ライフサイエンスコーパス: TTR

1 TTR also inhibited amyloid-dependent biofilm formation i

2 TTR amyloidoses are of particular interest regarding the

3 TTR and log-transformed INR variability were calculated

4 TTR tetramer dissociation precedes pathological TTR aggr

5 TTR-ASO treatment decreased LDL cholesterol in high-fat

6 TTR-ASO treatment of mice with genetic or diet-induced o

7 TTR-related causes were favorable predictors of survival

8 nested Cox regression models, including (1) TTR or log INR variability separately; (2) TTR and log I

9 Both AL amyloidosis and 2 of 10 TTR-noPN subjects were Congo red-positive.

10 myloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers without peripheral neuropathy (TTR

11 ) TTR or log INR variability separately; (2) TTR and log INR variability together; and (3) both predi

12 We present 2D terahertz-terahertz-Raman (2D TTR) spectroscopy, the first technique, to our knowledge

13 comparison of experimental and simulated 2D TTR spectra of bromoform (CHBr3), carbon tetrachloride (

14 bypass grafting (n = 1,033,255) to created 5 TTR groups: no 30-day readmission (n = 897,510), less th

15 Thirty of 31 patients (96.8%) achieved TTR stabilization after 6 weeks and 25 of 28 patients (8

16 rating effects of AD symptoms observed in AD/TTR(+/-) animal models after IDIF treatment and eventual

17 Adding TTR to ORBIT, ATRIA and HEMORR2HAGES led to improved pre

18 eding risk scores and investigated if adding TTR would improve their predictive value and clinical us

19 ence-specific because Lys-48 does not affect TTR aggregation.

20 ccur in cardiomyocytes exposed to aggregated TTR, and provide clues as to the molecular and physiolog

21 ecreasing circulating TTR levels or altering TTR-RBP4 binding could be a potential therapeutic approa

22 Amyloid TTR cytotoxicity results in mitochondrial potential modi

23 es (SMD=-1.27), CGI-S scores (SMD=-1.57) and TTR (SMD=-1.22).

24 a direct link between TTR-Abeta binding and TTR-mediated cytoprotection.

25 he treatment of familial chylomicronemia and TTR-mediated polyneuropathy.

26 ing strength between a particular ligand and TTR does not correlate well with its selectivity in plas

27 lecular interactions between the ligands and TTR were further characterized using molecular dynamics

28 Sections were stained with anti-PGP9.5, anti-TTR, and Congo red.

29 R stabilizes the homotetramer and attenuates TTR amyloidosis.

30 ban than with warfarin across center average TTR and individual TTR quartiles.

31 y impact on Alzheimer's disease (AD) because TTR has been shown to inhibit Abeta aggregation and deto

32 ructural features of the interaction between TTR and the Abeta(12-28) peptide (3), the essential reco

33 o better understand the interactions between TTR and THDCs, we determined the crystallographic struct

34 2A or L110A, providing a direct link between TTR-Abeta binding and TTR-mediated cytoprotection.

35 or log INR variability) but was weak between TTR and log INR variability (kappa=0.13).

36 is bound with similar high affinity in both TTR binding sites without the usual negative cooperativi

37 hesis, we have examined the effects of brain TTR on food intake and body weight and have further dete

38 al nerves, and transthyretin cardiomyopathy (TTR-CM), which primarily affects the heart.

39 eviously unknown anorectic action of central TTR in the control of energy balance, providing a potent

40 cise-induced anorexia, implying that central TTR may also play a functional role in modulating food i

41 These data show that decreasing circulating TTR levels or altering TTR-RBP4 binding could be a poten

42 ce of RBP4, we determined whether decreasing TTR levels with antisense oligonucleotides (ASOs) improv

43 nsgenically and treated with probe 4 display TTR.4 fluorescence in macrophage-like coelomocytes.

44 We divided TTR into 3 categories (high, >70%; moderate, 50% to 70%;

45 , but adding the 'labile INR' criteria (i.e. TTR <65%) to ATRIA, ORBIT and HEMORR2HAGES increased the

46 fic interest in the quest for more efficient TTR stabilizers, but a high selectivity is an almost uni

47 inol-binding protein 4 (RBP4), an endogenous TTR ligand, could be used as a diagnostic test for ATTR

48 Our analyses evaluated TTR groups for differences in risk-adjusted mortality (3

49 fficient binding to and imaging of exogenous TTR within intracellular organelles, including the mitoc

50 ction = .09 for DFS, .05 for OS, and .36 for TTR), although the stratified point estimates suggested

51 its components were moderate (kappa=0.56 for TTR and kappa=0.62 for log INR variability) but was weak

52 d the importance of metabolic activation for TTR binding.

