ライフサイエンスコーパス: PHF

1 PHF are fibers of amyloid nature that are composed of a

2 PHF are primarily composed of highly phosphorylated tau

3 PHF diagnosis is currently accomplished using serology o

4 PHF is caused by Neorickettsia risticii, and the recentl

5 PHF-1-immunoreactive thorn-shaped astrocytes were observ

6 PHF-Tau from Alzheimer disease brain was affinity-purifi

7 PHF/tau-positive dystrophic neurites were present in and

8 PHFs are composed of microtubule-associated protein tau,

9 PHFs are the first example of pathological aggregation a

10 in VHF and PHF rats (VHF vs. VC, P < 0.001; PHF vs. PC, P < 0.05).

11 hosphorylation at multiple sites (AT8, 12E8, PHF-1, and pS422), tauC3-immunoreactive tau fragmentatio

12 le of tau distributed among approximately 30 PHF phosphorylation sites as compared to 2-3 mol of phos

13 Using the tau (297-391) PHF-core fragment as a model, we further showed that pre

14 t hyperphosphorylation of Tau at Ser396/404 (PHF-1-reactive Tau, p-Tau), with no changes in pSer202 b

15 duces the protofilament's ability to adopt a PHF-like conformation by modifying a key glycine triad.

16 we provide clear structural evidence that a PHF, whether found in disease or assembled in vitro, is

17 of phosphorylated tau that inhibit abnormal PHF-tau, DYRK1A and GKS3B that reduce phosphorylated tau

18 ose molecular structure resembles that of AD PHF tau [S.

19 the insoluble characteristics typical of AD PHF/NFTs.

20 ified but each was indistinguishable from AD-PHFs in mass/nm length and density.

21 ar in mass/nm length, but less dense than AD-PHFs and Pick's disease filaments.

22 f PHF with hydrofluoric acid does not affect PHF solubility.

23 that injection of human wild-type Alzheimer PHF seeded aggregation of wild-type murine tau into an a

24 phorylation-dependent immunoprobes Tau-1 and PHF-1 with the aid of alkaline phosphatase demonstrated

25 hate-dependent anti-tau antibodies Tau-1 and PHF-1, that heat shock induces rapid dephosphorylation o

26 , as recognized by the antibodies PHF-13 and PHF-1, respectively.

27 Tau-1 (Ser-195/Ser-198/Ser-199/Ser-202) and PHF-1 (Ser-396/Ser-404) sites was increased, mostly in t

28 Thereafter, AT-8 and PHF-1 immunoreactivity accumulated in cell bodies and su

29 levant markers of dementia, beta-amyloid and PHF-tau, were profiled in formalin-fixed paraffin embedd

30 Since AT10 and PHF-27 are the only mAbs currently available that bind s

31 Since mAbs AT10 and PHF-27 had little or no affinity for fetal tau and biops

32 With the exception of AT10 and PHF-27, all the mAbs also labeled fetal tau and biopsy-d

33 hosphorylated tau immunostained with AT8 and PHF-1 antibodies.

34 with tau hyperphosphorylation at the AT8 and PHF-1 sites.

35 d later forms of phosphorylated tau (AT8 and PHF-1) in untreated 3xTg-AD mice.

36 ted tau in paired helical filaments (AT8 and PHF-1) show positive immunostaining on days 6-8.

37 endent monoclonal antibodies, tau-1, AT8 and PHF-1, we have found that the dephosphorylation of the a

38 ble-labeling experiments with fodrin CCP and PHF-1 were performed.

39 and throughout subsequent pregnancy (PC and PHF, respectively).

40 le tau phosphoepitopes (AT8, CP13, PT205 and PHF-1).

41 ed using <= 15-s ECGs (using RMSSD, SDSD and PHF indices) and investigate its association with atrial

42 ermine the frequency of occurrence of SF and PHF morphology in filaments assembled from these mutant

43 he liver, the finding of activated Stat3 and PHF/NF-kappa B suggests that these cytokines may play a

44 -wide, 10-75 nm long, frequently twisted and PHF-like filaments, with a mass per unit length (44 kDa/

45 endothelium-dependent relaxation in VHF and PHF rats (VHF vs. VC, P < 0.001; PHF vs. PC, P < 0.05).

46 ma cholesterol, which was reduced in VHF and PHF rats, plasma lipids were normal.

