ライフサイエンスコーパス: fibril formation

1 into a well-defined structural element upon fibril formation.

2 than doxycycline with complete abrogation of fibril formation.

3 stability but exhibit different kinetics of fibril formation.

4 equations accounting for nucleation-mediated fibril formation.

5 ial inhibitors of amylin oligomerization and fibril formation.

6 quent slow structural conversion step before fibril formation.

7 ons 8 (P8S) or 40 (P40S) completely reverted fibril formation.

8 syn within its amyloid region and circumvent fibril formation.

9 ation takes place, which efficiently retards fibril formation.

10 heir equimolar mixing to lead to accelerated fibril formation.

11 gomer formation and dramatically potentiates fibril formation.

12 d cross-linking pattern at an early stage of fibril formation.

13 interpeptide interactions are essential for fibril formation.

14 ammatory properties that are abrogated after fibril formation.

15 ified in vivo, whereas its absence abrogates fibril formation.

16 Abeta, while dimers strongly suppress Abeta fibril formation.

17 zes nonfibrillar aggregates, and accelerates fibril formation.

18 mation of peptides with a low propensity for fibril formation.

19 segments with a high propensity for amyloid fibril formation.

20 mechanistic effects of modulators on amyloid fibril formation.

21 n-containing conformers act as templates for fibril formation.

22 toxic oligomers frequently accumulate during fibril formation.

23 ity to form oligomers and slows down amyloid fibril formation.

24 encompasses all Abeta segments essential for fibril formation.

25 predict the resulting traction force and FN fibril formation.

26 to be the most toxic species produced during fibril formation.

27 leation enabling dimerisation and subsequent fibril formation.

28 d self-assembly processes, including amyloid fibril formation.

29 bin abolishes the cytotoxicity by preventing fibril formation.

30 re used to reveal multiple stages of amyloid fibril formation.

31 ative to Abeta will strongly inhibit amyloid fibril formation.

32 ecules have been identified that inhibit Tau fibril formation.

33 which suggests a physical basis for amyloid fibril formation.

34 nvolved in the prevention of in vivo amyloid fibril formation.

35 ation, or "seeding", is thought to propagate fibril formation.

36 substantially different from those of linear fibril formation.

37 ies for prevention or stimulation of amyloid fibril formation.

38 y reduces beta-cell apoptosis, by inhibiting fibril formation.

39 us were protected from protease digestion by fibril formation.

40 d at pH 10, causing repulsion and inhibiting fibril formation.

41 s prior to the "downhill" folding leading to fibril formation.

42 the aggregation process, whereas 36 activate fibril formation.

43 of triple helical assembly and second during fibril formation.

44 thermore, an inhibitory RNA aptamer prevents fibril formation.

45 urn nucleation is a critical step in Abeta40 fibril formation.

46 ers as the key step that leads ultimately to fibril formation.

47 nce in the energy landscape, it could impede fibril formation.

48 hibited a pronounced decrease in the rate of fibril formation.

49 ulated interest in the kinetics of Alphabeta fibril formation.

50 embrane permeabilization potential and rapid fibril formation.

51 abilize the tetramer, inhibiting TTR amyloid fibril formation.

52 ail, should lead to the known macromolecular fibril formation.

53 on but modulates the pH dependence of PAPf39 fibril formation.

54 ed that the C-terminal domain is involved in fibril formation.

55 lecular chaperone protection against amyloid fibril formation.

56 ge molar excess, completely prevents amyloid fibril formation.

57 therefore comprise the critical nucleus for fibril formation.

58 higher propensity for rapid aggregation and fibril formation.

59 and has been shown in vitro to inhibit IAPP fibril formation.

60 convenient probes of the process of amyloid fibril formation.

61 ncentration-dependent aggregation, including fibril formation.

62 e and beta-sheet end state, respectively, of fibril formation.

63 synthesized, nearly all potently inhibit TTR fibril formation.

64 s confirm that the compound prevents amyloid fibril formation.

65 xpressed mouse MBP similarly inhibited Abeta fibril formation.

66 earliest stages of aggregation, well before fibril formation.

