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1 cury and increase circulating levels of this neurotoxin.
2 s dopaminergic neurons against a PD-inducing neurotoxin.
3 ut seafood can also contain methyl mercury-a neurotoxin.
4  suggest a role of this metabolite as a weak neurotoxin.
5 crease soluble Abeta, likely the proximal AD neurotoxin.
6 used by consuming foods containing botulinum neurotoxin.
7 rmed for Clostridium botulinum and botulinum neurotoxin.
8 e world are exposed to lead, a developmental neurotoxin.
9 an illness caused by types A and B botulinum neurotoxin.
10 ol for discriminative detection of different neurotoxins.
11 roup of nonconventional "three-finger" snake neurotoxins.
12 NTs) form a large class of potent and deadly neurotoxins.
13 regulation of mAChRs by "three-finger" snake neurotoxins.
14 und to develop novel inhibitors of botulinum neurotoxins.
15  in survival in PC-12 cells treated with the neurotoxins.
16 cluding biogenic amines, cationic drugs, and neurotoxins.
17 of different brain cell types in response to neurotoxins.
18 ease, essential for maturing of spider venom neurotoxins.
19 otentially fatal paralytic illness caused by neurotoxins.
20 vant for heterodimerization of a subgroup of neurotoxins.
21 opening, as the target for these amphipathic neurotoxins.
22 inium (MPP(+)), the active metabolite of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,
23 e substantia nigra following exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,
24 ve effects associated with the mitochondrial neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
25 ormalities, the uptake of monoamines and the neurotoxin 1-methyl-4-phenylpyridinium was significantly
26 etitive OCT1 ligands, of which an endogenous neurotoxin, 1-benzyl-1,2,3,4-tetrahydroisoquinoline, was
27 vented the death of neurons treated with the neurotoxin, 1-methyl-4-phenylpyridinium (MPP(+)), which
28                Injection of the serotonergic neurotoxin 5,7-dihydroxytryptamine into the third ventri
29                     Sublethal amounts of the neurotoxin 5,7-dihydroxytryptamine known to specifically
30 -2a and human SH-SY5Y - after treatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the bi
31 ative injury following administration of the neurotoxin 6-hydroxydopamine.
32 e obtained when worms were exposed to the DA neurotoxin 6-hydroxydopamine.
33                                    Botulinum neurotoxin A (BoNT/A) belongs to the most dangerous clas
34                                    Botulinum neurotoxin A (BoNT/A) has intrinsic endoprotease activit
35                                    Botulinum neurotoxin A (BoNT/A) induces muscle paralysis by enzyma
36                                    Botulinum neurotoxin A (BoNT/A) is one of the most deadly toxins a
37       Here we present VHHs against botulinum neurotoxin A (BoNT/A) on the surface of red blood cells
38 lood cells to express VHHs against botulinum neurotoxin A (BoNT/A) on their surface and show that an
39 rapid and sensitive immunoassay of botulinum neurotoxin A (BoNT/A).
40 gned to address the light chain of Botulinum Neurotoxin A and Ricin Toxin A chain, which could be spe
41 scriptional response when exposed to MPTP, a neurotoxin able to mimic the selective cell loss observe
42 g and increased DA neuron survival following neurotoxin administration.
43 r alpha-bungarotoxin and similar snake alpha-neurotoxins also targeting alpha7 nAChR.
44            Acrylamide (AA) is a known lethal neurotoxin and carcinogen.
45 typing since botulism is caused by botulinum neurotoxin and does not require the presence of the bact
46  RNases (EARs): the human eosinophil-derived neurotoxin and eosinophilic cationic protein, and their
47               Using a catecholamine-specific neurotoxin and hyperinsulinemic-hypoglycemic clamps, we
48 e oligomeric (oAbeta), considered a proximal neurotoxin and neuroinflammatory stimuli.