47 Immunohistochemical localization of WT1 and PHF showed the presence of WT1 in approximately 42% of P

48 pecific mAb AT10 and 12 newly developed anti-PHF mAbs that recognize PHF-tau but not autopsy-derived

49 d S396/S404, as recognized by the antibodies PHF-13 and PHF-1, respectively.

50 immunostained with mouse monoclonal antibody PHF-1 to visualize neurofibrillary tangles.

51 subsequently recognized by the NFT antibody PHF-1.

52 mulation of disease-related proteins such as PHF-tau in the hippocampus of animals fed the control di

53 ectroscopy to investigate in vitro assembled PHFs from a truncated three-repeat tau isoform (K19) tha

54 Plaque-associated PHF/tau-positive dystrophic neurites were rare or absent

55 increase in phosphorylation was observed at PHF-1 (P-Ser396/P-Thr404), P-Ser202 and P-Thr231 sites o

56 tes recognized by the antibodies AT8, AT100, PHF-1, and TG3.

57 An ABI dependence was found in both PHF (p = 0.04) and TTP (p < 10(-4)).

58 In the current model, both PHF homologs coexist in the same NSL complex, although t

59 Experiments on K19 C322A PHFs further confirm the influence of disulfide bond for

60 ish the two Neorickettsia species that cause PHF.

61 ggest that N. findlayensis frequently causes PHF in horses in Alberta and Quebec.

62 n microscopy (TEM) were used to characterize PHF suspended in Tris-buffered saline (TBS), sodium acet

63 In contrast, PHF(FA) were dephosphorylated at all epitopes, with part

64 In contrast, PHFs from AD were ultrastructurally stable and uniform b

65 Neuronal protective effects and decreased PHF-1 immunoreactivity were observed in two animal model

66 and these ligand-based inhibitions decreased PHF-tau, DYRK1A and GSK3B levels.

67 Dephosphorylation of deglycosylated PHF tangles results in increased tau release.

68 fractions of human Alzheimer disease-derived PHFs for 24 h.

69 , retains TAI activity in vitro and disrupts PHFs isolated from AD brain tissues at 0.16 muM.

70 he microtubule-associated protein tau (i.e., PHF-tau).

71 imer disease, play a major role in effecting PHF insolubility in vivo.

72 em mass spectrometry was employed to examine PHF-Tau post-translational modifications, in particular

73 ed to PHF for 1 mo, those who were first fed PHF at 3.5 mo rejected PHF relative to CMF more than did

74 where repeated cases of Potomac horse fever (PHF) have occurred.

75 Potomac horse fever (PHF) is an acute and potentially fatal enterotyphlocolit

76 Horses develop Potomac horse fever (PHF) when they ingest aquatic insects containing encyste

77 risticii, the agent of Potomac horse fever (PHF), from snails (Pleuroceridae: Juga spp.) maintained

78 the causative agent of Potomac horse fever (PHF), which continues to be an important disease of hors

79 E tau adopts the AD paired helical filament (PHF) fold in the presence of the membrane at high protei

80 ractions leading to paired helical filament (PHF) formation.

81 hemistry of WT1 and paired helical filament (PHF) in serial sections was carried out.

82 The paired helical filament (PHF) is the major component of the neurofibrillary depos

83 rils displaying the paired helical filament (PHF) morphology characteristic of neurofibrillary tangle

84 structure as the AD paired-helical filament (PHF) tau but are unable to template additional monomers.

85 ated extensively in paired helical filament (PHF) tau from Alzheimer's disease (AD) brain, to a lesse

86 nding levels of the paired helical filament (PHF) tracer [(18)F]Flortaucipir, in all brain areas exam

87 of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins

88 inding affinity for paired helical filament (PHF)-tau pathology in Alzheimer's brains.

89 Paired helical filament (PHF)-tau, alpha-synuclein, and amyloid-beta lesions occu

90 Paired helical filament (PHF)/tau immunoreactive dystrophic neurites are a common

91 within the PHF6(*) (paired helical filament [PHF] residues 275-280) and PHF6 (residues 306-311) hexap

92 Paired helical filaments (PHF) are abnormal, approximately 20-25-nm wide periodica

93 Paired helical filaments (PHF) composed of hyperphosphorylated tau proteins are ch

94 The paired helical filaments (PHF) formed by the intrinsically disordered human protei

95 sition of tau into paired helical filaments (PHF) in neurofibrillary tangles (NFTs).

