ライフサイエンスコーパス: tau protein

1 g., amyloid-beta40, total and phosphorylated tau protein).

2 ated substrate, the intrinsically disordered Tau protein.

3 lular tangles containing hyperphosphorylated Tau protein.

4 viously reported fiber formed by VQIVYK from Tau protein.

5 igh molecular weight to low molecular weight Tau protein.

6 ation and posttranslational modifications of Tau protein.

7 ines associated with hyperphosphorylation of tau protein.

8 ct is translated into a full-length chimeric tau protein.

9 vo, and here we investigate its influence on tau protein.

10 regates of amyloid-beta (Abeta) peptides and tau protein.

11 mprised of aggregates of hyperphosphorylated tau protein.

12 s composed of abnormally hyperphosphorylated tau protein.

13 etal ions and the neurofibrillary tangles of Tau protein.

14 illary tangles (NFTs) comprising filamentous tau protein.

15 ntly reduced, as was the amount of insoluble tau protein.

16 whether this concept can also be applied to Tau protein.

17 ng from alpha-syn seeds to over 50% of total tau protein.

18 ates of amyloid-beta (Alphabeta) peptide and tau protein.

19 protective effects via direct proteolysis of TAU protein.

20 ary tangles comprised of hyperphosphorylated tau protein.

21 that appears to be suppressed in the native tau protein.

22 ide and abnormal hyperphosphorylation of the tau protein.

23 rd of mice transgenic for mutant human P301S tau protein.

24 ained inclusions made of hyperphosphorylated tau protein.

25 rd of mice transgenic for mutant human P301S tau protein.

26 perphosphorylation and filament formation of tau protein.

27 self-assembly of the microtubule-associated tau protein.

28 and intracellular neurofibrillary tangles of tau protein.

29 en decorated with the secondary antibody for tau protein.

30 ation on beta-amyloid, little is known about Tau protein.

31 loping PET tracers that bind specifically to tau protein.

32 model independent of expression of a mutant tau protein.

33 ociated with the pathological aggregation of tau protein.

34 ion of both ubiquitinated proteins and APP/p-Tau proteins.

35 rebrospinal fluid levels of beta-amyloid and tau proteins.

36 rranged in staggered arrays, cross-linked by tau proteins.

37 lation of Abeta oligomers and phosphorylated tau proteins.

38 lary tangles composed of hyperphosphorylated tau proteins.

39 gation of abnormally and hyperphosphorylated tau proteins.

40 ending on the combined activities of EBs and tau proteins.

41 on and clearance of amyloid beta (Abeta) and tau proteins.

42 We assessed CSF tau protein abnormalities in AD, a tauopathy with promin

43 Because PSP is associated with tau protein abnormalities, there is growing interest in

44 Furthermore, endogenous TAU protein abundance in human neuroblastoma SH-SY5Y cel

45 Aberrant tau protein accumulation drives neurofibrillary tangle (

46 protein, motor and behavioral deficits, and tau protein accumulation in neurons and tufted astrocyte

47 ENs were often dysmorphic, with pathological tau protein accumulation in Pick's disease.

48 njury, but not seizures, was associated with tau protein accumulation in this series.

49 r Braak stages, but asymmetrical patterns of tau protein accumulation within the sclerotic hippocampu

50 es were observed in total and phosphorylated tau proteins across conditions.

51 Intrinsically disordered proteins, such as tau protein, adopt a variety of conformations in solutio

52 ENT The stereotypical spread of pathological tau protein aggregates have recently been attributed to

53 aracterized by the formation of pathological tau protein aggregates in the brain and progressive neur

54 The deposition of tau protein aggregates in the brain is a pathological ha

55 However, in tauopathies, tau protein aggregates into insoluble filaments and neur

56 In Alzheimer's disease and tauopathies, tau protein aggregates into neurofibrillary tangles that

57 The formation and deposition of tau protein aggregates is proposed to contribute to cogn

58 treatment of neurodegenerative diseases with tau protein aggregates known as tauopathies.

59 7 is a PET radiotracer developed for imaging tau protein aggregates, which are implicated in neurolog

60 geous for the insight into the properties of tau protein aggregates.