49                              Acrylamide is a neurotoxin and potential carcinogen, but is found in var
50 ented the deleterious effects exerted by the neurotoxin and related metabolite quinolinic acid (QUIN)
51 inal type of experiment, the potency of pure neurotoxin and toxin complex was compared in animals pre
52 ility to copper, a metal that in excess is a neurotoxin and whose depletion constitutes a micronutrie
53 re it serves as a precursor to siderophores, neurotoxins and antibiotics.
54 early aggregation process are believed to be neurotoxins and causative agents in Alzheimer disease.
55                                 Spider venom neurotoxins and cytolytic peptides are expressed as elon
56 he scallop uses hepatopancreas to accumulate neurotoxins and kidney to transform to high-toxicity for
57 3FTx) family, with high sequence identity to neurotoxins and low identity to the well-characterized 3
58 t role in protecting the brain from cationic neurotoxins and other potentially toxic organic cations.
59 er and energy devices, as well as injectable neurotoxins and soft-tissue augmentation materials, amon
60 c dermatologic procedures, including energy, neurotoxin, and filler procedures, are safe when perform
61 dy demonstrates the suitability of botulinum neurotoxin, and serotype D in particular, as a basis for
62                                       Spider neurotoxins are commonly used as pharmacological tools a
63                 We determined that all three neurotoxins are enzymatically active.
64                                    Botulinum neurotoxins are known to have seven serotypes (BoNT/A-G)
65                                      Peptide neurotoxins are powerful tools for research, diagnosis,
66                                    Botulinum neurotoxins are the most poisonous substances known to h
67                                    Botulinum neurotoxins are the most toxic of all compounds.
68                                              Neurotoxins associated with Parkinson's disease fully en
69 idium botulinum and associates with nontoxic neurotoxin-associated proteins to form high-molecular we
70 ble treatment antitoxin which can target the neurotoxin at the extracellular level and cannot reverse
71 tive to the therapeutic effects of botulinum neurotoxin B (BoNT/B) than the animal models it is teste
72 replacing it with M/C/V/Q enhances botulinum neurotoxin B binding to human synaptotagmin II.
73                             Mutant botulinum neurotoxin B containing E1191M/S1199Y exhibits 11-fold
74 g neurotransmission than wild-type botulinum neurotoxin B in neurons expressing human synaptotagmin I
75                                    Botulinum neurotoxin B is a Food and Drug Administration-approved
76                     The engineered botulinum neurotoxin B provides a platform to develop therapeutic
77 g affinity to h-Syt II may improve botulinum neurotoxin B's therapeutic efficacy and reduce adverse e
78 arget influenza haemagglutinin and botulinum neurotoxin B, along with 6,286 control sequences to prob
79 en in the Syt II-binding pocket of botulinum neurotoxin B.
80  JCI, Selvaraj et al. report that in a mouse neurotoxin-based model of PD, reduced Ca2+ influx throug
81                                The steroidal neurotoxin (-)-batrachotoxin functions as a potent agoni
82  domain and replacing it with a C. botulinum neurotoxin binding domain.
83 rs were co-transported with both the tetanus neurotoxin-binding fragment and the membrane proteins th
84                           First, clostridial neurotoxins block neurotransmission to or from neurons b
85      Tetanus neurotoxin (TeNT) and botulinum neurotoxin (BoNT) are clostridial neurotoxins (CNTs) res
86                                    Botulinum neurotoxin (BoNT) binds to and internalizes its light ch
87                                    Botulinum neurotoxin (BoNT) detection provides a useful model for
88 ensitive detection of highly toxic botulinum neurotoxin (BoNT) from Clostridium botulinum is of criti
89 mats was quantified and the type of botulism neurotoxin (bont) genes associated with this organism we
90 t germinate, multiply, and produce botulinum neurotoxin (BoNT) in the immature intestine.
91 laccid paralysis of muscles due to botulinum neurotoxin (BoNT) intoxication.
92                                    Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum a
93 ic disease caused by the action of botulinum neurotoxin (BoNT) on nerve cells.
