ライフサイエンスコーパス: fibrillization

1 ses and in kinetic studies of self-assembly (fibrillization).

2 ll as toxic gains of function (increased tau fibrillization).

3 gap is the mechanism of Tau condensation and fibrillization.

4 the polypeptide chains during misfolding and fibrillization.

5 es, Congo red and Lacmoid, which inhibit its fibrillization.

6 loid fibrils, a subset of which also inhibit fibrillization.

7 rillizing proteins need to be "prepared" for fibrillization.

8 il (residues 17-21) that significantly slows fibrillization.

9 iophysical readouts for monitoring alpha-Syn fibrillization.

10 s resulted in oligomer loss and promotion of fibrillization.

11 inhibitors of alpha-Syn oligomerization and fibrillization.

12 nge may contribute to the kinetic control of fibrillization.

13 ntified as a specific inhibitor of alpha-syn fibrillization.

14 the dopamine-induced inhibition of alpha-syn fibrillization.

15 further oligomerizes to a tetramer, prior to fibrillization.

16 ecies that, as a peptide mixture, seed Abeta fibrillization.

17 transiently populated during the process of fibrillization.

18 isulfide bond that promotes dimerization and fibrillization.

19 the oligomerization of Abeta but inhibit its fibrillization.

20 ctly or indirectly on Abeta and inhibits its fibrillization.

21 now studied the effect of gelsolin on Abeta fibrillization.

22 ting that disease may arise from accelerated fibrillization.

23 most efficient inhibitor of alpha-synuclein fibrillization.

24 potential drugs on the intertwined stages of fibrillization.

25 ll tested compounds suggesting inhibition of fibrillization.

26 to investigate their modulatory role in tau fibrillization.

27 g an eight-fold reduction in the lag-time to fibrillization.

28 sure of amyloid-prone regions for subsequent fibrillization.

29 x may guide the search for suppressors of AB fibrillization.

30 in, which adopts a beta-sheet-rich fold upon fibrillization.

31 t in pathology and its relationship with tau fibrillization.

32 the complex factors affecting legume protein fibrillization.

33 f both species with subsequent inhibition of fibrillization.

34 tain alpha-sheet structure and form prior to fibrillization.

35 beta peptide and efficiently modulates Abeta fibrillization.

36 orphisms rather than a reliable indicator of fibrillization.

37 presence of nontoxic monomers and to prevent fibrillization.

38 bit both Abeta1-42 early oligomerization and fibrillization.

39 cal phenomena, including crystallization and fibrillization.

40 at destabilize protein structures and induce fibrillization.

41 rimary nucleation process underlying amyloid fibrillization.

42 omogenates were used to seed RT-QuIC-induced fibrillization.

43 ining compact monomer that was refractory to fibrillization.

44 eeded with infectious beta-solenoid fibrils) fibrillization.

45 oligomers and perturbs amyloid-beta (Abeta) fibrillization.

46 s known about how these molecules affect Tau fibrillization.

47 azine (ATPZ) series of compounds inhibit Tau fibrillization.

48 mers, leading to dimers that were capable of fibrillization.

49 then enter neighboring cells to seed further fibrillization.

50 tegrity of the protein and the conditions of fibrillization.

51 more critical to understand the kinetics of fibrillization.

52 K18 aggregation, and R3 is critical for K19 fibrillization.

53 lized underlying principle governing amyloid fibrillization.

54 sequently leads to a substantial increase in fibrillization.

55 azine ruthenium(II) complex to monitor Abeta fibrillization.

56 on between a small-molecule inhibitor of tau fibrillization, 3,3'-bis(beta-hydroxyethyl)-9-ethyl-5,5'

57 a candidate small molecule inhibitor of tau fibrillization, 3-(2-hydroxyethyl)-2-[2-[[3-(2-hydroxyet

58 aking the reversal of so-called irreversible fibrillization a significant challenge.