96 tes in the form of paired helical filaments (PHF) in the brains of patients with Alzheimer's disease

97 Paired helical filaments (PHF) occur in Alzheimer's diseased brains and are known

98 lubilize insoluble paired helical filaments (PHF) of Alzheimer disease.

99 the biogenesis of paired helical filaments (PHF) seen in Alzheimer's disease.

100 of aggregates, the paired helical filaments (PHF), incorporate about 20% of the full-length protein i

101 The formation of paired helical filaments (PHF), which are composed of hyperphosphorylated Tau prot

102 Paired helical filaments (PHFs) accumulate in the brains of subjects affected with

103 en I and insoluble paired helical filaments (PHFs) and collagen I of weak hydrogen bonding at proline

104 o the formation of paired helical filaments (PHFs) and neurofibrillary tangles (NFTs) in AD neurons.

105 the generation of paired helical filaments (PHFs) and neurofibrillary tangles, a key neuropathologic

106 Paired-helical filaments (PHFs) are an important diagnostic criterion of the inclu

107 s characterized by paired helical filaments (PHFs) composed of phosphorylated tau.

108 le, which contains paired helical filaments (PHFs) composed of the microtubule-associated protein tau

109 Ps to label native paired helical filaments (PHFs) from the postmortem brain of a patient with Alzhei

110 tes into insoluble paired-helical filaments (PHFs) in Alzheimer's disease (AD) and other tauopathies.

111 osphate content of paired helical filaments (PHFs) in Alzheimer's disease (AD) is a result of limited

112 sist of aggregated paired helical filaments (PHFs) in neurons.

113 h-molecular-weight paired helical filaments (PHFs) in the dentate gyrus of wild-type and mutant tau T

114 Paired helical filaments (PHFs) in the neurofibrillary tangles (NFTs) in Alzheimer

115 ely related to the paired helical filaments (PHFs) isolated from Alzheimer's disease (AD) brain tissu

116 he accumulation of paired helical filaments (PHFs) of hyperphosphorylated microtubule-associated prot

117 e tight bundles of paired helical filaments (PHFs) of tau protein found in Alzheimer's disease (AD) d

118 ein assembles into paired helical filaments (PHFs) that constitute the neurofibrillary tangles observ

119 o the formation of paired helical filaments (PHFs) which deposit into neurofibrillary tangles in Alzh

120 residues found in paired helical filaments (PHFs), and its expression is up-regulated in the brain i

121 mer's disease (AD) paired helical filaments (PHFs), building blocks of neurofibrillary tangles (NFTs)

122 like that found in paired helical filaments (PHFs), does not promote microtubule assembly leading to

123 myloid fibrils and paired helical filaments (PHFs).

124 the Tau MTBR forms paired helical filaments (PHFs).

125 form intraneuronal paired helical filaments (PHFs).

126 rillary tangles of paired helical filaments (PHFs).

127 sphorylated Tau as paired helical filaments (PHFs).

128 fibrillation into paired helical filaments (PHFs).

129 for AD paired helical or straight filaments (PHFs or SFs), but we did observe density for flortaucipi

130 to fibers termed "paired helical filaments" (PHFs).

131 nd accumulation of paired helical filaments-(PHF-) like fibrils.

132 Peak hyperemic flow (PHF) and time-to-peak (TTP) were computed and assessed a

133 as very good for RMSSD and SDSD and good for PHF.

134 significantly higher than those reported for PHF found either in AD (0.40 kDa/nm3) or CBD (0.33 kDa/n

135 tion' of PHF proteins is not responsible for PHF insolubility.

136 opment of diagnostic antibodies specific for PHF-tau since elevated tau levels are found in the cereb

137 of tau is either necessary or sufficient for PHF formation.

138 and help develop broad-spectrum vaccines for PHF.

139 The comparison of FTIR results for PHFs with collagen I gel and polyproline demonstrates th

140 -hydroxymethylethylene hydroxymethyl-formal (PHF), also known as Fleximer.

141 the response to protein hydrolysate formula (PHF) as a model system, we discovered the existence of a

142 ith PHF-tau and fetal tau, but differed from PHF-tau in their lack of the N-terminal insert which cha

143 three principal tau components resolved from PHF-tau on Western blots showed CML immunoreactivity ind

144 lycosylation alone, of AD P-tau and tau from PHF tangles restores their microtubule polymerization ac

145 ever the in vitro glycation of tau generates PHF that are insoluble in SDS and soluble in alkali.