61 phenotype through a mechanism independent of tau protein aggregation and identifies a critical role f

62 bilities to act as an antioxidant, to reduce tau protein aggregation and to improve energy metabolism

63 ium moiety, acts as a selective inhibitor of tau protein aggregation both in vitro and in transgenic

64 eractions of Abeta with three domains in the tau protein; all contain high beta-structure propensity

65 quence of the nonuniform distribution of MAP tau proteins along the bundle length.

66 sulin signaling modulates phosphorylation of tau protein, an early component in the development of Al

67 raneuronal inclusions of hyperphosphorylated tau protein and abnormal expression of brain-derived neu

68 and pseudo MS(n) were performed on oxidized Tau protein and acetylated bovine serum albumin to ident

69 caused by the dysfunction and aggregation of tau protein and an impairment of cellular protein degrad

70 01S tau transgenic mice express mutant human tau protein and develop progressive tau pathology.

71 peptide production, hyperphosphorylation of tau protein and endosomal abnormalities.

72 y tangles of hyperphosphorylated, aggregated tau protein and extracellular deposits of beta-amyloid p

73 se, which is characterized by changes in the tau protein and in the cleaved fragments of the amyloid

74 ments over a large temperature range for the tau protein and its hydration water, indicating intimate

75 lly disordered proteins, the K18 domain from Tau protein and N(TAIL) from measles virus nucleoprotein

76 lone can cause pathological abnormalities in tau protein and neurodegeneration in the absence of muta

77 iated by insoluble tangles of phosphorylated tau protein and plaques of amyloid peptides.

78 accumulation of soluble hyperphosphorylated TAU protein and slows down the disease progression in th

79 between cerebrospinal fluid (CSF) levels of tau proteins and alpha-synuclein, but not beta-amyloid 1

80 aggregation of the beta-amyloid (Abeta) and tau proteins and atrophy of medial temporal lobe (MTL) s

81 rs or amyloid-beta trimers, and pathological tau proteins and postsynaptic proteins correlated with A

82 associated with CSF levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals

83 ent of cerebrospinal fluid levels of orexin, tau proteins, and beta-amyloid 1-42 and polysomnographic

84 Levels of orexin, tau proteins, and beta-amyloid 1-42; macrostructural var

85 luble amyloid beta, total and phosphorylated tau proteins, and isoprostanes.

86 tests for prion diseases such as 14-3-3 and tau proteins, and together with PRNP gene sequencing the

87 Abnormalities in microtubule-associated tau protein are a key neuropathological feature of both

88 usions of hyperphosphorylated and aggregated tau protein are a pathological hallmark of several neuro

89 t effective therapies directly targeting the tau protein are currently lacking.

90 Deposits of abnormally phosphorylated tau protein are found in numerous neurodegenerative diso

91 ("hyperphosphorylation") and aggregation of Tau protein are hallmarks of Alzheimer disease and other

92 Lesions containing abnormal aggregated tau protein are one of the diagnostic hallmarks of Alzhe

93 Amyloid-beta and tau protein are the two most prominent factors in the pa

94 Intriguingly, Tau proteins are able to alleviate the effect of the Pri

95 Mutations in tau proteins are associated with a group of neurodegener

96 brillary tangles made of hyperphosphorylated tau proteins are closely associated with Alzheimer disea

97 Amyloid beta42, and tau proteins are established core cerebrospinal biomarke

98 Aggregated Tau proteins are hallmarks of Alzheimer disease and othe

99 c forms of amyloid-beta peptide (oAbeta) and tau proteins are likely to play a major role in Alzheime

100 rofibrillary deposits of hyperphosphorylated tau proteins are the diagnostic lesions of AD, but their

101 ofibrillary tangles (NFTs) of phosphorylated tau proteins, are a group of neurodegenerative diseases,

102 et al. identify a putative novel function of tau protein as a regulator of insulin signaling in the b

103 Several independent studies have implicated tau protein as central to Alzheimer's disease progressio

104 formation of the bonds between the connected tau proteins as they respond to mechanical stretch.