53 Assays of affinity for TTR and inhibition of its tendency to form fibrils were

54 at the French National Reference Center for TTR-FAP from June 1, 2013, to June 30, 2014.

55 uintiles based on their level of control for TTR, log INR variability, and WCM.

56 t characterization of peptide inhibitors for TTR aggregation, establishing a novel therapeutic strate

57 entify beta-strands F and H as necessary for TTR aggregation.

58 ly, no effective pharmacological therapy for TTR amyloidoses is available, mostly due to a substantia

59 een in the proportions of patients free from TTR events between the accelerated and standard epirubic

60 een in the proportions of patients free from TTR events between the CMF and capecitabine groups (HR 0

61 eiving accelerated epirubicin were free from TTR events.

62 ation using ASOs targeting SRB-1, A1AT, FXI, TTR, and ApoC III mRNAs.

63 genotype status for the transthyretin gene (TTR) in 3856 black participants in the Atherosclerosis R

64 A novel mutation in the transthyretin gene (TTR) in Indian patients with familial amyloid polyneurop

65 1.27 and HR=1.29, respectively) and at high TTR levels (HR=1.55 and HR=1.56, respectively), but not

66 The reference groups high TTR and stable anticoagulation each denote good control.

67 isk changed with TTR and to compare the high TTR, low TTR, and aspirin-treated patients, with TTR bei

68 credible in health care systems with higher TTRs.

69 Overall, we illustrate how TTR is yet another amyloidogenic protein exploiting nega

70 live Caenorhabditis elegans expressing human TTR transgenically and treated with probe 4 display TTR.

71 ned the crystallographic structures of human TTR in complex with perfluorooctanesulfonic acid (PFOS),

72 ICV TTR decreased neuropeptide Y (NPY) levels in the DMH and

73 This effect was not due to sickness as icv TTR did not cause a conditioned taste aversion.

74 r implications for therapeutic approaches in TTR amyloidosis.

75 l pathogenic role of proteolytic cleavage in TTR amyloid fibrillogenesis.

76 ed on 60 informative CpGs, which differed in TTR in the validation set [R vs. L class, P=2.9x10(-3),

77 as a biomarker to detect treatment effect in TTR-FAP drug trials.

78 of patients with CA and compared findings in TTR and AL-related disease.

79 es and frequency of ocular manifestations in TTR amyloidosis is presented.

80 Mutations in TTR and postoperative visual acuity.

81 been performed in AL amyloidosis but not in TTR amyloidosis and might give insight into this differe

82 Wild-type TTR staining was less prominent in TTR-FAP patients.

83 and PMNFD were all significantly reduced in TTR-FAP patients versus healthy controls, whereas TTR-no

84 that Lys-35 acts as a gatekeeper residue in TTR, strongly decreasing its amyloidogenic potential.

85 l molecules to the thyroxin-binding sites in TTR stabilizes the homotetramer and attenuates TTR amylo

86 binding cooperativity, to distinct sites in TTR, consistent with the data of x-ray analysis of TTR i

87 by ligands that occupy both binding sites in TTR.

88 r is widely accepted as the critical step in TTR amyloid fibrillogenesis.

89 logic therapies shown to improve survival in TTR-CM.

90 ests that further evaluation of tafamidis in TTR amyloid cardiomyopathy is warranted.

91 k or the HSF1 stimulator celastrol increased TTR transcription in parallel with that of HSP40, HSP70,

92 HSF1 construct into SH-SY5Y cells increased TTR transcription and protein production, which could be

93 Increasing TTR was associated with a stepwise decline in mortality.

94 Increasing TTR was significantly associated with reduction in prima

95 th heart failure in sinus rhythm, increasing TTR is associated with better outcome and improved net c

96 rin across center average TTR and individual TTR quartiles.

97 complications in association with individual TTR (iTTR), INR variability, and aspirin use and identif

98 ones, Tafamidis((R)) and diflunisal, inhibit TTR misfolding by stabilizing native tetrameric TTR; how

99 The ability to inhibit TTR fibrillogenesis is known for several classes of comp

100 amer in vivo in mice and humans and inhibits TTR cytotoxicity.