146 However, PHF is occurring in large numbers of horses in spite of

147 hippocampus, indicating that wild-type human PHFs were inefficient in seeding tau aggregates made of

148 tribute to the phosphorylation of Ser 262 in PHF-tau, and thus play a role in the pathogenesis of AD.

149 immunodominant phosphorylated amino acids in PHF-tau.

150 derived hyperpolarizing factor components in PHF rats.

151 bnormal tau aggregation, increased 3-fold in PHF-treated cells.

152 results suggest that tau becomes glycated in PHF-tau and glycation may play a role in stabilizing PHF

153 eactivity indicating that tau is glycated in PHF-tau; and insoluble PHF exhibited prominent CML immun

154 ve stress, 8-iso PGF2alpha, was increased in PHF animals (P < 0.01).

155 particular contact, which may be involved in PHF fibril formation, is proposed here as a possible aro

156 with an important role for beta structure in PHF formation, and may also help explain recent reports

157 Tau is hyperphosphorylated in PHFs, and phosphorylation of tau abolishes its ability t

158 ries of protein solvent to analyze insoluble PHF, only alkali or exhaustive proteolysis are effective

159 at tau is glycated in PHF-tau; and insoluble PHF exhibited prominent CML immunoreactivity on top of t

160 ions of soluble PHF-tau as well as insoluble PHF from AD brains.

161 Sarkosyl-insoluble PHFs were visualized by electron microscopy.

162 soluble matrix consistent with the insoluble PHFs/NFTs which may contribute to neuronal degeneration

163 Intact PHFs were effectively dephosphorylated only at the two N

164 studied in vitro dephosphorylation of intact PHFs, PHFs with filamentous structure abolished by formi

165 The results indicate that intact PHFs, but not PHF(FA) or fetal tau display differential

166 The evidence that cells can internalize PHFs, leading to formation of aggresome-like bodies, ope

167 We found that cells internalized PHFs through an endocytic mechanism and developed intrac

168 rain cytosol (AD P-tau) self-aggregates into PHF-like structures on incubation at pH 6.9 under reduci

169 of the molecule can also self-assemble into PHF.

170 s 297-391 of full-length tau) assembles into PHF-like fibrils in vitro without the need for other add

171 AD P-tau inhibits its self-association into PHF.

172 mechanism of initiation of tau assembly into PHFs is not well understood.

173 totic cell death, sequestration of Pin1 into PHFs may contribute to neuronal death.

174 Given the importance of this irreversible PHF formation in neurodegenerative disease, Tau aggregat

175 Tau (p-Tau) at the Alzheimer's disease-like PHF-1 phospho-epitope.

176 d Ser214, and the peptide recognition of mAb PHF-27 was markedly increased when both the primary site

177 NFT and was co-localized with the NFT marker PHF-1 and the amyloid P component (AP).

178 at colocalized with the mature tangle marker PHF-1.

179 Moreover, PHFs from CBD have been shown to be primarily composed o

180 at enables reliable identification of muscle PHFs by light microscopy.

181 se in combination with dissolution of native PHFs to quantify the activity of Tau aggregation inhibit

182 e results indicate that intact PHFs, but not PHF(FA) or fetal tau display differential dephosphorylat

183 the presence of WT1 in approximately 42% of PHF-positive neurofibrillary tangle containing-neurons.

184 In the spinal cord, 87% of PHF-1-labeled cells colocalize with the transglutaminase

185 eurites were often present in the absence of PHF/tau-positive plaque-associated dystrophic neurites.

186 tested for Ehrlichia risticii, the agent of PHF, by nested PCR using primers specific to the 16S rRN

187 However, the structural basis of PHF assembly at atomic detail is largely unknown.

188 In a limited study, 43 confirmed cases of PHF occurred between the 1994 and 1996 seasons; of these

189 luorescence to demonstrate colocalization of PHF-1-immunoreactive tau and the transglutaminase-cataly

190 Deglycosylation of PHF tangles by endoglycosidase F/N-glycosidase F convert

191 ate of PHF and complete dephosphorylation of PHF with hydrofluoric acid does not affect PHF solubilit

192 The extent of dephosphorylation of PHF(FA) was equal or more effective than in fetal tau, e

193 d control cases and to examine the effect of PHF accumulation.