67 id nucleation and subsequent protofibril and fibril formation.

68 and possibly even largely caused) by amyloid fibril formation.

69 role of Abeta's N-terminal domain in amyloid fibril formation.

70 ligomers to more compact oligomers preceding fibril formation.

71 ation in collagen interaction and control of fibril formation.

72 rmediates that likely regulate the timing of fibril formation.

73 ole in formation of oligomeric and seeds for fibril formation.

74 onomers, indicative of on-pathway events for fibril formation.

75 ouse AF defect model, with abundant collagen fibril formation.

76 tes pericellular BM protein accumulation and fibril formation.

77 th a nucleation-polymerization mechanism for fibril formation.

78 then significantly accelerated D76N beta2-m fibril formation.

79 remarkable efficacy in accelerating amyloid fibril formation.

80 f amyloidogenic proteins, preempting amyloid fibril formation.

81 cubated at 37 degrees C and pH 6.0 to induce fibril formation.

82 of prefibrillar species formed early during fibril formation.

83 o rationalize some aspects of alphaS amyloid fibril formation.

84 romote apoA-I structural changes and amyloid fibril formation.

85 experimental model of cell-mediated collagen fibril formation.

86 ture, membrane binding, oligomerization, and fibrils formation.

87 e amyloidogenic TDP-43 peptide that disrupts fibril formation also eliminates neurotoxicity, supporti

88 During amyloid fibril formation, amyloidogenic polypeptides misfold and

89 nability of Httex1-7Q/15Q to undergo amyloid fibril formation and an inverse correlation between fibr

90 These results provide a mechanism for hIAPP fibril formation and could explain the remarkable stabil

91 tate in the free energy landscape that slows fibril formation and creates a stable population of olig

92 Kinetically, N17 accelerates fibril formation and destabilizes nonfibrillar intermedi

93 protein nucleobindin 1 (NUCB1) prevent hIAPP fibril formation and disaggregate preexisting hIAPP fibr

94 Differences in Col5a2(-/-) and Col5a1(-/-) fibril formation and embryonic survival suggest that alp

95 rophobic Abeta-sequence approach each other, fibril formation and expulsion of water molecules occur

96 anism is proposed whereby membranes nucleate fibril formation and facilitate the in-register alignmen

97 ation that precedes, and likely facilitates, fibril formation and growth.

98 sh a new modality for covalent inhibition of fibril formation and illuminate a path for future optimi

99 tem and has been shown to accelerate amyloid fibril formation and increase their toxicity.

100 er, the part(s) of the N-domain critical for fibril formation and maintenance of the [PSI(+)] phenoty

101 cs the behavior of nitrated Abeta related to fibril formation and neuronal toxicity.

102 ata demonstrate that Aha1 contributes to tau fibril formation and neurotoxicity through Hsp90.

103 -sheet breakers are able to inhibit in vitro fibril formation and prevent the beta sheet folding of p

104 rty against beta-amyloid and alpha-synuclein fibril formation and protective capacity against Abeta-i

105 of peach cultivars inhibits Abeta and alphaS fibril formation and protects PC12 cell lines against Ab

106 otein properties, DNA-RNA complexes, amyloid fibril formation and protein suspensions in a crowded en

107 e been found to inhibit amyloid beta (Abeta) fibril formation and reduce neuron cell toxicity in vitr

108 The structural basis of the fibril formation and stabilization is still debated and

109 d alpha-syn mutants that promote oligomer or fibril formation and tested the toxicity of these mutant

110 ecies of beta2-microglobulin, preventing its fibril formation and the associated cytotoxicity and res

111 stic relationship between Abeta oligomer and fibril formation and the cytotoxicity of these aggregate

112 In this study, we analyze the rates of fibril formation and the monomer-fibril equilibrium for

113 t of Asian spices, is known to disrupt Abeta fibril formation and to reduce AD pathology in mouse mod

114 icacy of these compounds on inhibiting Abeta fibril formation and toxicity in vitro was assessed usin

115 n, the role of lipid membrane composition in fibril formation and toxicity is not well understood.