101 Adding 'labile INR' (TTR < 65%) to ORBIT, ATRIA and HEMORR2HAGES significantl

102 tructures of unlabeled and deuterium-labeled TTR are essentially identical, subunit exchange kinetics

103 e of our previously reported bivalent ligand TTR 'superstabiliser' family, is notably more potent tha

104 d parent dust contaminants in a radio-ligand TTR binding assay; 2,2',4,4'-tetrahydroxybenzophenone, p

105 oronic acid-substituted stilbenes that limit TTR amyloidosis in vitro.

106 5 and HR=1.56, respectively), but not at low TTR levels.

107 ed with TTR and to compare the high TTR, low TTR, and aspirin-treated patients, with TTR being treate

108 Since lowering TTR levels increases renal clearance of RBP4, we determi

109 ts engineered nontetramer-forming monomer (M-TTR, F87M/L110M) inhibit CsgA amyloid formation in vitro

110 ot significantly compromise the ability of M-TTR to inhibit CsgA amyloidogenesis.

111 ibit CsgA amyloid formation in vitro, with M-TTR being the more efficient inhibitor.

112 reatment effectively achieved and maintained TTR stabilization and was well tolerated.

113 as available in only 18.7% of patients (mean TTR: 49.5% +/- 22.3%).

114 essive systemic disorder caused by misfolded TTR monomers that cumulatively deposit in the heart and

115 without amyloidosis that degraded misfolded TTR (misTTR) without reactivity to the physiological tet

116 misTTR inhibits fibrillogenesis of misfolded TTR under micromolar concentrations.

117 ed with low log INR variability, at moderate TTR levels (HR= 1.27 and HR=1.29, respectively) and at h

118 atients and APP23 AD model mice produce more TTR is unknown.

119 tion carriers without peripheral neuropathy (TTR-noPN; n = 10), (3) healthy controls (n = 20), (4) di

120 with X-ray crystallographic analysis of nine TTR.ligand complexes.

121 an efficient tool for the discovery of novel TTR-binders from the Tox21 inventory.

122 e mutation in the 33rd position of exon 2 of TTR in 1 patient of 1 pedigree, confirming the diagnosis

123 id was detected in 70% of TTR-FAP and 20% of TTR-noPN subjects.

124 ON: Cutaneous amyloid was detected in 70% of TTR-FAP and 20% of TTR-noPN subjects.

125 racerebroventricular (icv) administration of TTR in normal growing rats decreased food intake and bod

126 onsistent with the data of x-ray analysis of TTR in complex with both ligands.

127 While the in vivo analysis of TTR in mammalian models is complex, time- and resource-c

128 The standard treatment of familial cases of TTR amyloidosis has been liver transplantation.

129 o TTR, crystal structures were determined of TTR in complex with four of the identified compounds inc

130 The destabilizing effects of TTR deuteration are rather similar in character to those

131 and familial amyloid cardiomyopathy forms of TTR amyloidoses.

132 The natural history of TTR-CM is poorly characterized, which presents difficult

133 icts warfarin adverse effects independent of TTR.

134 Chronic icv infusion of TTR in Otsuka Long-Evans Tokushima Fatty rats reversed h

135 an 80-95% decrease in circulating levels of TTR and RBP4.

136 e risk for adverse events at given levels of TTR.

137 ds are known, understanding the mechanism of TTR aggregation can lead to additional inhibition approa

138 ledge about both the molecular mechanisms of TTR aggregation in tissue and the ensuing functional and

139 Several models of TTR amyloid fibrils have been proposed, but the segments

140 o those observed for aggressive mutations of TTR such as L55P (associated with familial amyloid polyn

141 ion (ChIP) assays demonstrated occupation of TTR promoter heat shock elements by HSF1 in APP23 hippoc

142 This review provides a brief overview of TTR-CM and the challenges of identifying clinically mean

143 dentified a new mechano-enzymatic pathway of TTR fibrillogenesis in vitro, catalysed by selective pro

144 and efficacy with respect to progression of TTR amyloid cardiomyopathy.

145 tion relationships due to oxidative PTPMs of TTR should contribute to the understanding of pathophysi

146 =1.57, P<0.001) independently, regardless of TTR levels.

147 (WARCEF) trial to assess the relationship of TTR with the WARCEF primary outcome (ischemic stroke, in

148 ligands within the thyroxine binding site of TTR can stabilize the tetrameric integrity and is a pote

149 bility of the two thyroxine binding sites of TTR to discriminate between different ligands, this feat

150 n-label trial evaluated the stabilization of TTR tetramers using 20 mg of tafamidis daily at week 6 (

151 lyphenols, which protect the native state of TTR by specifically interacting with its thyroxine bindi

152 Isotope labeling is used for the study of TTR by NMR, neutron diffraction, and mass spectrometry (

153 and safety of tafamidis for the treatment of TTR-CM.