94                                    Botulinum neurotoxin (BoNT) serotype A is the most lethal known to
95 covered which produces two toxins: botulinum neurotoxin (BoNT) serotype B and a novel BoNT reported a
96 c method for the detection of four botulinum neurotoxin (BoNT) serotypes responsible for human botuli
97  different sdAb specific for the 7 botulinum neurotoxin (BoNT) serotypes, enabling recognition of the
98  simultaneous on-site detection of botulinum neurotoxin (BoNT) types A, B, and E in complex matrixes,
99 ny of the seven known serotypes of botulinum neurotoxin (BoNT), all of which disrupt synaptic transmi
100 east one of the seven serotypes of botulinum neurotoxin (BoNT/A-G).
101 ic proteins for humans and include botulinum neurotoxins (BoNT) and tetanus neurotoxin (TeNT).
102                                    Botulinum neurotoxins (BoNT) are the most potent toxins known and
103                                    Botulinum neurotoxins (BoNT/A-G) act by blocking synaptic vesicle
104 mics approach, we report here that all three neurotoxins, BoNT/A2, /F4, and /F5, are produced by C. b
105                                    Botulinum neurotoxins (BoNTs) and tetanus neurotoxin (TeNT) are th
106                                    Botulinum neurotoxins (BoNTs) and tetanus toxin (TeNT) are the mos
107                                     Botulium neurotoxins (BoNTs) are among the most lethal toxins kno
108                                    Botulinum neurotoxins (BoNTs) are among the most poisonous biologi
109                                    Botulinum neurotoxins (BoNTs) are highly potent bacterial proteins
110                                    Botulinum neurotoxins (BoNTs) are highly potent toxins that cleave
111                                    Botulinum neurotoxins (BoNTs) are produced by various species of c
112                                    Botulinum neurotoxins (BoNTs) are synthesized by Clostridium botul
113                                    Botulinum neurotoxins (BoNTs) are the most toxic proteins for huma
114                                    Botulinum neurotoxins (BoNTs) are the most toxic substances known.
115                                    Botulinum neurotoxins (BoNTs) are used in a wide variety of medica
116                                    Botulinum neurotoxins (BoNTs) are zinc endopeptidases that block r
117                                    Botulinum neurotoxins (BoNTs) cleave SNARE proteins in motor neuro
118                                How botulinum neurotoxins (BoNTs) cross the host intestinal epithelial
119                                    Botulinum neurotoxins (BoNTs) form a large class of potent and dea
120                                    Botulinum neurotoxins (BoNTs) possess unique specificity for nerve
121                                    Botulinum neurotoxins (BoNTs) produced by Clostridium botulinum ar
122     Clostridium botulinum produces botulinum neurotoxins (BoNTs), highly potent substances responsibl
123                                    Botulinum neurotoxins (BoNTs), the most potent toxins known, are p
124                                    Botulinum neurotoxins (BoNTs), which are highly toxic proteins res
125 of the dinoflagellate Karenia brevis and its neurotoxin, brevetoxin (PbTx).
126                           It produces potent neurotoxins (brevetoxins [PbTxs]), which negatively impa
127 eveloping fetuses are most at risk from this neurotoxin but health effects of highly exposed populati
128 ng neuronal resistance to Alphabeta or other neurotoxins by decreasing mitochondrial activity and sub
129 ay increase human exposure to MeHg, a potent neurotoxin, by increasing MeHg production as well as bio
130 calcium-dependent and inhibited by botulinum neurotoxin C, demonstrating the involvement of SNARE-dep
131  not when syntaxin-1 is cleaved by botulinum neurotoxin C.
132 ory failure, ultimately resulting in reduced neurotoxin clearance along the optic nerves, could be an
133                              The clostridial neurotoxins (CNTs) are the most toxic proteins for human
134  botulinum neurotoxin (BoNT) are clostridial neurotoxins (CNTs) responsible for the paralytic disease
135                                 Cyclic imine neurotoxins competitively inhibit biotinylated-alpha-bun
136 num HA is a component of the large botulinum neurotoxin complex and is critical for its oral toxicity
137                                 Cyclic imine neurotoxins constitute an emergent family of neurotoxins
138 convert the inactive prodrug Daun02 into the neurotoxin daunorubicin.