59 a hydrophobic interface can promote amyloid fibrillization, although the underlying mechanism is sti

60 est that methylene blue inhibits tau amyloid fibrillization and accelerates tau droplet gelation via

61 for in vivo evaluation must both prevent tau fibrillization and achieve significant brain levels.

62 al modifications of synuclein that favor its fibrillization and aggregation in inclusions in neurons

63 nsight into the early stages of beta-amyloid fibrillization and can be used to enhance the understand

64 This study explored protein fibrillization and characterization, demonstrating signi

65 es that are both effective inhibitors of tau fibrillization and display significant brain-to-plasma e

66 chanisms underlying halpha-Syn intraneuronal fibrillization and its contribution to PD pathogenesis,

67 s of PD, the processes that govern alpha-syn fibrillization and LB formation remain poorly understood

68 design of drugs that inhibit alpha-synuclein fibrillization and might arrest disease progression.

69 ng the cause and effect relationship between fibrillization and neurodegeneration.

70 r Abeta was dependent on the degree of Abeta fibrillization and on the concentration of fAbeta.

71 We found that it markedly accelerates aSyn fibrillization and results in the formation of fibrils w

72 rate that UBQLN2 droplets catalyze alpha-syn fibrillization and suggest that small molecules targetin

73 n play an active role in preventing aberrant fibrillization and suggest the molecular mechanism where

74 utant p53 amyloids suggests means to control fibrillization and the associated pathologies through mo

75 Herein, the fibrillization and toxicity of amide-to-ester mutants of

76 ing backbone amide bonds are compared to the fibrillization and toxicity of the 19-20 E-olefin Abeta

77 matic data defining factors affecting A beta fibrillization and, thus, should be valuable in the desi

78 ation may exist between the rate of in vitro fibrillization and/or oligomerization and the progressio

79 plasma and CSF, where it prevents Abeta from fibrillization, and helps to maintain it in the soluble

80 eta-sheet conformation, surfactant activity, fibrillization, and seeding capability.

81 leading to LB formation, including seeding, fibrillization, and the formation of inclusions that rec

82 , activation energies of oligomerization and fibrillization are estimated to be 5.5 and 12.1 kCal/mol

83 y enable inhibition of one or more stages of fibrillization as a potential therapeutic strategy.

84 cules were found to interfere with Abeta1-40 fibrillization as determined by transmission electron mi

85 ntains a BRICHOS domain, which reduces Abeta fibrillization as well as neurotoxicity in vitro and in

86 uclein-deficient neurons lacked amyloid-like fibrillization, as determined by thioflavine S staining.

87 e amyloid-forming peptides leads to enriched fibrillization at an air-water interface.

88 We found TDP-43 inhibited Abeta fibrillization at initial and oligomeric stages.

89 lts or RNAs and provided visual evidence for fibrillization at the droplet surface/solvent interface

90 ained via immunization are unable to prevent fibrillization at the same substoichiometric concentrati

91 ynuclein is necessary and sufficient for its fibrillization based on the following observations: 1) h

92 These data support that Abeta fibrillization begins within AD vulnerable neurons, lead

93 Studies of the in vitro fibrillization behavior of the mutant proteins suggest t

94 l domain affected not only the extent of PrP fibrillization but also its kinetics, lowering the react

95 ctic" mutation (AbetaE22G) accelerated Abeta fibrillization but decreased the abundance of nonfibrill

96 drug candidates that inhibit alpha-synuclein fibrillization but do not block its oligomerization coul

97 t not fibrillization, compounds that inhibit fibrillization but not oligomerization, and compounds th

98 echanism for substoichiometric inhibition of fibrillization by a variety of chaperones.

