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1 nd peripheral site inhibitors (gallamine and fasciculin).
2 d with a K(S) of 0.4+/- 0.2 mM measured with fasciculin.
3  with its peptidic inhibitor, the neurotoxin fasciculin.
4 n of the AChE was resistant to inhibition by fasciculin.
5  anionic site ligands, such as propidium and fasciculin.
6 hat the dissociation of fluorescently-tagged fasciculin 2 (a specific and selective peptide inhibitor
7                  The peripheral site ligand, fasciculin 2 (FAS2), a peptide of 6.5 kDa with a net cha
8                                              Fasciculin 2 (Fas2), a three-fingered peptide of 61 amin
9 The availability of a crystal structure of a fasciculin 2 (Fas2)-acetylcholinesterase complex affords
10 lation of the protein-protein complex, where fasciculin 2 appears to sterically block access of ligan
11                                              Fasciculin 2 binds to the gorge entrance of acetylcholin
12                            To assess whether fasciculin 2 can sterically block access of a ligand to
13                                 For the AChE-fasciculin 2 complex, the corresponding constants were k
14 interact with the acylation site in the AChE-fasciculin 2 complex.
15 is of the relaxation times in the absence of fasciculin 2 gave estimates of the N-methylacridinium as
16                                  When excess fasciculin 2 was added, the prominent relaxation shifted
17 ased by more than 3 orders of magnitude when fasciculin 2 was bound, consistent with a pronounced ste
18 ium with AChE in the presence and absence of fasciculin 2 were measured by fluorescence temperature j
19 n, we synthesized a fluorescent conjugate of fasciculin 2, a snake alpha-neurotoxin that tightly bind
20 ral site where inhibitors like propidium and fasciculin 2, a snake neurotoxin, bind and interfere wit
21  one-time blockade of AChEs with fluorescent fasciculin 2, AChEs are removed from synapses initially
22 er, when AChEs are continuously blocked with fasciculin 2, the removal rate increases substantially (
23 ation of acetylcholinesterase complexed with fasciculin 2.
24 nteraction with human AChE in the absence of fasciculin 2.
25 .1-1 ms range was observed in the absence of fasciculin 2.
26 formed by one of the apo forms of neurotoxin fasciculin-2 (FAS2) and its high-affinity binding protei
27                               The neurotoxin fasciculin-2 (FAS2) is a picomolar inhibitor of synaptic
28 nesterase (mAChE) and the protein neurotoxin fasciculin-2.
29                                              Fasciculin, a selective peptidic inhibitor of acetylchol
30 tors, measurements of phosphorylation of the fasciculin-AChE complex by AChE inactivation gave mislea
31 rylodan at the 262 position are unaltered by fasciculin addition.
32                    Capping of the gorge with fasciculin, although it does not displace the bound liga
33 ns of the conformationally flexible proteins fasciculin and calmodulin, as well as the less flexible
34  sample transitions between the substates of fasciculin and calmodulin, GNEIMO simulations show the t
35 resence of two inhibitors of different size, fasciculin and huperzine.
36                    Analysis of inhibition of fasciculin association rates by these substrates reveale
37 at part of their epitope overlapped with the fasciculin binding site.
38 ]-4-methylcoumarin (EMPC) that resulted from fasciculin binding, decreased from 0.002 in wild-type hu
39 sochromic shift of the emission maximum with fasciculin binding.
40 onal change in the acylation site induced by fasciculin binding.
41                                         Like fasciculin, binding of these monoclonal antibodies in th
42 cholinesterase active site is disrupted with fasciculin bound.
43                                              Fasciculin, but not tacrine, on the other hand, dramatic
44  demonstrate that a fluorescently conjugated fasciculin can be used to monitor total, active, and OP-
45  and application to the acetylcholinesterase-fasciculin complex is illustrated.
46 GNEIMO with replica exchange to the study of fasciculin conformational dynamics produced sampling of
47 ecular dynamics trajectories of apo forms of fasciculin, corresponding to different conformational su
48      To this end, we constructed a synthetic fasciculin gene with an appropriate leader peptide for e
49 , and the peripheral site peptide inhibitor, fasciculin, had no effect on the anisotropy decay of flu
50 ith partial occlusion by loops II and III of fasciculin in the complex.
51                                         When fasciculin is present, the gorge width distribution is a
52 the acrylodan in the complex with the tip of fasciculin loop II.
53 c obstruction seen in the crystal structure, fasciculin may inhibit acetylcholinesterase by combined
54 he 287 position, in a manner consistent with fasciculin reducing the segmental motion of the peptide
55  6H9, and 5E8 interfered with the binding of fasciculin to the complexed enzyme, suggesting that part
56 t, the binding of the polypeptide neurotoxin fasciculin to the peripheral site of AChE dramatically d
57 formational effect induced by the binding of fasciculin to the peripheral site.
58  inhibition of the binding of the neurotoxin fasciculin to the peripheral site.
59                               The neurotoxin fasciculin was used to report specifically on interactio
60                                    Moreover, fasciculin, which binds at the mouth of the gorge, well
61 acity to influence the binding of a peptide, fasciculin, which inhibits catalysis peripherally by sea

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