105 Tau protein assembles into paired helical filaments (PHF

106 cid inhibitor of the fibril formation of the tau protein associated with Alzheimer's disease, and a n

107 -1 (TTBK1) is involved in phosphorylation of tau protein at specific Serine/Threonine residues found

108 NSE and tau protein at the 6-hour time point were both significa

109 nt evidence has suggested that truncation of tau protein at the caspase cleavage site D421 precedes h

110 e generated four singly pseudophosphorylated Tau proteins (at Thr(231), Ser(262), Ser(396), and Ser(4

111 exhibit accumulation of hyperphosphorylated tau protein (AT8 antibody), an early precursor to the fo

112 g30 murine tauopathy model expresses a human tau protein bearing two frontotemporal dementia with Par

113 gate their likelihood of fitting into VQIVYK tau protein binding channel model.

114 Normal tau protein binds and stabilizes the microtubules in neu

115 Tau protein binds to a highly anionic MT surface to stab

116 We perform Monte Carlo simulations of tau proteins bound to a cylinder that mimics a microtubu

117 t autoantibodies that recognized recombinant tau protein but not the immunogen were detected in the P

118 s can form not only by the full-length human Tau protein, but also by the three repeated (K19) or fou

119 re composed of insoluble hyperphosphorylated Tau protein, but the mechanisms underlying the conversio

120 l (mTau) that overexpresses wild-type murine tau protein by twofold compared with endogenous levels.

121 We generated pseudophosphorylated Tau proteins by mutating Ser/Thr to Glu and, as controls

122 still unclear which specific domains in the tau protein can interact with Abeta oligomers and what c

123 Tau protein can transfer between neurons transneuronally

124 In the model, inverted pairs of tau proteins can dynamically cross-link parallel MTs via

125 SK-3beta) by attacking both beta-amyloid and tau protein cascades has been identified as a promising

126 that a sequence of progressive misfolding of tau proteins, circuit-based transfer to new cell populat

127 sect the molecular characteristics of native tau protein conformers from TgP301S tau mice and show th

128 plex is present to load beta(2), a truncated tau protein containing only domains III-V will suffice.

129 Astrocytic-tau protein correlated with the presence of both traumat

130 etitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other

131 of molecular probes capable of detection of tau protein deposits in vitro.

132 aggregated beta-amyloid peptides (Abeta) and tau protein derived intracellular tangles.

133 Pathological tau proteins derived from human AD brains (AD-tau) act a

134 heet peptide inhibits the aggregation of the tau-protein-derived peptide Ac-VQIVYK-NH2 (AcPHF6).

135 peptides 1 that inhibit the aggregation of a tau-protein-derived peptide.

136 As a consequence, Tau protein detaches from microtubules and eventually ag

137 ), which are composed of hyperphosphorylated Tau protein dissociating from microtubules, is one of th

138 ocytic tau pathology by expressing the human tau protein driven by the glial fibrillary acidic protei

139 fruit fly Drosophila melanogaster expresses Tau proteins (dTau) that are homologous to hTau, we aime

140 All four singly pseudophosphorylated Tau proteins exhibited loss-of-function effects.

141 We assessed Tau protein expression in primary breast cancer specimen

142 High Tau protein expression is associated with better prognos

143 al distribution of mRNA expression and total tau protein expression levels were largely in agreement,

144 ing and reformation of the bonds between the tau proteins facilitate the extension of axons up to app

145 tive production of small amounts of abnormal tau protein facilitates dysfunction and accumulation of

146 MAP tau proteins fail in clusters of 10-100 elements located

147 er's disease (AD) and other tauopathies, the tau protein forms fibrils, which are believed to be neur

148 In Alzheimer's disease, the tau protein forms intracellular amyloid fibrils in which

149 and experimental IR spectra suggest that the tau-protein fragments form extended beta-strands that ar

150 iochemical and histochemical profiles of the tau protein from the rTg4510 transgenic mouse model in w

151 ly induced seizure models, mice with reduced tau protein had less severe seizures than control mice.

152 aged Tg mice of both sexes expressing human tau proteins harboring a pathogenic P301L MAPT mutation

153 In Alzheimer disease and other tauopathies, Tau protein has a reduced affinity toward microtubules.

154 SIGNIFICANCE STATEMENT: The tau protein has a relevant role in the transport of carg

155 olecules that inhibit the aggregation of the tau protein have been identified, little is known about

156 rivatives as imaging probes for pathological tau protein have great potential, but have not been well

157 re composed of misfolded hyperphosphorylated tau proteins; however, the link between tau abnormalitie

158 ons in axonal transport can exacerbate human tau protein hyperphosphorylation, formation of insoluble

159 er's disease neurofibrillary pathology using tau protein immunohistochemistry.