99 ta indicate that dopamine inhibits alpha-syn fibrillization by inducing structural changes in alpha-s

100 oth in vitro and in vivo, suppresses amyloid fibrillization by promoting an alternative fibril struct

101 t Asn-181) significantly reduces the rate of fibrillization by promoting intermolecular disulfide for

102 pseudophosphorylation and glycation promoted fibrillization by shifting equilibrium toward the fibril

103 We demonstrate that fibrillization can be disrupted with a new class of inhi

104 The process of Tau fibrillization can be replicated in vitro, and a number

105 rom the amorphous aggregation channel to the fibrillization channel.

106 mpounds that inhibit oligomerization but not fibrillization, compounds that inhibit fibrillization bu

107 We investigated the fibrillization conditions of two constructs and found th

108 Under the same fibrillization conditions, Arctic Abeta40 exhibits a hig

109 tiple conformations in fibrils, depending on fibrillization conditions.

110 ucible and sensitive to subtle variations in fibrillization conditions.

111 The effect of bead mass on fibrillization correlated (R(2) = 0.96) with variations

112 Fibrillization correlates with the distinct clustering o

113 suggesting mutagenesis approaches to inhibit fibrillization could improve this important drug.

114 proved critical for the nucleation of Sup 35 fibrillization de novo and displayed a conformation comm

115 Notably, D(L)-Cu-SMOHs inhibit amyloid fibrillization effectively with pronounced chirality dis

116 y little is understood about its folding and fibrillization energy landscape.

117 Dopamine inhibition of alpha-syn fibrillization generated exclusively spherical oligomers

118 Several critical factors for fibrillization have been identified.

119 e process of alpha-synuclein aggregation and fibrillization holds pivotal roles in Parkinson's diseas

120 eracts with one of the phenylalanines during fibrillization; however, it is not known if aromatic-aro

121 es)) in prion disease and by analogy prevent fibrillization in amyloid diseases.

122 e mechanism that prevents soluble Abeta from fibrillization in biological fluids is not clear.

123 dopamine autoxidation can prevent alpha-syn fibrillization in dopaminergic neurons through a novel m

124 thenium(II) complexes for monitoring protein fibrillization in highly fluorescent media.

125 ein homologs could be attenuating halpha-Syn fibrillization in mice, and therefore, we systematically

126 s by which gyrating beads accelerate amyloid fibrillization in microtiter plate assays are unclear.

127 pharmacological approach to the role of tau fibrillization in neurodegeneration.

128 acologic and genetic modulators of alpha-Syn fibrillization in neurons.

129 o observe the initial stages of beta-amyloid fibrillization in situ.

130 igh affinity were also capable of triggering fibrillization in the absence of other inducers.

131 (SP) and that agitation is not required for fibrillization in this setting.

132 hAChE variants, only hAChE-S enhances Abeta fibrillization in vitro and Abeta deposition and toxicit

133 analogous to the relationship between Abeta fibrillization in vitro and familial AD.

134 investigate the molecular details of peptide fibrillization in vitro by perturbing this process throu

135 each of which has been shown to promote tau fibrillization in vitro when present at high stoichiomet

136 n microscopy as a quantitative assay for tau fibrillization in vitro, the interaction between synthet

137 recruit RNA, leading to faster rates of tau fibrillization in vitro.

138 he amide-to-ester Abeta 1-40 mutants prevent fibrillization; in fact several exhibit hastened amyloid

139 3), The extent of Abeta fibrillization increases with peptide concentration.

140 res required for the fatty acid class of tau fibrillization inducer using recombinant full-length tau

141 asurements when conducted in the presence of fibrillization inducers has been questioned.