139 inals exposed to spider or snake presynaptic neurotoxins degenerate as a result of calcium overload a
140 ne-coated nanoparticle (RBCNP) with a unique neurotoxin-derived targeting moiety.
141  of nanomolar concentrations of cyclic imine neurotoxins directly in shellfish samples.
142 Zalophus californianus) exposed to the algal neurotoxin domoic acid are treated in veterinary rehabil
143 reconstituted evoked exocytosis in botulinum neurotoxin E-treated neurons.
144 was developed for the detection of botulinum neurotoxin-E (BoNT/E).
145 leukotrienes (CysLT), and eosinophil-derived neurotoxin (EDN) release.
146 ilia and IL-5, IL-13, and eosinophil-derived neurotoxin (EDN), which stayed consistent after 6 weeks.
147            Human LYNX1, belonging to the Ly6/neurotoxin family of three-finger proteins, is membrane-
148                          Mercury is a potent neurotoxin for humans, particularly if the metal is in t
149                           Although botulinum neurotoxin for refractory bladder pain syndrome/intersti
150               Luteovirid coat protein-insect neurotoxin fusions represent a promising strategy for tr
151 lostridial organism containing more than two neurotoxin gene clusters.
152  Clostridium botulinum strain Af84 has three neurotoxin gene clusters: bont/A2, bont/F4, and bont/F5.
153                                          The neurotoxin genes were then deleted independently in the
154 xin fulfills a plethora of functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and
155 ethylation, however, SAM is converted to the neurotoxin homocysteine and must be excreted or drawn ba
156 e versuta (Blue Mountains funnel-web spider) neurotoxin (Hvt) and onion leaf lectin, in tobacco (Nico
157                                    MeHg as a neurotoxin impacts on the human central nervous systems
158 ound that expression of four insect specific neurotoxins improved the efficacy of M. acridum against
159                     For facial injections of neurotoxin in saline, 30-gauge needles were associated w
160 first time that, during exposure to an HIV-1 neurotoxin in vivo, alteration of GluN2B-containing NMDA
161 betaOs), increasingly recognized as proximal neurotoxins in AD, impair organelle transport in culture
162 eta peptide have been implicated as proximal neurotoxins in Alzheimer's disease.
163  and degeneration as well as accumulation of neurotoxins in brain such as beta-amyloid (Abeta) in Alz
164 f amyloid-beta (Abeta) oligomers, AD-related neurotoxins, in the brains of rats and adult nonhuman pr
165 notoxin ImI and a chimeric Naja oxiana alpha-neurotoxin indicating that the major role in alpha-Ctx b
166 fed on these fusion proteins showed signs of neurotoxin-induced paralysis.
167 nd PLD1 positively control fusion of tetanus neurotoxin insensitive vesicle-associated membrane prote
168                                      Tetanus neurotoxin-insensitive vesicular-associated membrane pro
169 cision placement of agents (e.g., tracers or neurotoxins) into small brain regions of the infant and
170 ut less well understood aspects of botulinum neurotoxin intoxication.
171 peptide (AbetaOs) are thought to be proximal neurotoxins involved in early neuronal oxidative stress
172                                    Botulinum neurotoxin is considered as one of the most toxic food-b
173 e, convenient, and rapid assay for botulinum neurotoxins is therefore highly desirable for addressing
174 though its contamination by mercury, a known neurotoxin, is a growing concern.
175 Tetrodotoxin (TTX), a small molecular weight neurotoxin, is responsible for poisoning events that tra
176 sTx-1 exhibits two different functions; as a neurotoxin it inhibits L-type Ca(2+) channels, and as a
177 tamate analogs, like the classic excitotoxic neurotoxins kainic acid, domoic acid, and NMDA; the ther
178    Domoic acid (DA) is a naturally occurring neurotoxin known to harm marine animals.
179 manganese and zinc, and higher uptake of the neurotoxin lead.
