from various species presents a consi

185 d small molecule drugs that inhibit specific snake venom toxins show considerable promise for tacklin

186 between antivenom antibodies and epitopes on snake venom toxins, a high-throughput immuno-profiling s

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

188 Snake venoms, with a direct genetic basis and clearly de