142 courses performed in the presence of anionic fibrillization inducers revealed that increasing concent

143 Eight potential fibrillization inhibitor compounds reported in the liter

144 It also provides a structural basis for fibrillization inhibitors.

145 During fibrillization, inhibitory DAPHs alter the folding of Su

146 candidates that reduce amyloid 1-42 peptide fibrillization interact with the most neurotoxic species

147 It is likely that oligomeric fibrillization intermediates (protofibrils), rather than

148 There is mounting evidence that fibrillization intermediates, or protofibrils, but not m

149 Tau fibrillization is a potential therapeutic target for Alz

150 ow the rate of superoxide dismutase-1 (SOD1) fibrillization is affected by 12 different beads with a

151 Amyloid fibrillization is an exceedingly complex process in whic

152 Importantly, while not required for LLPS, fibrillization is enhanced in protein-rich droplets.

153 emonstrated that alpha-synuclein (alpha-syn) fibrillization is inhibited by dopamine, and studies to

154 Amyloid fibrillization is multistep process involving soluble ol

155 on with fibrillization rate, suggesting that fibrillization is not necessary for synuclein-induced ye

156 fibrillize under native conditions and that fibrillization is promoted by two solvent-exposed patche

157 This TFE-induced fibrillization is quite unusual, because most amyloidoge

158 cause of insulin's inhibitory effect on IAPP fibrillization, it has been suggested that insulin may a

159 Using fibrillization kinetics and chemical stability assays, w

160 The fibrillization kinetics depended on peptide and TFE conc

161 ble to describe the classic types of amyloid fibrillization kinetics identified in our literature sur

162 stent with the documented differences in the fibrillization kinetics of the two mutants.

163 stacked beta-sheet-seeded solutions lead to fibrillization kinetics similar to homogeneously seeded

164 r a conformational change to promote amyloid fibrillization leads to direct competition between unfol

165 The fibrillization leads to reduced adsorption of Abeta42 to

166 Inhibition of fibrillization leads to the accumulation of nonfibrillar

167 2), The onset of fibrillization limits the concentration of oligomers in

168 Both inducer micellization and tau fibrillization made significant contributions to light s

169 ibility that the toxicity of alpha-synuclein fibrillization may derive from an oligomeric intermediat

170 lt in neuronal damage, and inhibitors of Tau fibrillization may hold promise as therapeutic agents.

171 gregation through intermediate formation and fibrillization may underlie the activity of other induce

172 Wild-type sTREM2 also inhibited AB fibrillization (measured by imaging and thioflavin T flu

173 itative analysis and characterization of the fibrillization mechanisms predicted by the network Hamil

174 We uncovered two fibrillization mechanisms that govern the structural con

175 ules that prevent tau oligomerization and/or fibrillization might have therapeutic value.

176 Neither the mechanism of alpha-syn fibrillization nor the degradative process for alpha-syn

177 Further-more, the aggressive fibrillization of a C179S mutant of this fragment highli

178 The fibrillization of a truncated tau fragment that contains

179 e that apoE promotes both the deposition and fibrillization of Abeta, ultimately affecting clearance

180 LLPS and fibrillization of ACC(1-13)K(n) are triggered by ATP thr

181 vitro experiments that revealed tau-mediated fibrillization of alpha-synuclein protein at low concent

182 ired for inclusion formation and follows the fibrillization of alpha-synuclein.

183 the assay was demonstrated by following the fibrillization of beta-amyloid peptide 1-42 (Abeta42) as

184 B) the fibrillization of endogenous fibronectin is partially ha

185 o form filaments, and these peptides promote fibrillization of full-length human alpha-synuclein in v

186 In vitro, fibrillization of full-length, unphosphorylated recombin

187 yloid-prevention capabilities for inhibiting fibrillization of hIAPP.

188 Here we present the amyloid-like beta-sheet fibrillization of HN along with characterization of its

189 arker of fluid-phase endocytosis, and induce fibrillization of intracellular full-length Tau.