180                                The botulinum neurotoxin light chain (LC) protease has become an impor
181                                       Potent neurotoxins like tetrodotoxin (TTX) and saxitoxin (STX)
182        Glycosylphosphatidylinositol-anchored neurotoxin-like receptor binding proteins, such as lynx
183                                          The neurotoxin-like region of the rabies virus glycoprotein
184 y some other three-finger toxins, long alpha-neurotoxin Ls III and nonconventional toxin WTX.
185 ains 7, 8, and 9 of the highly potent marine neurotoxin maitotoxin (1), the largest secondary metabol
186 streamwater concentrations and export of the neurotoxin methyl mercury (MeHg) to freshwater ecosystem
187 t receives gestational exposure (E17) to the neurotoxin methylazoxymethanol (MAM).
188  Microbial production of the bioaccumulative neurotoxin methylmercury (MeHg) is stimulated in newly f
189 c trace metal into the highly bioaccumulated neurotoxin methylmercury (MeHg).
190 ributes to the bioaccumulation of the potent neurotoxin methylmercury in the marine food web.
191  LTCC blockers were neuroprotective in mouse neurotoxin models of PD, and isradipine is currently und
192 gainst anatoxin-a (ATX), the smallest potent neurotoxin (Mol.
193 se species contain the highest levels of the neurotoxin monomethylmercury (MMHg) and therefore presen
194 eria that produce the potent bioaccumulative neurotoxin monomethylmercury remains one of the greatest
195                                           PD neurotoxin MPP(+) inhibits neddylation of both parkin an
196 P2D6 are fully capable of activating the pro-neurotoxin MPTP and inducing neuronal damage, which is e
197 and astrocytic inflammatory responses to the neurotoxin MPTP and reduced striatal dopamine turnover.
198  in different lineages to function as potent neurotoxins, myotoxins, or hemotoxins.
199 nd female P301S tau transgenic mice with the neurotoxin N-(2-chloroethyl)-N-ethyl-bromobenzylamine (D
200                Monomethylmercury (MMHg) is a neurotoxin of concern in the Canadian Arctic due to its
201 neurotoxins constitute an emergent family of neurotoxins of dinoflagellate origin that are potent ant
202                                       Insect neurotoxins offer an alternative to chemical insecticide
203  we studied the effect of this environmental neurotoxin on PP2A activity and tau hyperphosphorylation
204  < 0.001, r = 0.7353] and eosinophil-derived neurotoxin [p < 0.01, r = 0.7059]).
205           Annonaceous acetogenins (AAGs) are neurotoxins possibly responsible for atypical Parkinsoni
206       Here we describe the purification of a neurotoxin precursor processing protease from the venom
207 y of the protease in propeptide removal from neurotoxin precursors by cleavage C-terminal of the PQM.
208 es mimicking the predicted cleavage sites of neurotoxin precursors.
209 ns, the genes of a specialized heterodimeric neurotoxin predate the origin of rattlesnakes and were p
210                      Domoic acid is a potent neurotoxin produced by certain marine microalgae that ca
211            The HIV-1 Tat protein is a potent neurotoxin produced during HAND that induces activation
212                    Methylmercury is a potent neurotoxin produced in natural environments from inorgan
213    Outbreaks are caused by bird ingestion of neurotoxins produced by Clostridium botulinum, a spore-f
214 e first report of three enzymatically active neurotoxins produced in a single strain of Clostridium b
215               The highly poisonous botulinum neurotoxins, produced by the bacterium Clostridium botul
216  samples were tested for botulinum toxin and neurotoxin-producing Clostridium species.