116 rmore, cABC is a potent inhibitor of amyloid fibril formation and, by slowing the rate of its aggrega

117 ions in tau can lead to tau oligomerization, fibril formation, and neurodegenerative disease, includi

118 ordered protein aggregation, such as amyloid fibril formation, and not with stable molten globules st

119 eta-amyloid (Abeta) in vitro, inhibits Abeta fibril formation, and suppresses the Alzheimer's disease

120 an has a different effect on the kinetics of fibril formation, and this effect seems to be associated

121 The early stages of fibril formation are difficult to capture in solution.

122 documented, but the consequences on collagen fibril formation are less clear.

123 se folding intermediates, which occur during fibril formation, are the toxic species in the amyloid-r

124 implicates Abeta peptides self-assembly and fibril formation as crucial events in the pathogenesis o

125 lizes the disulfide-bonded dimer and impairs fibril formation as determined by electron microscopy.

126 that the compound inhibits unseeded amyloid fibril formation as well as disaggregates IAPP amyloid.

127 opy cannot be directly used to study amyloid fibrils formation, as it was proposed by some authors.

128 s involved in the initial stages of glucagon fibril formation at acidic pH.

129 signing therapeutics that target Abeta(1-40) fibril formation at an early stage of the disease.

130 APf39Delta1-13 are capable of seeding PAPf39 fibril formation at neutral pH, suggesting that these va

131 agen (C7), a protein essential for anchoring fibril formation at the dermal-epidermal junction (DEJ).

132 collagen, a protein essential for anchoring fibril formation at the dermal-epidermal junction.

133 and fluorescence spectroscopy, we monitored fibril formation at the ultrastructural, secondary confo

134 deposition in tgSwe mice by increasing Abeta fibril formation because heparanase-induced fragmentatio

135 threshold monomer concentration below which fibril formation becomes biologically irrelevant.

136 ions in PKCgamma accelerate the amyloid-like fibril formation both in cultured cells and in vitro.

137 uctural transitions not seen before, namely, fibril formation both in hydrophobic regions L17-A21 and

138 , the N-terminal region is not necessary for fibril formation but modulates the pH dependence of PAPf

139 cesses in explaining the kinetics of amyloid fibril formation but predict fibril length distributions

140 a-TC3 and NMuMG HS to stimulate IAPP maximal fibril formation, but desulfated HS from both cell types

141 s one of the most potent inhibitors of hIAPP fibril formation, but its inhibition mechanism is not un

142 t in SP had little effect on the kinetics of fibril formation, but physiologic levels of Zn(2+) stron

143 ay an important role at the stage of initial fibril formation, but the stage of fibril elongation is

144 the engineered forms of NUCB1 prevent hIAPP fibril formation by a mechanism where protofibril-like s

145 Purified PrP-AA potently blocked fibril formation by a toxic 21-amino acid fragment of th

146 ectively accelerating and preventing amyloid fibril formation by Abeta(42).

147 This diboronic acid inhibits fibril formation by both wild-type TTR and a common dise

148 pression of islet amyloid polypeptide (IAPP) fibril formation by compound 1 was demonstrated by thiof

149 ength hIAPP did not modulate the kinetics of fibril formation by full-length hIAPP.

150 isotope labeling to monitor the kinetics of fibril formation by human islet amyloid polypeptide (hIA

151 Misfolding and amyloid fibril formation by human islet amyloid polypeptide (hIA

152 insights into the mechanism of amyloid-like fibril formation by multi-domain proteins.

153 small unilamellar vesicles inhibits amyloid fibril formation by Orb2A.

154 Here, we show that fibril formation by PAP(248-286) is accelerated dramatic

155 of the effects of specific SP components on fibril formation by PAP(248-286) revealed that this effe

156 reticulum export, subcellular targeting, and fibril formation by Pmel17 and thus for establishing fun

157 Although acidic pH promotes amyloid fibril formation by this and many other proteins, the mo

158 Intracellular fibril formation by Ure2p produces the non-Mendelian gen

159 h, named kinetic inhibition, aims to prevent fibril formation by using small ligands that stabilize t

160 We show that the timescale for fibril formation can be estimated from the population of

161 the molecular interactions mediating amyloid fibril formation could be harnessed to generate antibodi

162 Inhibitors of pathological amyloid fibril formation could be useful in the development of t

163 However, fitting kinetic fibril formation data to a complex model including expli

164 d AL-12, AL-09, kappaI Y87H, and AL-103 H92D fibril formation; delayed fibril formation for AL-103; a

165 that models that are suitable for nucleated fibril formation do not fit our aggregation data.