190 Internalized Tau aggregates induce fibrillization of intracellular Tau in these naive recip

191 ains has been widely described yet templated fibrillization of LB-alphaSyn often fails to propagate i

192 Here, the fibrillization of lentil protein prepared using various

193 introduces another layer of complexity into fibrillization of metastable proteins, a need for tunabl

194 hanisms involved in the self-association and fibrillization of monomeric soluble proteins into insolu

195 The fibrillization of monomeric Tau to filaments is a multis

196 The fibrillization of mouse alpha-synuclein is slowed by WT

197 nant factor controlling the accumulation and fibrillization of nascent Abeta in endosomes and, in TgC

198 Here, we examine the role of this segment in fibrillization of PrP23-144 using a deletion variant, De

199 Fibrillization of purified recombinant alpha-synuclein i

200 elated anionic detergents greatly accelerate fibrillization of recombinant alpha-synuclein at low mic

201 To address this issue, the fibrillization of recombinant full-length four-repeat hu

202 T-QuIC) test, which is based on prion-seeded fibrillization of recombinant prion protein (rPrPSen), i

203 ic prion protein conversion prevent in vitro fibrillization of recombinant prion protein, suggesting

204 In vitro, fibrillization of recombinant tau can be induced by trea

205 Misfolded tau has the capacity to seed the fibrillization of soluble tau, leading to the prion-like

206 h gelsolin showed that gelsolin inhibits the fibrillization of synthetic Abeta 1-40 and Abeta 1-42 at

207 s that hyperphosphorylation, misfolding, and fibrillization of tau impair synaptic plasticity and cau

208 Fibrillization of tau protein is a hallmark lesion in Al

209 gnificantly more effective at preventing the fibrillization of tau than the Abeta(1-42) peptide which

210 This mechanism is analogous to the fibrillization of the Abeta(1-42) peptide and may be imp

211 Fibrillization of the Abeta1-40 peptide under similar co

212 observations suggest that the nucleation and fibrillization of the PAPf39 peptide are a tug-of-war be

213 rils were found to be able to cross-seed the fibrillization of the parent protein, although these rea

214 conformational changes that occurred during fibrillization of the pathologic form of Htt-exon1 (NtQ4

215 Fibrillization of the protein amyloid beta is assumed to

216 ation can be reproduced in vitro in a seeded fibrillization of the recombinant prion protein variant

217 sity, can be reproduced in vitro in a seeded fibrillization of the recombinant prion protein variant

218 rriers, can be reproduced in vitro in seeded fibrillization of the Y145Stop prion protein variant.

219 Implications of fibrillization on the administration of HN is discussed.

220 that Hsp31 is able to suppress the in vitro fibrillization or aggregation of alphaSyn, citrate synth

221 cause they impair tau functions, promote tau fibrillization, or perturb tau gene splicing, thereby le

222 ilitating human disorders indicates a shared fibrillization pathway that may initiate or accelerate n

223 were attained, the rate-limiting step in the fibrillization pathway was tau dimer formation.

224 oligomers are obligate intermediates in the fibrillization pathway, we characterized the mechanism o

225 large length and time scales associated with fibrillization pose challenges for simulation studies of

226 volves a complex interplay between alpha-syn fibrillization, posttranslational modifications, and int

227 Fibrillization proceeded after intermediate formation wi

228 Thermodynamic signatures of this enhanced fibrillization process from our simulations are in good

229 but unchanged vibrational spectra during the fibrillization process suggests that a cooperative confo

230 mutants and documented their effects on the fibrillization process.

231 cal cross-linking) significantly hampers the fibrillization process.

232 ld be exploited in the dissection of protein fibrillization processes as well as in the therapeutics

233 ns could be used to ascertain their relative fibrillization propensities.

234 roughput reporter assays, and predicting the fibrillization propensity of amyloid beta with data gene

235 thin the N terminus of aSyn that hinders the fibrillization propensity of its aggregation-prone core.

236 t temperatures simulated, the results on the fibrillization propensity of the seven short de novo des

237 Here, we demonstrate the LLPS/fibrillization properties of a family of chimeric peptid

238 ed the secondary structure, aggregation, and fibrillization properties of the two Abeta40 variants an

239 noubiquitination on the phase separation and fibrillization properties of these two amyloidogenic pro

240 eet conformation and the fastest aggregation/fibrillization properties.

241 uence cause different disease phenotypes and fibrillization properties.