160 perphosphorylation and filament formation of tau protein in Alzheimer's disease and other tauopathies

161 expansion disorders, Parkinson's disease and tau protein in Alzheimer's disease.

162 twisted filaments similar to those formed by tau protein in Alzheimer's neurofibrillary tangles.

163 etic variability linked to altered levels of tau protein in cerebrospinal fluid.

164 f serum neurofilament light chain (NF-L) and tau protein in comparison to CSF markers (NF-L and phosp

165 While mutant tau protein in frontotemporal dementia and parkinsonism

166 el and substantial alterations of endogenous tau protein in glaucoma, including abnormal subcellular

167 eta plaques and intracellular aggregation of tau protein in neurofibrillary tangles (NFTs) (1, 2).

168 or imaging aggregates of hyperphosphorylated tau protein in neurofibrillary tangles, a process that o

169 intracellular lesions of hyperphosphorylated Tau protein in P301S Tau transgenic mice.

170 haracterized by aggregates of phosphorylated tau protein in the brain [2, 3].

171 Aggregation of tau protein in the brain is associated with a class of n

172 myloid-beta peptides and hyperphosphorylated tau protein in the brain.

173 3) show increased accumulation of oligomeric tau protein in the CNS and enhanced loss of motor neuron

174 Increased concentrations of tau protein in the CSF and an increase in brain atrophy

175 d reduced levels of total and phosphorylated tau protein in the CSF of treated AD patients.

176 au aggregates from one cell directly contact Tau protein in the recipient cell to trigger further agg

177 ning the molecular mechanism of the neuronal Tau protein in the tubulin heterodimer assembly has been

178 ar membrane and aggregates of GFP-conjugated Tau protein in three dimensions.

179 regation of purified recombinant full-length tau protein in vitro was examined as a function of membr

180 gregates of the Alzheimer disease-associated Tau protein in vivo is vital for the development of ther

181 her demonstrated that ERalpha interacts with tau protein in vivo.

182 dies to detect oligomeric and phosphorylated Tau proteins in a non-transgenic rodent model of parasag

183 tification of Myelin Basic Protein (MBP) and Tau proteins in cerebrospinal fluid (CSF) and serum, obt

184 ques and accumulation of hyperphosphorylated tau proteins in neurofibrillary tangles.

185 ABEL) trap to prolong measurements of single tau proteins in solution.

186 Pathological changes to the tau protein, including conformational changes and aggreg

187 Pathological tau protein inclusions have long been recognized to defi

188 Based on the stiffness and viscosity of tau proteins inferred from single-molecule force spectro

189 rogression and to interact with the neuronal tau protein inhibiting its aggregation into fibrillar ta

190 ation of PP2A/Balpha and deregulation of Fyn-Tau protein interactions have been linked to enhanced ta

191 ese findings provide novel information about tau-protein interactions in human brains, and they descr

192 ing a biochemical cascade that drives normal tau protein into a pathological state found in a variety

193 s study, we microinjected normal and mutated Tau protein into cultured cells expressing fluorescent t

194 self-assembly of the microtubule associated tau protein into fibrillar cell inclusions is linked to

195 d to be essential for the aggregation of the tau protein into the amyloids associated with Alzheimer'

196 Our data integrate Tau protein into the class of amyloidogenic proteins and

197 accumulation of aggregated beta-amyloid and tau proteins into plaques and tangles is a central featu

198 Misfolding of tau proteins into prions and their propagation along neu

199 t of quantification for the full-length 2N4R tau protein is 0.03pM, a value unaltered when the assay

200 Abnormal hyperphosphorylation of tau protein is a characteristic feature of a class of ne

201 Intracellular deposition of tau protein is a hallmark lesion of Alzheimer's disease.

202 osition of aggregates of hyperphosphorylated tau protein is a hallmark of tauopathies like Alzheimer

203 Accumulation of pathological tau protein is a major hallmark of Alzheimer's disease.

204 cumulation of neurotoxic hyperphosphorylated TAU protein is a major pathological hallmark of Alzheime