194 vation as well as an increased expression of PHF-tau, paralleled by increased levels of reactive oxyg

195 alpha-Syn-dependent, increased formation of PHF-1-reactive Tau, suggesting convergent overlapping pa

196 Module-B likewise result in the formation of PHF-like structures.

197 al antibody to isolate a soluble fraction of PHF-Tau in a conformation unique to human AD brain.

198 he relationship between the heterogeneity of PHF-tau and the appearance of abnormal filaments, the ul

199 s suggest that the 'hyperphosphorylation' of PHF proteins is not responsible for PHF insolubility.

200 The cross-linking of PHF tau occurs both intra-molecularly and inter-molecula

201 beta-strands result in a significant loss of PHF aggregation efficiency, highlighting the importance

202 Three months of PHF exposure led to acceptance similar to that at 1 mo o

203 orresponding matched control preparations of PHF/NFTs, none of these phosphorylated neuronal cytoskel

204 nges in the CD spectrum following removal of PHF by centrifugation suggest that PHF-tau possesses a h

205 of horses presenting with clinical signs of PHF.

206 quantitative assays to establish solvents of PHF.

207 In TBS the CD spectrum of PHF was observed to have a spectral pattern consistent w

208 does not affect the phosphorylation state of PHF and complete dephosphorylation of PHF with hydrofluo

209 tes the self-assembly of tau into tangles of PHF and straight filaments by neutralizing the inhibitor

210 each of the six tau isoforms into tangles of PHF and straight filaments, and the microtubule binding

211 d Lys-353, suggesting that ubiquitination of PHF-Tau may be an earlier pathological event than previo

212 asitism, and facilitate our understanding of PHF pathogenesis.

213 s from the assemblies formed by a variety of PHF/tau-related peptide constructs containing the motifs

214 au isoform (K19) that represents the core of PHFs.

215 cantly contribute to hyperphosphorylation of PHFs in the C-terminus.

216 Electron microscope images of PHFs show pairs of twisted ribbons with 80 nm periodicit

217 demonstrates that the secondary structure of PHFs is polyproline II.

218 le information of the molecular structure of PHFs, as previous studies have failed to identify signs

219 Indeed, in vitro studies of PHFs have usually been performed in the presence of addi

220 d only phosphorylation dependent epitopes on PHF-tau.

221 ariant rapidly forms long and highly ordered PHFs.

222 it suggests that filamentous tau in the PHF (PHF-tau) makes a substantial contribution to the overall

223 d in vitro dephosphorylation of intact PHFs, PHFs with filamentous structure abolished by formic acid

224 d to microtubules and is believed to precede PHF assembly.

225 t the anti-CML antibody labels predominantly PHF in aggregates.

226 This is remarkable as tau-protein, PHF's primary constituent, has a high abundance of helix

227 pes in the paired helical filament proteins (PHF) found in AD brain.

228 newly developed anti-PHF mAbs that recognize PHF-tau but not autopsy-derived normal adult tau on West

229 se who were first fed PHF at 3.5 mo rejected PHF relative to CMF more than did infants exposed at you

230 ating the formation of degradation-resistant PHF tangles.

231 phosphorylated tau might prevent or reverse PHF formation in Alzheimer's disease.

232 st immediately with increasing PAD severity, PHF was, in contrast, relatively well preserved until la

233 sis are effective in completely solubilizing PHF, while a variety of denaturants are ineffective.

234 of normal brains and preparations of soluble PHF-tau as well as insoluble PHF from AD brains.

235 It was found that soluble PHF-Tau is ubiquitinated at its microtubule-binding doma

236 and glycation may play a role in stabilizing PHF aggregation leading to tangle formation in AD.

237 apidly induced transcription factors, Stat3, PHF/NF-kappa B, and others are responsible for activatio

238 well as archival DNA samples from suspected PHF cases to estimate the prevalence of N. findlayensis

239 hosphorylation-dependent epitopes (AT8, T3P, PHF-1, 12E8, AT6, AT18, AT30) in tau proteins.