242 of each bead and that bead's effect on SOD1 fibrillization rate was with regard to bead mass.

243 rease in the lag time and an increase in the fibrillization rate, consistent with promotion of both f

244 s measured, and we found no correlation with fibrillization rate, suggesting that fibrillization is n

245 cular basis for why Abeta42 exhibits greater fibrillization rates than Abeta40.

246 sease, suggesting it participates in the tau fibrillization reaction pathway.

247 qualitatively reproducing all aspects of the fibrillization reaction.

248 Induction of measurable tau fibrillization required an alkyl chain length of at leas

249 uld also be peracetylated with aspirin after fibrillization, resulting in supercharged fibrils, with

250 d levels, HSA inhibits the kinetics of Abeta fibrillization, significantly increasing the lag time an

251 nique model system in which to study protein fibrillization, since its three disulfide bridges are re

252 n was achieved concomitant with promotion of fibrillization, suggesting that oligomer and fibril form

253 Our results suggest that the fibrillization temperature (temperature above which fibr

254 bril stability and that by rank ordering the fibrillization temperatures of various sequences, PRIME2

255 e a model for Cu(II) binding to Abeta during fibrillization that is independent of peptide oligomeric

256 celles or vesicles can serve to nucleate tau fibrillization, that this mechanism underlies the activi

257 sicles can serve to nucleate alpha-synuclein fibrillization, that this mechanism underlies the induce

258 act of posttranslational modification on tau fibrillization, the ability of recombinant full-length f

259 off-pathway aggregation relative to amyloid fibrillization; these include non-linear semilog plots o

260 We conclude that TDP-43 inhibits Abeta fibrillization through its interaction with Abeta and ex

261 (1:1 ratio) collected as a function of Abeta fibrillization time, which indicates that the Cu(II) env

262 developed a seeding-based model of alpha-syn fibrillization to generate a neuronal model that reprodu

263 s study, we develop a minimal model of Abeta fibrillization to investigate the onset of AD over a lon

264 eneration link alpha-Syn oligomerization and fibrillization to the onset and progression of PD.

265 ns play a pivotal role in selecting the LLPS-fibrillization transition pathway.

266 n and might be the site of nucleation during fibrillization under conditions without denaturants.

267 stingly, methylene blue, an inhibitor of Tau fibrillization under evaluation in Alzheimer disease cli

268 hrough which anionic surfactants promote tau fibrillization using a combination of electron microscop

269 rt timescales, an understanding of how Abeta fibrillization usually starts to dominate at a longer ti

270 ive assay of anionic micelle-induced protein fibrillization was characterized using tau protein, the

271 Abeta fibrillization was delayed specifically in the presence

272 The fibrillization was reversible, and the dissociation reac

273 To this end, the kinetics of PAPf39 peptide fibrillization was studied using a battery of biophysica

274 alpha-synuclein can directly cross-seed tau fibrillization, we administered preformed alpha-synuclei

275 amyloidogenic oligomerization and contingent fibrillization were abolished.

276 Mutants that display inhibited beta-sheet fibrillization were associated with those previously ide

277 "Refolding" and fibrillization were initiated by rapid dilution into pho

278 , reaction progress curves for wild-type tau fibrillization were sigmoidal and correlated well with m

279 , calpain-cleaved soluble alpha-syn inhibits fibrillization, whereas calpain-cleaved fibrillar alpha-

280 phorylation at serine 26 (S26) impairs Abeta fibrillization while stabilizing its monomers and nontox

281 The addition of anionic inducers led to fibrillization with nucleation-dependent kinetics.

282 hosphatidylserine vesicles, also induced tau fibrillization with resultant filaments originating from

283 lipid vesicles, also induced alpha-synuclein fibrillization, with resultant filaments originating fro

284 raneuronal onset of Abeta42 accumulation and fibrillization within cell bodies, neurites, and synapse

285 it reduced oligomerization, aggregation, and fibrillization yet maintained cell signaling properties,