154 floor ceiling effects that limit the use of TTR and INR variability as separate measures.

155 1 was either suppressive or had no effect on TTR expression confirming the differential effects of HS

156 nfirming the differential effects of HSF1 on TTR transcription in different cell types.

157 fibrils formed from wild-type TTR and other TTR variants.

158 tetramer dissociation precedes pathological TTR aggregation.

159 ansthyretin familial amyloid polyneuropathy (TTR-FAP).

160 By immune-targeting sparsely populated TTR misfolding intermediates (i.e. monomers), we achieve

161 olecule for Parkinson's disease, as a potent TTR aggregation inhibitor.

162 nts and 230 (53.1%) metabolites as potential TTR binders.

163 As promising TTR therapies are in development, increased awareness an

164 hway that includes the transthyretin protein TTR-52, as well as CED-7, NRF-5 and CED-6.

165 nship between time in the therapeutic range (TTR) and clinical outcomes in heart failure patients in

166 Percent time in therapeutic range (TTR) and international normalized ratio (INR) variabilit

167 warfarin, percent time in therapeutic range (TTR) and international normalized ratio (INR) variabilit

168 ved incorporating time in therapeutic range (TTR) in warfarin-treated patients.

169 Time in Therapeutic Range (TTR) was available in only 18.7% of patients (mean TTR:

170 nts, reflected by time in therapeutic range (TTR).

171 rfarin arms with times in therapeutic range (TTRs) of 55.2% to 64.9%, making the results less credibl

172 2 (MAF=3.2%, P=1.27 x 10(-9)) tagging a rare TTR variant (MAF=0.4%, P=2.14 x 10(-11)).

173 cent excess (MPE) or tracer-to-tracee ratio (TTR)) and amino acid concentration (i.e. unlabelled only

174 Circulating RBP4, TTR, B-type natriuretic peptide (BNP), and troponin I (T

175 nical prediction algorithm composed of RBP4, TTR, left ventricular ejection fraction, interventricula

176 inversely correlated with time to recovery (TTR) (r = -0.272, P = .02).

177 r epigenetic changes and time to recurrence (TTR).

178 cin would improve time to tumour recurrence (TTR); and whether use of oral capecitabine instead of cy

179 dies, and transcription termination regions (TTRs) showed strong positive correlation with gene expre

180 reading of H3S10ph at RT transition regions (TTRs) is accompanied by aberrant transcription initiatio

181 on-Severity Scale (CGI-S), time to response (TTR), discontinuation rate and individual adverse effect

182 was assessed by estimating time to results (TTR), prioritising/assigning putative therapeutic target

183 The mean (+/-SD) TTR was 57% (+/-28.5%).

184 This specific truncation of Ser52Pro TTR was generated readily in vitro by limited proteolysi

185 ution crystallographic structure of Ser52Pro TTR.

186 ychotics (SGAs) were associated with shorter TTR (SMD=-0.27) and a lower incidence of extrapyramidal

187 ides and the positive effect exerted by some TTR stabilizers for modulating the TTR-Abeta interaction

188 Pan-specific TTR antibodies do not possess such fibril inhibiting pro

189 ng sites and lacked the ability to stabilize TTR.

190 equally weighted method, adding standardized TTR to standardized log-transformed INR variability usin

191 ts and their metabolites for THDCs targeting TTR, we developed a quantitative structure-activity rela

192 developed an antibody (misTTR) that targets TTR residues 89-97, an epitope buried in the tetramer bu

193 misfolding by stabilizing native tetrameric TTR; however, their minimal effective concentration is i

194 t reactivity to the physiological tetrameric TTR (phyTTR).

195 ere, we report that both human WT tetrameric TTR (WT-TTR) and its engineered nontetramer-forming mono

196 We hypothesized that TTR might have broad antiamyloid activity because the bi

197 We now show that TTR expression in SH-SY5Y human neuroblastoma cells, pri

198 Here we show that TTR fibrillogenesis by the mechano-enzymatic pathway is

199 We show that TTR-52 binds to PS exposed on the injured axon, and can

200 These discoveries suggest that TTR is an effective antibiofilm agent that could potenti

201 The TTR 26-57 segment bears many of these aggressive amyloid

202 The TTR variant was associated with an increased risk of inc

203 ls, have provided a structural model for the TTR-Abeta interaction, as well as for the ternary comple

204 loidosis, and more than 100 mutations in the TTR gene are involved in familial amyloid polyneuropathy

205 The compounds were found to bind in the TTR hormone binding sites as predicted.

206 ased occupancy of heat shock elements in the TTR promoter by HSF1.