217 epod Calanus finmarchicus co-occurs with the neurotoxin-producing dinoflagellate, Alexandrium fundyen
218 this paper we present a scheme for modelling neurotoxin production in C. botulinum Group I type A1, b
219 ship between HIV replication, HO-1 loss, and neurotoxin production in MDM that likely reflects proces
220 crophage HO-1 deficiency, and the associated neurotoxin production, is a conserved feature of infecti
221 does not prevent HO-1 loss or the associated neurotoxin production.
222 red to detect the trace amount of endogenous neurotoxin (QA).
223 be for the selective detection of endogenous neurotoxin quinolinic acid (QA) whose elevated level in
224                                          The neurotoxin quinolinic acid may impair blood-brain barrie
225 rtant neuroactive metabolites, including the neurotoxin, quinolinic acid (QUIN), the neuroprotective
226 toxin (TTX) is one of the most potent marine neurotoxins reported.
227 ration is induced by some animal presynaptic neurotoxins, representing an appropriate and controlled
228 icardial application of a selective afferent neurotoxin, resiniferatoxin, selectively lowered diastol
229 errence against predation, while it achieves neurotoxin resistance through point mutations in sodium
230 r muscle, sophisticated eyes, and remarkable neurotoxin resistance.
231 Pseudomonas aeruginosa exotoxin A, Botulinum neurotoxin, ricin, and Zika virus.
232 pression changes induced by the Parkinsonian neurotoxin rotenone and opposed by those induced by clio
233 AR by epicardial application of the afferent neurotoxin, RTX, selectively lowered diastolic blood pre
234 -beta-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinj
235 us animals such as scorpions produce diverse neurotoxins selected to hit targets in the nervous syste
236 en-labelled studies have suggested botulinum neurotoxin serotype A (BoNT-A) to be an effective treatm
237                                    Botulinum neurotoxin serotype A (BoNT/A) causes a debilitating and
238  (4,7-ACQ) based inhibitors of the botulinum neurotoxin serotype A (BoNT/A) light chain were synthesi
239 says for colorimetric detection of botulinum neurotoxin serotype A light chain (BoLcA).
240 analogues of dual antimalarial and botulinum neurotoxin serotype A light chain (BoNT/A LC) inhibitor
241 gosaccharide GD1a can associate to botulinum neurotoxin serotype A when expressed as individual trisa
242 ate minimal binding epitope of the botulinum neurotoxin serotype A.
243                     Stichodactyla helianthus neurotoxin (ShK) is an immunomodulatory peptide currentl
244 d and functionally characterized to date are neurotoxins specifically targeted to receptors, ion chan
245  agent vincristine, antimalarial quinine and neurotoxin strychnine, are synthesized in several differ
246 orescent recognition agent for the botulinum neurotoxin subtype A (BoNT/A) using the virtual screenin
247 oxicity is indirect, resulting from released neurotoxins such as the HIV-1 protein transactivator of
248                                      Tetanus neurotoxin (TeNT) and botulinum neurotoxin (BoNT) are cl
249    Botulinum neurotoxins (BoNTs) and tetanus neurotoxin (TeNT) are the most toxic proteins for humans
250                                      Tetanus neurotoxin (TeNT) causes neuroparalytic disease by enter
251                                      Tetanus neurotoxin (TeNT) is among the most poisonous substances
252 AREs (synaptobrevins/VAMP1/2/3 using tetanus neurotoxin (TeNT), also in TI-VAMP/VAMP7 knock-out (KO)
253 ude botulinum neurotoxins (BoNT) and tetanus neurotoxin (TeNT).
254 ignificant capacity to store psychosine, the neurotoxin that accumulates in Krabbe disease.