166 are intermediates in the process of amyloid fibril formation, either as precursors of fibrils or as

167 ls from IAPP cytotoxicity by modulating IAPP fibril formation extracellularly and also, after uptake

168 H, and AL-103 H92D fibril formation; delayed fibril formation for AL-103; and did not promote any fib

169 ormation for AL-103; and did not promote any fibril formation for AL-12 R65S, AL-103 delP95aIns, or k

170 tive deviation of Ile leads to prediction or fibril formation for the NININI peptide.

171 re, we examined their effects on the amyloid fibril formation from Alzheimer's amyloid beta (Abeta) (

172 Fibril formation from IAPP was stimulated equally by IAP

173 mary, neither binding to nor acceleration of fibril formation from the amyloidogenic peptide IAPP is

174 Our data indicate that fibril formation greatly affects hydroxyproline and prol

175 with the length of time that the process of fibril formation has been allowed to progress and with t

176 The molecular mechanism of epitaxial fibril formation has been investigated for GAV-9 (NH(3)(

177 importance of the amino terminus of SAA for fibril formation has been well documented, the influence

178 inhibited both Abeta(1-40) and D76N beta2-m fibril formation in a Ca(2+)-independent manner.

179 ify the interactions that inhibit or promote fibril formation in atomic detail.

180 phobic regions L17-A21 and G37-A42 preceding fibril formation in hydrophilic region E22-A30.

181 Abeta(42) and reduces aggregation levels and fibril formation in mixtures.

182 ce detection is used to simultaneously probe fibril formation in polyglutamine peptides, the aggregat

183 e of [Ru(phen)(2)dppz](2+) to monitor alphaS fibril formation in real-time and to detect and quantify

184 N-terminal htt acetylation retarded fibril formation in solution and promoted the formation

185 , as the result of markedly reduced collagen fibril formation in the infarct area due to impaired fib

186 scopy images show that PADK inhibits Abeta42 fibril formation in the solution.

187 e-rich repeat domain and regulating collagen fibril formation in vitro and in vivo Some nine tyrosine

188 ort that APFs are in a distinct pathway from fibril formation in vitro and in vivo.

189 BP enhances islet amyloid polypeptide (IAPP) fibril formation in vitro Now we report that polymeric C

190 ved peptides and compared their capacity for fibril formation in vitro with that of their VLITL-delet

191 the role of sulfated GAGs on AL oligomer and fibril formation in vitro, a kappa1 LC purified from uri

192 d monomeric TTR, the best inhibitor of Abeta fibril formation in vitro, did not bind Abeta monomers i

193 Abeta fibril seeds promoted CAA mutant Abeta fibril formation in vitro.

194 otently inhibit TTR dissociation and amyloid fibril formation in vitro.

195 n peptides modulates aggregation and amyloid fibril formation in vitro.

196 h affinities of 1-10 nm and inhibit AbetapE3 fibril formation in vitro.

197 While it has been generally recognized that fibril formation in vivo may be greatly assisted or acce

198 oved efficient in inhibiting alpha-synuclein fibril formation induced by PMCA.

199 ulfate A, on the other hand, showed a strong fibril formation inhibition for all proteins.

200 Fibril formation involves a spontaneous nucleation event

201 Amyloid fibril formation is associated with a number of debilita

202 In this study, a reduced level of hAM fibril formation is confirmed by transmission electron m

203 A critical step of beta-amyloid fibril formation is fibril elongation in which amyloid-b

204 cs slower: time-resolved imaging showed that fibril formation is highly suppressed, with aggregates f

205 e both formed under conditions where amyloid fibril formation is observed but differ in molecular wei

206 Fibril formation is pH dependent; all proteins form fibr

207 Cu(II)-induced beta2m fibril formation is preceded by the formation of discret

208 sis for UCH-L1s involvement in proteinacious fibril formation is still elusive, especially in regard

209 ind and enter cells to trigger intracellular fibril formation is unknown.

