ライフサイエンスコーパス: fibril formation

1 id nucleation and subsequent protofibril and fibril formation.

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

3 ligomers to more compact oligomers preceding fibril formation.

4 ation in collagen interaction and control of fibril formation.

5 rmediates that likely regulate the timing of fibril formation.

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

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

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

9 fic, as the reversed reaction inhibited sRPT fibril formation.

10 tes pericellular BM protein accumulation and fibril formation.

11 th a nucleation-polymerization mechanism for fibril formation.

12 then significantly accelerated D76N beta2-m fibril formation.

13 in an isolated V(L) domain is essential for fibril formation.

14 remarkable efficacy in accelerating amyloid fibril formation.

15 f amyloidogenic proteins, preempting amyloid fibril formation.

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

17 ucine to valine mutation, is responsible for fibril formation.

18 o rationalize some aspects of alphaS amyloid fibril formation.

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

20 experimental model of cell-mediated collagen fibril formation.

21 stability but exhibit different kinetics of fibril formation.

22 equations accounting for nucleation-mediated fibril formation.

23 ial inhibitors of amylin oligomerization and fibril formation.

24 quent slow structural conversion step before fibril formation.

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

26 syn within its amyloid region and circumvent fibril formation.

27 ation takes place, which efficiently retards fibril formation.

28 gomer formation and dramatically potentiates fibril formation.

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

30 interpeptide interactions are essential for fibril formation.

31 ammatory properties that are abrogated after fibril formation.

32 zes nonfibrillar aggregates, and accelerates fibril formation.

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

34 segments with a high propensity for amyloid fibril formation.

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

36 toxic oligomers frequently accumulate during fibril formation.

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

38 encompasses all Abeta segments essential for fibril formation.

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

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

41 bin abolishes the cytotoxicity by preventing fibril formation.

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

43 ative to Abeta will strongly inhibit amyloid fibril formation.

44 ecules have been identified that inhibit Tau fibril formation.

45 which suggests a physical basis for amyloid fibril formation.

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

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

48 substantially different from those of linear fibril formation.

49 ies for prevention or stimulation of amyloid fibril formation.

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

51 us were protected from protease digestion by fibril formation.

52 ution and that the hydrophobic effect drives fibril formation.

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

54 the aggregation process, whereas 36 activate fibril formation.

55 of triple helical assembly and second during fibril formation.

56 thermore, an inhibitory RNA aptamer prevents fibril formation.

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

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

59 of Abeta42 oligomer dynamics during amyloid fibril formation.

60 is widely used as a model system for amyloid fibril formation.

61 DMNDC efficiently reports on the kinetics of fibril formation.

62 nsights into the role of GAGs during amyloid fibril formation.

63 and species involved in oligomerization and fibril formation.

64 gation-prone regions significantly slow down fibril formation.

65 on to rPfMSP8 prevented rPfMSP2 amyloid-like fibril formation.

66 EL glycations at Lys-16 of Abeta1-42 delayed fibril formation.

67 of prenucleation and oligomerization, before fibril formation.

68 orphology of fibrils, and forces driving the fibril formation.

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

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

71 of prefibrillar species formed early during fibril formation.

72 than doxycycline with complete abrogation of fibril formation.

73 heir equimolar mixing to lead to accelerated fibril formation.

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

75 Abeta, while dimers strongly suppress Abeta fibril formation.

76 mechanistic effects of modulators on amyloid fibril formation.

77 predict the resulting traction force and FN fibril formation.

78 leation enabling dimerisation and subsequent fibril formation.

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

80 ge molar excess, completely prevents amyloid fibril formation.

81 earliest stages of aggregation, well before fibril formation.

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

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

84 During amyloid fibril formation, amyloidogenic polypeptides misfold and

85 pothesis is that PSMalpha3 toxicity requires fibril formation; an alternative is that toxicity is cau

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

87 the lag phase and early elongation phase of fibril formation and can inhibit amyloid fibril formatio

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

89 Kinetically, N17 accelerates fibril formation and destabilizes nonfibrillar intermedi

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

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

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

93 nder conditions which would normally lead to fibril formation and found that the degree of tetramer s

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

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

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

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

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

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

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

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

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

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

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

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

106 ng epithelial cells and promotes fibronectin fibril formation and survival, whereas blockade of Sfrp2

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

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

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

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

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

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

113 eptides are only transiently redirected from fibril formation, and eventually almost all Abeta monome

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

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

116 d (Abeta) plaques and fibrils, inhibit Abeta fibril formation, and significantly reduce Abeta-induced

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

118 t a likely contributor to early oligomer and fibril formation, and thus a potential critical mechanis

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

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

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

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

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

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

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

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

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

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

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

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

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

132 recapitulating the entire process of amyloid fibril formation, beginning with thousands of free monom

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

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

135 reduce neurotoxicity associated with Abeta42 fibril formation both in vitro and in vivo In this study

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

137 T can be used not only as a test for amyloid fibrils formation but also for the comparative study of

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

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

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

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

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

143 provide evidence for the inhibition of ApoE4 fibril formation by ApoE3.