205 The aberrant accumulation of tau protein is a pathological hallmark of a class of neu

206 Aggregated tau protein is associated with over 20 neurological diso

207 perphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenera

208 Abnormal metabolism of the tau protein is central to the pathogenesis of a number o

209 n of anisotropy values obtained from trapped tau protein is conspicuously bimodal while those obtaine

210 Interest on Tau protein is fast increasing in Alzheimer's disease (A

211 Intracellular accumulation of tau protein is hallmark of sporadic Alzheimer's disease

212 osphorylation, and that of mutant but not WT Tau protein is maintained in tauopathies by Hsp90.

213 d other neurodegenerative disorders in which tau protein is not genetically modified remain unknown.

214 The Tau protein is the major component of intracellular fila

215 The tau protein is thus widely felt to play a key role in pr

216 Here, we show that the Tau protein is toxic due to its aggregation propensity,

217 cal for ONOO(-)-mediated oligomerization, as tau proteins lacking all Tyr residues fail to generate o

218 berrant phosphorylation and/or expression of Tau protein, leading to a time-dependent accumulation of

219 Abnormal folding of tau protein leads to the generation of paired helical fi

220 ilure of large groups of interconnecting MAP tau proteins leads to detachment of MT filaments from th

221 at the viscoelastic behavior specifically of tau proteins leads to mechanical breaking of microtubule

222 levels were positively correlated with total tau protein levels (r = 0.32; P = .03) and strictly rela

223 Total tau protein levels and seizure severity were highly corr

224 s highly interconnected with tau, preserving tau protein levels and synergizing with it to assemble M

225 We demonstrate that endogenous tau protein localizes to McTNs and is both necessary and

226 e findings suggest that other regions of the tau protein may be crucial in regulating normal function

227 Thus, propagation of Tau protein misfolding among cells can be mediated by re

228 Seventy-four percent of pCR cases were tau protein negative; the odds ratio for pCR was 3.7 (95

229 the Abeta peptide (amyloid plaques) and the tau protein (neurofibrillary tangles) in the brains of a

230 sites, the four singly pseduophosphorylated Tau proteins often functioned similarly, as did the four

231 ectrochemical biosensor for the detection of tau protein - one of the possible markers for the predic

232 date, the presence of the hypophosphorylated tau protein (P-tau) in plasma from patients with acute T

233 oE genotypes display distinct phosphorylated tau protein (p-tau) staining patterns.

234 regional accumulation of hyperphosphorylated tau protein (p-tau).

235 ich include tauopathy made of phosphorylated tau protein (P-tau).

236 IDPs, such as alpha-synuclein, tau protein, p53, and BRCA1, are attractive targets for

237 e, we found evidence for hyperphosphorylated tau protein (paired helical filament-I tau), which has b

238 In addition, our findings suggest that tau protein pathology in these areas may contribute to t

239 kinase 3beta, cyclin-dependent kinase 5, and tau protein phosphatase 2A.

240 pathology, including beta-amyloid 42, total tau protein, phosphorylated tau 181, and soluble amyloid

241 lpha7nAChR activation mediates Abeta-induced tau protein phosphorylation.

242 ve demonstrated that hyperphosphorylation of tau protein plays a role in neuronal toxicities of alpha

243 orms, all of the doubly pseudophosphorylated Tau proteins possessed enhanced microtubule assembly act

244 pecific for the 3-NT modification, as mutant tau proteins pseudophosphorylated at each Tyr residue ar

245 rly, we elucidated the importance of certain Tau protein regions and unique residues, including the r

246 The tau protein regulates the stability and assembly of micr

247 Amyloid deposition and tau protein-related neuronal injury in early Alzheimer's

248 On the other hand, the tau protein repeats with the characteristic U-turn shape

249 insight into the regulatory mechanism of the tau protein's microtubule binding activity.