210 With regard to fibril formation kinetics and resistance against denatur

211 The presence of surfaces influences the fibril formation kinetics of peptides and proteins.

212 At pH 7, Ca(2+) rendered the fibril formation kinetics slower: time-resolved imaging

213 dynamic stability and a significant delay in fibril formation kinetics with respect to AL-103.

214 A model of fibril formation kinetics, including end-joining, is dev

215 insights into how polyphenols inhibit Abeta fibril formation, knowledge that could be useful for des

216 stabilizing TTR and thus preventing amyloid fibril formation, known to cause polyneuropathy.

217 The N-terminal domain shortened the collagen fibril formation lag phase and tyrosine sulfation was re

218 Ile-25 of the MinD-interacting domain affect fibril formation, membrane binding ability of MinE and M

219 ed oligomers are alpha-helical, resistant to fibril formation, more prone to disaggregation, enzymati

220 turally compatible with PAPf39, yet no mixed fibril formation occurs between the truncated variants a

221 In contrast, GAGs did not enhance fibril formation of a non-amyloidogenic kappa1 LC purifi

222 dge) drug candidates for AD that inhibit the fibril formation of Abeta peptides and eliminate their n

223 oss in PD occurs is unknown, aggregation and fibril formation of alpha-syn are considered to be key p

224 less effective the sHsps were at inhibiting fibril formation of alpha-syn.

225 egation of alpha-lactalbumin and the amyloid fibril formation of alpha-synuclein in comparison with H

226 In this work, we compare fibril formation of alphaS and betaS at pH 7.3 and mildl

227 ICHOS domains from Bri2 and pro-SP-C prevent fibril formation of amyloid beta-peptides (Abeta(40) and

228 Fibril formation of beta2-microglobulin and associated i

229 bin prevents the fatty acid-promoted de novo fibril formation of beta2-microglobulin even at substoic

230 Our data show that haptoglobin prevents fibril formation of beta2-microglobulin under conditions

231 e importance of these charged side chains in fibril formation of betaS.

232 A mechanism is proposed for the mini-fibril formation of Col108 in which the axial periodicit

233 Here, we analyze fibril formation of full-length PABPN1.

234 from structure-based designs can disrupt the fibril formation of full-length proteins, including thos

235 Amyloid fibril formation of GLP-1 was monitored using thioflavin

236 y, which show that EGCG efficiently inhibits fibril formation of hCT by preventing the initial associ

237 ide may play an important role in inhibiting fibril formation of hCT.

238 s a transient intermediate to beta-sheet and fibril formation of pEAbeta (3-42).

239 Aggregation and amyloid fibril formation of peptides and proteins is a widesprea

240 form fibrils: An attractive surface retards fibril formation of peptides with a high tendency for fi

241 ormation, while the same surface accelerates fibril formation of peptides with a low propensity for f

242 Misfolding and fibril formation of phosphorylated alpha-syn isoforms we

243 al the molecular nature of self-assembly and fibril formation of proteins and peptides, it is yet unc

244 Fibril formation of R3Abeta2m was potently prevented by

245 mutations on protein stability and in vitro fibril formation of single and double restorative mutant

246 terized an all-D-amino-acid inhibitor of the fibril formation of the tau protein associated with Alzh

247 or chemical denaturants, causes amyloid-like fibril formation of this protein.

248 lycosaminoglycans on the kinetics of amyloid fibril formation of three AL cardiac amyloidosis light c

249 The MD results indicate that the binding and fibril formation on the membrane surface depends on the

250 e to soluble oligomeric species that precede fibril formation or are formed by fibril fragmentation,

251 depleted of PrP-AA had little effect on PrP fibril formation or PrP neurotoxicity.

252 s that target the process of LC aggregation, fibril formation, or organ damage.

