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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
30 -2a and human SH-SY5Y - after treatment with neurotoxin 6-hydroxydopamine (6-OHDA), leading to the bi
38 lood cells to express VHHs against botulinum neurotoxin A (BoNT/A) on their surface and show that an
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
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
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
54 early aggregation process are believed to be neurotoxins and causative agents in Alzheimer disease.
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
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
74 g neurotransmission than wild-type botulinum neurotoxin B in neurons expressing human synaptotagmin I
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
80 JCI, Selvaraj et al. report that in a mouse neurotoxin-based model of PD, reduced Ca2+ influx throug
83 rs were co-transported with both the tetanus neurotoxin-binding fragment and the membrane proteins th
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
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
104 mics approach, we report here that all three neurotoxins, BoNT/A2, /F4, and /F5, are produced by C. b
122 Clostridium botulinum produces botulinum neurotoxins (BoNTs), highly potent substances responsibl
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
132 ory failure, ultimately resulting in reduced neurotoxin clearance along the optic nerves, could be an
134 botulinum neurotoxin (BoNT) are clostridial neurotoxins (CNTs) responsible for the paralytic disease
136 num HA is a component of the large botulinum neurotoxin complex and is critical for its oral toxicity
139 inals exposed to spider or snake presynaptic neurotoxins degenerate as a result of calcium overload a
142 Zalophus californianus) exposed to the algal neurotoxin domoic acid are treated in veterinary rehabil
146 ilia and IL-5, IL-13, and eosinophil-derived neurotoxin (EDN), which stayed consistent after 6 weeks.
152 Clostridium botulinum strain Af84 has three neurotoxin gene clusters: bont/A2, bont/F4, and bont/F5.
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
158 ound that expression of four insect specific neurotoxins improved the efficacy of M. acridum against
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
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
167 nd PLD1 positively control fusion of tetanus neurotoxin insensitive vesicle-associated membrane prote
169 cision placement of agents (e.g., tracers or neurotoxins) into small brain regions of the infant and
171 peptide (AbetaOs) are thought to be proximal neurotoxins involved in early neuronal oxidative stress
173 e, convenient, and rapid assay for botulinum neurotoxins is therefore highly desirable for addressing
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
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
188 Microbial production of the bioaccumulative neurotoxin methylmercury (MeHg) is stimulated in newly f
191 LTCC blockers were neuroprotective in mouse neurotoxin models of PD, and isradipine is currently und
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
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.
199 nd female P301S tau transgenic mice with the neurotoxin N-(2-chloroethyl)-N-ethyl-bromobenzylamine (D
201 neurotoxins constitute an emergent family of neurotoxins of dinoflagellate origin that are potent ant
203 we studied the effect of this environmental neurotoxin on PP2A activity and tau hyperphosphorylation
207 y of the protease in propeptide removal from neurotoxin precursors by cleavage C-terminal of the PQM.
209 ns, the genes of a specialized heterodimeric neurotoxin predate the origin of rattlesnakes and were p
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
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
223 be for the selective detection of endogenous neurotoxin quinolinic acid (QA) whose elevated level in
225 rtant neuroactive metabolites, including the neurotoxin, quinolinic acid (QUIN), the neuroprotective
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
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
238 (4,7-ACQ) based inhibitors of the botulinum neurotoxin serotype A (BoNT/A) light chain were synthesi
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
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
249 Botulinum neurotoxins (BoNTs) and tetanus neurotoxin (TeNT) are the most toxic proteins for humans
252 AREs (synaptobrevins/VAMP1/2/3 using tetanus neurotoxin (TeNT), also in TI-VAMP/VAMP7 knock-out (KO)
256 elevated loadings of methylmercury (MeHg; a neurotoxin that biomagnifies through foodwebs) due to oi
259 eurotoxin type A (BoNT/A) is a highly potent neurotoxin that elicits flaccid paralysis by enzymatic c
261 with 1-methyl-4-phenylpyridinium (MPP(+)), a neurotoxin that inhibits complex I of electron transport
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
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
277 sensitive detection of Clostridium botulinum Neurotoxin Type A (BoNT/A) in complex, real-world media.
281 ent with infant botulism, produced botulinum neurotoxin type B (BoNT/B) and another BoNT that, by use
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
292 aightforward detection between OP and non-OP neurotoxins was successfully achieved with cyclic voltam
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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