250 Microtubule bundles cross-linked by tau protein serve a variety of neurological functions in

251 To identify other neurotoxic tau protein species, we performed biochemical analyses o

252 Tau protein spreads from the entorhinal cortex to the hi

253 Human tau protein spreads to these regions and coaggregates wi

254 ctedly, Pin1 knockdown or KO decreased P301L tau protein stability and abolished its robust tauopathy

255 trate that Pin1 knockdown or KO increased WT tau protein stability in vitro and in mice and that Pin1

256 TauD proteins substituted at residues surrounding the ac

257 nt models for the intracellular transport of Tau protein suggest motor protein-dependent co-transport

258 (phosphorylated tau) and non-specific (total tau) protein targets.

259 HtrA1 has also been reported to cleave the tau protein (Tau) and the amyloid protein precursor (APP

260 f hyperphosphorylated microtubule-associated tau protein (tau, gene MAPT) are typical of AD.

261 , such as the beta-amyloid (Abeta(1-42)) and tau proteins (tau).

262 characterized by intracellular aggregates of tau proteins, termed tauopathies, include Alzheimer's di

263 by mutations in the MAPT gene, encoding the tau protein that accumulates in intraneuronal lesions in

264 nd Tau release is modified by changes in the Tau protein that are associated with tauopathies.

265 lusions containing abnormally phosphorylated tau protein that co-localized in some instances with mut

266 fications of the microtubule (MT)-associated tau protein that promote its pathological self-assembly

267 s lithium attenuates iron efflux by lowering tau protein that traffics amyloid precursor protein to f

268 identify a region (positions 272-289) in the tau protein that, in the fibrillar state, either forms p

269 ll-length proteins, including those, such as tau protein, that lack fully ordered native structures.

270 R2-fragment ((273)GKVQIINKKLDL(284)) of the Tau protein, that TMAO can counteract the denaturing eff

271 rainstem nuclei in our model expressed human tau protein, the development of neurofibrillary tangles,

272 Here, we report that tau protein, the primary constituent of Alzheimer neurof

273 gments from the Alzheimer's amyloid-beta and tau proteins, the PrP prion protein, insulin, islet amyl

274 ve tauopathy characterized by aggregation of Tau protein through the repeat domain to form intraneuro

275 0 mice) which overexpresses a mutant form of tau protein, to examine the effects of tauopathy on hipp

276 mice), which overexpresses a mutant form of tau protein, to examine the effects of tauopathy on hipp

277 , which overexpresses a mutant form of human tau protein, to investigate the effects of tau pathology

278 The components of a Tau protein triage system consisting of CHIP/Hsp70 and o

279 hology in astrocytes by expressing the human tau protein under the control of the glial fibrillary ac

280 ate the interaction between microtubules and tau proteins under mechanical loading.

281 We identified hyperphosphorylated tau protein using AT8 immunohistochemistry and compared

282 r(404)) and four doubly pseudophosphorylated Tau proteins using the same sites.

283 We found that the exogenous mutant tau protein was restricted in MEC without spreading to o

284 S-100b, neuron specific enolase (NSE), and tau protein were assayed as MBIs preoperatively and post

285 Oligomeric and phosphorylated Tau proteins were detected 4 and 24 h and 2 weeks post-T

286 eudophosphorylated and corresponding control Tau proteins were expressed transiently in PC12 and CHO

287 albumin (HSA), beta-casein, and recombinant Tau proteins were submitted to in source decay in the MA

288 tion limits of 0.30nM for MBP and 0.15nM for Tau proteins which were sufficient for the levels to be

289 rotofilaments comprising residues 306-378 of tau protein, which adopt a combined cross-beta/beta-heli

290 of aggregates formed of hyperphosphorylated tau protein, which are associated with synapse and neuro

291 Tau protein, which contains two naturally occurring cyst

292 scenario has recently been observed for the tau protein, which has four repeats.

293 phorylation at most phosphorylation sites of tau protein, which is known to play a crucial role in th

294 ell-known IDPs is the microtubule-associated tau protein, which regulates microtubule growth in the n

295 We review evidence that the -amyloid and tau proteins, which aggregate to form senile plaques and

296 ion sites from in vivo phosphorylated tau (p-tau) protein, which is associated with Alzheimer's disea

297 brillary tangles made of hyperphosphorylated tau protein with neuronal loss.

298 strate that transgenic mice expressing human tau protein with this mutation develop neurodegeneration

299 odel and then correlated the levels of these tau proteins with memory loss.

300 by insoluble deposits of hyperphosphorylated tau protein within brain neurons.