240 buildup of hippocampal Abeta plaques and tau PHF in 11-month TgF344-AD rats but had no effect on wild

241 e highly phosphorylated polypeptides of tau (PHF-tau), with these polypeptides expressing no exons 3

242 ostained for hyperphosphorylated tau (p-tau; PHF-1) and assessed in accordance with the harmonized ev

243 and more limited in their distribution than PHF-1 or AP-immunoreactive NFT.

244 etry data for ubiquitin itself indicate that PHF-Tau is modified by three polyubiquitin linkages, at

245 We now show that PHF tangles isolated from AD brains are glycosylated, wh

246 emoval of PHF by centrifugation suggest that PHF-tau possesses a higher fraction of alpha-helical str

247 These data suggest that PHF/tau-positive dystrophic neurites are a common compon

248 icrotubule assembly leading to the view that PHF formation leads to microtubule deficiency in Alzheim

249 nsformed infrared spectroscopy, we find that PHFs are comprised of alpha-helices.

250 We also find that PHFs are very stable, as judged by their high melting te

251 Electron microscope studies have shown that PHFs from CBD differ from those of AD by being wider and

252 htau becomes phosphorylated at the PHF-1 (Ser-396/404) and TAU-1/AT8 (Ser-199/202) epitopes

253 increase in tau hyperphosphorylation at the PHF-1 epitope in pre-symptomatic R6/2 mice, whereas symp

254 ve thermal transitions were observed for the PHF samples in acetate buffer and water, consistent with

255 and it suggests that filamentous tau in the PHF (PHF-tau) makes a substantial contribution to the ov

256 These mAbs include the PHF-tau specific mAb AT10 and 12 newly developed anti-PH

257 e observed, indicating a perturbation of the PHF structure by the lipids.

258 to be responsible for the maintenance of the PHF structure.

259 ted form is the major protein subunit of the PHF.

260 Therefore, the PHF structure alone is insufficient for defining the pat

261 e deficiency in the antibody response to the PHF vaccines and the heterogeneity of E. risticii isolat

262 Using the PHF-core tau fragment (residues 297 - 391) as a model, w

263 ess dense mass, which appeared to divide the PHFs into two protofilament-like strands.

264 cular mechanisms leading to formation of the PHFs and accumulations of proteins in IBM muscle are not

265 phorylated, using a battery of antibodies to PHF/tau, neurofilament, and beta-amyloid protein.

266 similar in the ultrastructural appearance to PHF.

267 Among infants exposed to PHF for 1 mo, those who were first fed PHF at 3.5 mo rej

268 urrent to Tau aggregation cascade leading to PHF formation.

269 urrently available that bind specifically to PHF-tau, these data suggest that double phosphorylation

270 12/Ser214 and Thr231/Ser235 may be unique to PHF-tau.

271 tubule density was surprisingly unrelated to PHFs (P = 0.8).

272 tructure abolished by formic acid treatment (PHF(FA)) and fetal human tau protein.

273 Remarkably, the true PHF-specific antibodies recognized peptide sequences pho

274 , they can be considered as the first "true" PHF-specific antibodies capable of distinguishing tau is

275 A field study of horses vaccinated with two PHF vaccines indicated a poor antibody response, as dete

276 Ultrastructurally, PHFs from CBD were shown to be a heterogeneous populatio

277 In vivo, PHF tau, and high and medium molecular weight neurofilam

278 a pasture in Siskiyou County, Calif., where PHF is enzootic and were maintained for several weeks in

279 n the present study, we investigated whether PHF/tau-positive dystrophic neurites are located in all

280 We studied whether PHFs released from degenerating neurons could be taken u

281 ble with AT8 antibody and later changes with PHF-1 antibody.

282 pected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects wit

283 Glutamine levels correlated with PHF-1 immunostained hyperphosphorylated tau.

284 ed from E. risticii strains from horses with PHF.

285 ocalized to NFTs and immunoprecipitated with PHF-tau, but also is one of the few proteins known to un

286 B-positive neurities do not co-localize with PHF-1 or AT8 (hyperphosphorylated tau) immunoreactive ne

287 -like cells shared phosphorylated sites with PHF-tau and fetal tau, but differed from PHF-tau in thei

288 man recombinant tau in vitro as well as with PHFs isolated from NFTs from AD brains.

289 ly one pT-P motif in tau and copurifies with PHFs, resulting in depletion of soluble Pin1 in the brai

290 e diminution in AD and its relationship with PHFs has been performed.