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

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

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

147 as HW-155, were effective inhibitors of the fibril formation by hIAPP(.)

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

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

150 omers to form oligomers and then accelerates fibril formation by increasing the proliferation rate of

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

152 small unilamellar vesicles inhibits amyloid fibril formation by Orb2A.

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

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

155 ermolecular disulfide bonds initiate amyloid fibril formation by recruitment of monomers.

156 Here we propose that fibril formation by these amyloidogenic molecules reflec

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

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

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

160 y and explains the irreversible pathological fibril formation caused by the Asp mutations identified

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

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

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

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

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

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

167 stabilize specific oligomers during amyloid fibril formation, facilitating the structural characteri

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 ace now invite to formulate hypotheses about fibril formation, growth and stability.

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

177 Atomistic description of protein fibril formation has been elusive due to the complexity

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

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

180 ed molecular chaperones that inhibit amyloid fibril formation; however, their mechanisms of action re

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

182 of fibril formation and can inhibit amyloid fibril formation in a dose-dependent manner.

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

184 erstanding of how protein nucleators mediate fibril formation in cells remains elusive.

185 a(3) or genetic loss of GPVI reduced amyloid fibril formation in cultured platelets and decreased the

186 pseudomelanosomes indicating altered amyloid fibril formation in five of the nine variants.

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

188 (RPT), an amyloidogenic domain essential for fibril formation in melanosomes.

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

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

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

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

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

194 contrasting ways: decreasing the lag time of fibril formation in the presence of LMW-heparin and slow

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

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

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

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

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

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

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

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

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

204 Fibril formation involves a spontaneous nucleation event

205 Amyloid fibril formation is a hallmark of neurodegenerative dise

206 Amyloid fibril formation is associated with a number of debilita

207 Amyloid fibril formation is central to the etiology of a wide ra

208 n of compounds capable of inhibiting amyloid-fibril formation is critical to the development of poten

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

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

211 Therefore, understanding how fibril formation is initiated and maintained in the join

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

213 Fibril formation is observed when either the V(L) or C(L

214 Fibril formation is pH dependent; all proteins form fibr

215 A critical step in collagen fibril formation is the proteolytic removal of N- and C-

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

217 process of LB formation, rather than simply fibril formation, is one of the major drivers of neurode

218 With regard to fibril formation kinetics and resistance against denatur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 ary structure during pH- and heparin-induced fibril formation of apolipoprotein A-I (apoA-I) associat

234 Fibril formation of beta2-microglobulin and associated i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 Fibril formation of R3Abeta2m was potently prevented by

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

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

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

253 The proposed mechanism of fibril formation of transthyretin (TTR) involves self-as

254 tein states that arise during the process of fibril formation often coexist with mature fibrils and a

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

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

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

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

259 5a) plays a major role in the AL-103 amyloid fibril formation process.

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

261 s susceptible to biophysical aggregation and fibril formation, promoted by manual agitation and eleva

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

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

264 Amyloid fibril formation results from a destabilizing mutation i

265 gn and optimization of inhibitors of amyloid-fibril formation, revealing in particular the important

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

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

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

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

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

271 gh the polyglutamine domain is important for fibril formation, the dynamic, C-terminal proline-rich d

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

273 of excited states of the two peptides to the fibril formation time scales using an empirical formula,

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

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

276 iseases, detection and inhibition of amyloid fibril formation using FPs can provide insights on devel

277 By monitoring fibril formation using Thioflavin T fluorescence and far

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

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

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

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

282 teolytic cleavage of procollagen to initiate fibril formation was significantly reduced with inhibiti

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

284 -3-gallate (EGCG), known to inhibit alphaSYN fibril formation, was investigated.

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

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

287 The free energies for fibril formation were -12.36, -8.10, and -10.61 kcal mol

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

289 Lys-28 of Abeta1-42 had the least impact on fibril formation, whereas CEL glycations at Lys-16 of Ab

290 mechanism by which BAX can be sequestered by fibril formation, which can prevent it from initiating M

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 protein primary sequence trigger cross-beta fibril formation, with insights that have direct implica

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