207 d variant show that it docks better into the TTR T4 pocket than tafamidis, so far the only drug on th

208 d by some TTR stabilizers for modulating the TTR-Abeta interaction have been previously studied.

209 nd results in the rapid self-assembly of the TTR 26-57 region into amyloid fibrils.

210 Lys-35 is part of the TTR basic heparin-binding motif.

211 gment of the TTR variant, the portion of the TTR sequence that previously has been reported to be the

212 Molecular aspects related to the role of the TTR stabilizer iododiflunisal (IDIF, 5) on the TTR-Abeta

213 brils was the residue 49-127 fragment of the TTR variant, the portion of the TTR sequence that previo

214 R stabilizer iododiflunisal (IDIF, 5) on the TTR-Abeta complex have been also examined.

215 nteraction and of the ability to protect the TTR native state for polyphenols, both stilbenoids and f

216 We thus confirm that the TTR fold keeps a generic residual aggregation propensity

217 be 4 is dark in aqueous buffers, whereas the TTR.4 complex exhibits a fluorescence emission maximum a

218 tional interactions of its linker within the TTR central channel.

219 12 representatives were selected, and their TTR binding affinities were studied with isothermal titr

220 Three TTR mutations, Glu89Lys, Gly47Arg, and homozygous Gly6Se

221 These chemicals competitively bind to TTR with 50% inhibition (IC50) values at or below 10 muM

222 idate structural details in their binding to TTR, crystal structures were determined of TTR in comple

223 Domains with structural homology to TTR exist in a number of proteins, including the M14B su

224 Tolcapone binds specifically to TTR in human plasma, stabilizes the native tetramer in v

225 ycycline exhibited greater potential towards TTR fibril disaggregation in vitro compared to the paren

226 Transthyretin (TTR) amyloidoses are familial or sporadic degenerative c

227 Transthyretin (TTR) amyloidosis is a progressive systemic disorder caus

228 Transthyretin (TTR) forms misfolded beta-sheet aggregates responsible f

229 Transthyretin (TTR) is a blood and cerebrospinal fluid transporter of t

230 Transthyretin (TTR) is a homotetrameric protein.

231 Transthyretin (TTR) is a plasma homotetrameric protein implicated in fa

232 Transthyretin (TTR) is an amyloidogenic protein, the amyloidogenic pote

233 of patients were studied: (1) transthyretin (TTR) familial amyloidotic polyneuropathy (FAP; n = 20),

234 ndividuals with amyloidogenic transthyretin (TTR) mutations.

235 pe (ATTRwt) or mutant (ATTRm) transthyretin (TTR) CA.

236 Circulating transthyretin (TTR) is a critical determinant of plasma retinol-binding

237 es: C-reactive protein (CRP), transthyretin (TTR), and concanavalin A (Con A).

238 amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily affecting the peripher

239 polipoprotein C-III and human transthyretin (TTR) in transgenic mice.

240 srupting chemicals (THDCs) is transthyretin (TTR), a thyroid hormone transporter in vertebrates.

241 jugate duplex targeting mouse transthyretin (TTR) indicated that GNA is well tolerated in the seed re

242 Wild-type and mutant transthyretin (TTR) can misfold and deposit in the heart, peripheral ne

243 on of model proteins, namely, transthyretin (TTR), avidin, concanavalin A (conA), and human serum amy

244 Dissociation of the native transthyretin (TTR) tetramer is widely accepted as the critical step in

245 dation of the nonglycosylated transthyretin (TTR) D18G misfolded client.

