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1 ultiple species and is the major allergen in bee venom.
2  is dispensable for the allergic response to bee venom.
3  vespid venom, but not in those treated with bee venom.
4 tudied after adding glutamate and sPLA2 from bee venom.
5     Melittin is the primary peptide in honey bee venom.
6  originally isolated from the European honey bee venom.
7 s of Mycobacterium chelonae infections after bee venom acupuncture.
8 ic skin and soft tissue infections following bee venom acupuncture.
9               B cells specific for the major bee venom allergen phospholipase A2 (PLA) were isolated
10               B cells specific for the major bee venom allergen PLA isolated from nonallergic beekeep
11 depot effect, prolonging the availability of bee venom allergens at the site of administration.
12 increased by adding rSSMA of other important bee venom allergens.
13    We retrospectively analyzed data from 190 bee venom-allergic and 809 vespid venom-allergic patient
14 and/or Ves v 1, and 78.3% of single-positive bee venom-allergic patients had sIgE to Api m 1.
15  while a bee/vespid ratio >= 5.33 identified bee venom allergy with 50.6% sensitivity, both with 100%
16 t-off approach with the intradermal test for bee venom allergy, while sensitivity for vespid venom al
17 n secreted phospholipase A(2) (sPLA(2), from bee venom and bovine pancreas) and a transition-state an
18             Although very different from the bee venom and mammalian hyaluronidase sequences, the E.
19 ients and controls, sIgE to rSSMA Api m 1 of bee venom and to Ves v 1 and Ves v 5 of wasp venom were
20 d from beekeepers who displayed tolerance to bee venom antigens and allergic patients before and afte
21                                          The bee venom antimicrobial peptide, melittin, besides showi
22            Molecular dynamics simulations of bee venom apamin, and an analogue having an Asn to Ala s
23                               Sensitivity of bee venom Api m 1 could be increased by adding rSSMA of
24 antibacterial, and antioxidant properties of bee venom (apitoxin), its application for promoting grow
25 la2g10 In the periphery, an sPLA(2) found in bee venom (bee venom PLA(2)) administered with the incom
26 ptor sequences of Bmem specific to the major bee venom (BV) allergen Api m 1 before and after ultra-r
27                                        Honey bee venom (BV) allergies are very common; however, the l
28 he ImmunoCAP system for routine diagnosis of bee venom (BV) allergy.
29 optimal formulation of liposomes loaded with bee venom (BV) and coated with PEG (BV-Lipo-PEG).
30           This study explored the effects of bee venom (BV) encapsulated nano-chitosan (BV-CSNPs) on
31   Here, we investigated the putative role of bee venom (Bv) in human FOXP3-expressing Treg homeostasi
32         The secreted phospholipase A(2) from bee venom (bvPLA(2)) contains a membrane binding surface
33  finding was explained by demonstrating that bee venom-derived phospholipase A2 (PLA2) activates T ce
34 ) or diets added with 0.1, 0.2, or 0.3 mg of bee venom encapsulated nano-chitosan (BV-CSNPs) per kg o
35  IgG4-switched memory B cells expanded after bee venom exposure.
36 otherwise) increased sensitivity for sIgE to bee venom from 85.7% to 94.6% and for vespid venom from
37 (TPN), a 21 amino acid peptide isolated from bee venom, has been reported to inhibit Kir1.1 and Kir3.
38 ied distinct sensitization profiles in honey bee venom (HBV) allergy, some of which were dominated by
39 rted (beta/alpha)8 barrel resembling that of bee venom hyaluronidase, and a novel, EGF-like domain, c
40 ially inhibited sPLA2 OS2 but not sPLA2 from bee venom-induced arachidonic acid release.
41    Whereas activation of the inflammasome by bee venom induces a caspase-1-dependent inflammatory res
42 protein toxin originally isolated from honey bee venom, inhibits only certain eukaryotic inward-recti
43 in (TPN), a small protein derived from honey bee venom, inhibits the GIRK1/4 and ROMK1 channels with
44                            Here we show that bee venom is detected by the NOD-like receptor family, p
45         Melittin, the major component of the bee venom, is an amphipathic, cationic peptide with a wi
46  complex with melittin, a major component of bee venom, is often used as a model system of protein-pr
47 ally evolved gain-of-function variant of the bee venom lytic peptide melittin identified in a high-th
48 o occurs if cells are reacted in medium with bee venom melittin, which penetrates cells and forms mem
49         Among the different sPLA(2)s tested, bee venom, Naja naja, and porcine and human pancreatic P
50 cial catalysis by phospholipase A2 (PLA2) of bee venom on zwitterionic vesicles of 1-palmitoyl-2-oleo
51                    UCL1684, a mimetic of the bee venom peptide apamin, sits atop the canopy and occlu
52 es of the cecropin A and residues 2-9 of the bee venom peptide mellitin.
53 ry conductance values and sensitivity to the bee venom peptide toxin, apamin.
54 ere synthesized encompassing portions of the bee venom peptide, apamin, and the sequence KWLAESVRAGK
55 c example of membrane-induced folding is the bee-venom peptide melittin that is largely unstructured
56                  Kinetic characterization of bee venom phospholipase A(2) activity at bile salt+phosp
57  activity of the synthetic analogues against bee venom phospholipase A(2) suggests that cacospongiono
58 ATX generates LPA from CHO cells primed with bee venom phospholipase A(2), and ATX-mediated LPA produ
59 ing phosphatidylcholine (PC), using snake or bee venom phospholipase A(2).
60          Interfacial catalytic constants for bee venom phospholipase A2 (bvPLA2) have been obtained f
61               The basis for tight binding of bee venom phospholipase A2 (bvPLA2) to anionic versus zw
62 pheles stephensi mosquitoes that express the bee venom phospholipase A2 (PLA2) gene from the gut-spec
63 pecific suppressor T cell (Ts) hybridoma and bee venom phospholipase A2 (PLA2)-specific Ts hybridoma
64 ipoprotein were active, LDL was treated with bee venom phospholipase A2 (PLA2).
65 oxalate) has been developed to determine how bee venom phospholipase A2 sits on the membrane.
66  activity of the synthetic analogues against bee venom phospholipase A2 suggests that the cacospongio
67                                           In bee venom phospholipase A2, histidine-34 probably functi
68 onphospholipid as a novel substrate of honey bee venom phospholipase A2.
69  and with a structurally divergent group III bee venom PLA(2) (bvPLA(2)).
70      In this study, we demonstrate that both bee venom PLA(2) and murine sPLA(2)-X have adjuvant acti
71 he periphery, an sPLA(2) found in bee venom (bee venom PLA(2)) administered with the incomplete Ag OV
72                                We found that bee venom PLA2 induced a T helper type 2 (Th2) cell-type
73                         Here we examined how bee venom PLA2 is sensed by the innate immune system and
74 nd enzymatic activity of membrane-associated bee venom PLA2, covering a pressure range up to 2 kbar.
75 ns to three membrane peptides: melittin from bee venom, the transmembrane domain of the M2 protein fr
76 A (from moth) with residues 2-9 of melittin (bee venom)], three fluorescence signals report oxidative
77 f allergen-specific B cells before and after bee venom tolerance induction.
78                        Pretreatment with the bee venom toxin apamin enhanced this response.
79          Melittin, the main component of dry bee venom, was used as a model amphipathic alpha-helical
80    Here, by modifying a toxin from the honey bee venom, we have successfully engineered an inhibitor
81 melittin, the active molecule of apitoxin or bee venom, were investigated on human red blood cells (R