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 entially neutralize the proteases present in snake venom.

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

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

9 lectin purified from Calloselasma rhodostoma snake venom.

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

11 e protection to mice against Echis carinatus snake venom.

12 ered peptide toxin superfamily isolated from snake venoms.

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

14 members of this protein family occurring in snake venoms.

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

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

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

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

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

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

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

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

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

24 Snake venoms are complex protein mixtures encoded by sev

25 Many snake venoms are known for their antithrombotic activity

26 Snake venoms are rich in protein and peptide toxins that

27 Snake venoms are variable protein mixtures with a multit

28 -4 does not afford direct protection against snake venom because it is actually a poor inhibitor of s

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

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

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

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

33 Snake venom consists of toxin proteins with multiple dis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 Snake venom hemorrhagic metalloproteinase toxins that ha

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

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

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

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

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

54 Snake venom is a natural substance that contains numerou

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

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

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

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

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

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

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

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

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

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

65 Elapid snake venom neurotoxins exert their effects through high

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 -3'dN) were corroborated by a combination of snake venom phosphodiesterase digestion in the presence

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

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

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

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

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

88 Enhanced stability against snake venom phosphodiesterase resulted from modification

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

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

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

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

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

94 e incorporation increases resistance against snake venom phosphodiesterase.

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

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

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

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

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

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

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

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

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

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

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

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

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

108 The snake venom protein rhodocytin and the endogenous protei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 The snake venom toxin trimucytin-stimulated a similar patter

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

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

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

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