246 blished that the formation of transthyretin (TTR) amyloid fibrils is linked to the destabilization an

247 ization and ligand binding of transthyretin (TTR) and the chaperone domain from prosurfactant protein

248 creased neuronal synthesis of transthyretin (TTR) may favorably impact on Alzheimer's disease (AD) be

249 The Ser52Pro variant of transthyretin (TTR) produces aggressive, highly penetrant, autosomal-do

250 The ability of transthyretin (TTR) to bind Abeta-peptides and the positive effect exer

251 This is the case of transthyretin (TTR), a homotetrameric protein whose dissociation into i

252 c thyroxine transport protein transthyretin (TTR) forms amyloid fibrils upon dissociation and monomer

253 The visceral protein transthyretin (TTR) is frequently affected by oxidative post-translatio

254 mic amyloid precursor protein transthyretin (TTR) is known to inhibit amyloid-beta (Abeta) aggregatio

255 The plasma protein transthyretin (TTR) is linked to human amyloidosis.

256 soleucine at codon 122 of the transthyretin (TTR) gene (V122I), present in 3.43% of African American

257 amyloidosis, mutation in the transthyretin (TTR) protein is the most common type.

258 signed to bind selectively to transthyretin (TTR).

259 ls is the hormone transporter transthyretin (TTR).

260 Wild type transthyretin (TTR) is responsible for senile systemic amyloidosis, and

261 short polypeptide fragment of transthyretin, TTR (105-115), directly correlates to their supramolecul

262 ate stabilizers are promising drugs to treat TTR amyloidoses.

263 so far the only drug on the market to treat TTR amyloidoses.

264 famidis, a small-molecule drug used to treat TTR-related amyloidosis in the clinic.

265 tions are being assessed in clinical trials (TTR gene silencing).

266 inhibits fibril formation by both wild-type TTR and a common disease-related variant, V30M TTR, as e

267 ardiac amyloid fibrils formed from wild-type TTR and other TTR variants.

268 l structures of tolcapone bound to wild-type TTR and to the V122I cardiomyopathy-associated variant s

269 beta toxicity was demonstrated for wild-type TTR but not L82A or L110A, providing a direct link betwe

270 to amyloid oligomers or fibrils of wild-type TTR or to its T4-stabilized form, which resists tetramer

271 Wild-type TTR staining was less prominent in TTR-FAP patients.

272 hs of time to variously aggregated wild-type TTR, a condition that characterizes senile systemic amyl

273 e of overt cardiac abnormalities among V122I TTR carriers was low.

274 ficant difference in mortality between V122I TTR allele carriers and noncarriers, a finding that cont

275 the risk of incident heart failure in V122I TTR variant carriers (124 participants [3%]) versus nonc

276 R and a common disease-related variant, V30M TTR, as effectively as does tafamidis, a small-molecule

277 uantity of full-length wild-type and variant TTR, the main component of the ex vivo fibrils was the r

278 ol-binding protein (RBP) by Ser52Pro variant TTR stabilizes the native tetrameric assembly, but neith

279 The primary endpoint was TTR, defined as time from randomisation to first invasiv

280 AP patients versus healthy controls, whereas TTR-noPN subjects had intermediate reductions.

281 d to examine how the event risk changed with TTR and to compare the high TTR, low TTR, and aspirin-tr

282 e patients who presented to Mayo Clinic with TTR amyloidosis between January 1, 1970, and November 1,

283 l and poorest control quintile compared with TTR and log INR variability, but not for major bleeding.

284 ed by x-ray analysis of their complexes with TTR.

285 ame approaches were used in conjunction with TTR and/or unlabelled concentration only, or when using

286 o develop PTM, and inversely correlates with TTR.

287 ctional group does not react covalently with TTR on the time scale required for cellular imaging, but

288 Patients with TTR amyloidosis have been noted to have ocular, especial

289 In this large cohort of patients with TTR amyloidosis, female sex and decreased VA were associ

290 Of 108 examined eyes in 54 patients with TTR amyloidosis, there were 26 eyes (24%) in 13 patients

291 tion alterations often seen in patients with TTR amyloidosis.

292 Fifteen patients with TTR-FAP underwent a complete neurologic examination, inc

293 In these 15 patients with TTR-FAP, IVCM measurement permitted rapid, noninvasive e

294 he place of IVCM in monitoring patients with TTR-FAP.

295 low TTR, and aspirin-treated patients, with TTR being treated as a time-dependent covariate.

296 osulfate probe 4 does react selectively with TTR without labeling the remainder of the cellular prote

297 d that these THDCs interacted similarly with TTR via the residue Ser117A, but their binding poses wer

298 y 50% in high-fat diet-fed mice treated with TTR-ASOs, demonstrating improved insulin sensitivity.

299 Treatment with TTR-ASOs, but not control ASOs, decreased insulin levels

300 Preincubation of WT-TTR with small molecules that occupy the T4 binding site

301 report that both human WT tetrameric TTR (WT-TTR) and its engineered nontetramer-forming monomer (M-T