253 ed along the obligatory nucleation-dependant fibril formation pathway.

254 e trapped intermediate states throughout the fibril formation pathways to examine the structural chan

255 ue that such soluble Abeta oligomers are off fibril formation pathways, they may nonetheless share so

256 ar weight oligomers can be generated via non-fibril formation pathways.

257 n oligomers arising along the aggregation or fibril-formation pathways are important in the genesis o

258 hat have elucidated important aspects of the fibril formation process in vitro, and a magic angle spi

259 le of oxidation of Met-86 and Met-148 in the fibril formation process.

260 5a) plays a major role in the AL-103 amyloid fibril formation process.

261 ion of IbpA resulted in a defect in the IbpA fibril formation process.

262 ght on the molecular species involved in the fibril formation process.

263 city focus on the nuclei or oligomers in the fibril formation process.

264 Owing to the enhanced fibril formation propensity, racemic Abeta42 was less pr

265 is study, we have examined the amyloidogenic fibril formation properties of PG-1 in comparison with a

266 ted leucine-rich repeat domain inhibited the fibril formation rate, and full-length fibromodulin show

267 islet amyloid deposition by inhibiting hIAPP fibril formation, rather than degrading hIAPP.

268 ed HS from both cell types still accelerated fibril formation relative to IAPP alone.

269 tide motif in repeat R3, a crucial motif for fibril formation, shows strikingly low variability of al

270 apeutic landscape to include RNA inhibitors, fibril formation stabilisers and inhibitors, and immunot

271 ppers', the successful inhibition of amyloid fibril formation strengthens the hypothesis that amyloid

272 cal pH regime (5 +/- 0.5) was identified for fibril formation suggesting the involvement of at least

273 show dramatically altered pH sensitivity for fibril formation supporting the importance of these char

274 gth-dependent effects on Httex1 oligomer and fibril formation that were previously not observed using

275 Upon acid-induced amyloid fibril formation, the 2D IR spectra reveal that the C-te

276 on to the initiation, rate, and mechanism of fibril formation, the helical nature of htt(NT) and its

277 the size of the fibril nucleus, the work for fibril formation, the nucleation barrier, the equilibriu

278 ) to measure the kinetic properties of Abeta fibril formation under different conditions during the p

279 med amyloid-like fibrils within hours during fibril formation under near physiological conditions.

280 By monitoring fibril formation using Thioflavin T fluorescence and far

281 showed a markedly different pH dependence of fibril formation versus that of PAPf39.

282 mine how this pattern is generated, collagen-fibril formation was examined in mice lacking a tectorin

283 Unexpectedly, fibril formation was independent of the presence of the

284 hown with AFM imaging that the inhibition of fibril formation was not complete with any of the compou

285 n the spontaneous reactions, the lag time of fibril formation was rather uniform for the mutants M129

286 Abeta fibril formation was validated by thioflavin T (ThT) flu

287 -3-gallate (EGCG), known to inhibit alphaSYN fibril formation, was investigated.

288 e the contribution of disulfide formation to fibril formation, we have compared the assembly of tau(2

289 Because heparin affects collagen fibril formation, we investigated whether tyrosine sulfa

290 n, with a clear and well-defined pathway for fibril formation, where the effects of lipid interaction

291 affects the self-assembly process of amyloid fibril formation, which results in their conformational

292 e insights into polyQ solution structure and fibril formation while also suggesting an approach to th

293 Zn(2+) helps stabilize the fibril formation, while also acting as a cofactor to cat

294 The N-terminal N17 promotes amyloid fibril formation, while the C-terminal Proline Rich Doma

295 rmation of peptides with a high tendency for fibril formation, while the same surface accelerates fib

296 y grows to 50-70% within the early stages of fibril formation, while they mostly anneal block-wisely

297 The investigated methods detected fibril formation with equal sensitivities.

298 ell-studied model system of systemic amyloid fibril formation, with a clear and well-defined pathway

299 and the lag time prior to the observation of fibril formation, with truncated species exhibiting the

300 s into a structure that may nucleate amyloid fibril formation (Yeung, P.