255                        Gambierol is a potent neurotoxin that belongs to the family of marine polycycl
256  elevated loadings of methylmercury (MeHg; a neurotoxin that biomagnifies through foodwebs) due to oi
257                            Mercury (Hg) is a neurotoxin that can be particularly harmful to top preda
258                         Here, we show that a neurotoxin that causes a disease that mimics PD upon adm
259 eurotoxin type A (BoNT/A) is a highly potent neurotoxin that elicits flaccid paralysis by enzymatic c
260             Methylmercury (MeHg) is a potent neurotoxin that has been demonstrated to biomagnify in A
261 with 1-methyl-4-phenylpyridinium (MPP(+)), a neurotoxin that inhibits complex I of electron transport
262             Methylmercury (MeHg) is a potent neurotoxin that is biomagnified approximately 1-10 milli
263                          Ammonia is a potent neurotoxin that is detoxified mainly by the urea cycle i
264 -tetrahydropyridine (MPTP) is a dopaminergic neurotoxin that replicates most of the clinical features
265 xicity of the venom is mainly due to various neurotoxins that belong to two distinct structural and i
266 llate produces brevetoxins, which are potent neurotoxins that cause neurotoxic shellfish poisoning an
267    Brevetoxins (BTXs) are very potent marine neurotoxins that increased in geographical distribution
268                                              Neurotoxins that mimic Parkinson's disease increased Cav
269                                              Neurotoxins that mimic Parkinson's disease target TRPC1
270 ellate Karenia brevis, which produces potent neurotoxins that negatively impact coastal marine ecosys
271  alpha-Conotoxins are disulfide-rich peptide neurotoxins that selectively inhibit neuronal nicotinic
272 t North American rattlesnakes do not produce neurotoxins, the genes of a specialized heterodimeric ne
273 etwork excitability in the presence of HIV-1 neurotoxins; these changes may inform the development of
274 ate-receptor binding assay, the cyclic imine neurotoxins tightly bound to the coated Torpedo nicotini
275 iche, starting by middle age, amplified upon neurotoxin treatment and associated with an exacerbated
276                                              Neurotoxin treatment decreased TRPC1 expression, TRPC1 i
277 sensitive detection of Clostridium botulinum Neurotoxin Type A (BoNT/A) in complex, real-world media.
278                                    Botulinum neurotoxin type A (BoNT/A) is a highly potent neurotoxin
279 ssociated protein 25 (SNAP-25) for botulinum neurotoxin type A (BoNT/A).
280 012 is a recombinant derivative of Botulinum neurotoxin Type A (BoNT/A).
281 ent with infant botulism, produced botulinum neurotoxin type B (BoNT/B) and another BoNT that, by use
282                                The botulinum neurotoxin type D is one of seven highly potent toxins p
283                                    Botulinum neurotoxin type E (BoNT/E) is a member of a family of se
284 ent was prevented by expression of botulinum neurotoxin type E.
285 duces the recently described novel botulinum neurotoxin type H (BoNT/H).
286 e of 62 (SD 22) treatments of 70.2 (SD 20.8) neurotoxin units.
287 d by examining the enzymatic activity of the neurotoxins upon peptide substrates, which mimic the tox
288 tect against dopaminergic deficits caused by neurotoxins via increased neurogenesis in the subventric
289 eurocognitive diseases through metabolism to neurotoxins via the kynurenine pathway, a role for kynur
290            In the first, the potency of pure neurotoxin was compared with that of progenitor toxin co
291          The enzymatic activity of all three neurotoxins was assessed by examining the enzymatic acti
292 aightforward detection between OP and non-OP neurotoxins was successfully achieved with cyclic voltam
293                            Using a selective neurotoxin, we also demonstrate differential drive of th
294  and antagonist responses nicotine and known neurotoxins were detected from tobacco extract and snake
295 rticular interest as methylmercury (MeHg), a neurotoxin which bioaccumulates through foodwebs, can re
296 various species of clostridia and are potent neurotoxins which cause the disease botulism, by cleavin
297 mercury (MeHg(+) ) is one of the most potent neurotoxins, which damages the brain and nervous system
298 and epitope, and these compounds bind to the neurotoxin with a high degree of predisposition but with
299 is the first discovery of a single botulinum neurotoxin with BoNT/A antigenicity and BoNT/F light cha
300 supernatants and tested each immune-captured neurotoxin with full-length substrates vesicle-associate

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