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1 europathy were identified, 60 primary and 41 transthyretin.
2 tion of the beta-Amyloid Peptide Abeta42 and transthyretin.
3 n in the peripheral nervous system of mutant transthyretin.
4 y-binding to the thyroxine-carrying protein, transthyretin.
5 erence (RNAi) could reduce the production of transthyretin.
6 ial infiltration, usually by light chains or transthyretin.
7 xplorations of pathological conformations of transthyretin.
8 hibits amyloid formation by both WT and L55P transthyretin.
9 raction between RBP4 and its binding partner transthyretin.
10 c fragment of the disease-associated protein transthyretin.
11 biophysical properties to recombinant human transthyretin.
12 r seed further amyloid aggregation of native transthyretin.
16 eover, the treatment increased expression of transthyretin, accompanied by reduction of intracellular
17 s and Schwann cells of nerves with deposited transthyretin aggregates but the pattern also extended t
21 in a reticular/pericellular pattern, whereas transthyretin amyloid (ATTR) more commonly showed patchy
23 o reactivity to the Abeta precursor protein, transthyretin amyloid aggregates, or irrelevant proteins
27 model of patients with wild-type or variant transthyretin amyloid cardiomyopathy and heart failure (
31 s study explored the prevalence of wild-type transthyretin amyloid in cAS by myocardial biopsy, its i
32 used by the deposition of hepatocyte-derived transthyretin amyloid in peripheral nerves and the heart
36 , 37%), localized AL (N = 3, 10%), wild-type transthyretin amyloidosis (ATTR) (N = 1, 3.3%), and amyl
42 mically to bind human AA, ALkappa, ALlambda, transthyretin amyloidosis (ATTR), and Abeta amyloid depo
46 In univariable analyses, the presence of transthyretin amyloidosis amyloid had the highest hazard
47 epidemiology, and therapeutic strategies for transthyretin amyloidosis and highlight diagnostic pitfa
48 kilogram of body weight) in 32 patients with transthyretin amyloidosis and then evaluated ALN-TTR02 (
50 e, oral TTR stabilizer under development for transthyretin amyloidosis cardiomyopathy (ATTR-CM) that
51 years) using inputs from the ATTR-ACT trial (Transthyretin Amyloidosis Cardiomyopathy Clinical Trial)
58 who when compared with whites with wild-type transthyretin amyloidosis, a phenotypically similar cond
63 esidues 105-115 of the amyloidogenic protein transthyretin and a DNA origami construct is used to for
64 11-residue peptide derived from the protein transthyretin and clusters of this fibre-forming peptide
65 loidogenesis, we produced recombinant murine transthyretin and human/murine transthyretin heterotetra
66 y showed that the placenta actively produces transthyretin and in preeclampsia, a significant amount
67 here were 28 patients (25 men) with Ala97Ser transthyretin and late onset (59.9 +/- 6.0 years) disabl
71 4 patients: 5 amyloid light chain, 5 amyloid transthyretin, and 4 control with hypertensive heart dis
72 he plasma proteins, fibrinogen, fibronectin, transthyretin, and alpha-fetoprotein, an essential featu
73 tetrameric protein complexes (streptavidin, transthyretin, and hemoglobin) in the gas phase was unde
76 mon systemic amyloidoses (ALlambda, ALkappa, transthyretin, and reactive amyloidosis), with Congo red
77 n techniques with primers designed to detect transthyretin, apolipoprotein AI, apolipoprotein AII, fi
79 f diagnosis and 25% of patients with amyloid transthyretin (ATTR) amyloidosis die within 24 months of
81 oidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially infl
82 onoclonal immunoglobulin light-chain (AL) or transthyretin (ATTR) type-and healthy volunteers (n = 5)
83 e C, holo hemoglobin-alpha, ovalbumin, human transthyretin, avidin, bovine serum albumin, concanavali
84 lity in CA, with an amyloid burden effect in transthyretin, but an idiosyncratic effect in light chai
87 d qRT-PCR, we investigated the production of transthyretin by preeclamptic placentae and whether tran
88 id systems, beta-amyloid peptide (Abeta) and transthyretin, by these designed alpha-sheet peptides.
90 nd that changes in the tertiary structure of transthyretin can be associated with disruptions to the
96 st common of these conditions, but wild-type transthyretin cardiac amyloidosis (ATTRwt) is increasing
97 Technetium-99 m pyrophosphate protocols for transthyretin cardiac amyloidosis diagnosis have variabl
98 ing have transformed our ability to diagnose transthyretin cardiac amyloidosis noninvasively and unma
99 registry analysis of patients with suspected transthyretin cardiac amyloidosis referred for technetiu
101 primarily affects the peripheral nerves, and transthyretin cardiomyopathy (TTR-CM), which primarily a
102 ongoing phase 3 ATTR-ACT study (Tafamidis in Transthyretin Cardiomyopathy Clinical Trial), an interna
105 Systemic amyloid deposition of aggregated transthyretin causes hereditary and sporadic amyloidoses
107 c placentae secreted similar levels of total transthyretin compared to normotensive placentae (2352 +
110 uction of both mutant and nonmutant forms of transthyretin, establishing proof of concept for RNAi th
111 neuropathy (SFN) is an important feature of transthyretin familial amyloid polyneuropathy (TTR-FAP).
113 een shown to delay neurologic progression of transthyretin familial amyloid polyneuropathy, there are
114 ate phenotypic presentations of the disease: transthyretin familial amyloid polyneuropathy, which pri
117 ology and thermodynamic stability of natural transthyretin fibrils with those of fibrils generated in
121 siRNAs are being explored to knock-down the transthyretin gene to prevent the related form of amyloi
122 he noncovalently associated complex of human transthyretin, generated by collision-induced dissociati
126 binant murine transthyretin and human/murine transthyretin heterotetramers and compared their structu
127 PP, neprilysin, insulin-degrading enzyme and transthyretin in MCAT, AbetaPP, MCAT/AbetaPP and wild-ty
129 ion of retinol-binding protein 4 (RBP4) with transthyretin in the serum would reduce serum RBP4 and r
130 fferent sources (alpha-synuclein, Sup35, and transthyretin) induced NADPH oxidase-dependent NETs in v
135 yretin by preeclamptic placentae and whether transthyretin is carried into the maternal circulation v
137 aggregation of circulating proteins, such as transthyretin, is a severe and usually fatal condition.
138 ecursor proteins, including serum amyloid A, transthyretin, islet amyloid polypeptide, and amyloid be
142 pid, dose-dependent, and durable lowering of transthyretin levels was observed in the two trials.
145 common Greek-key beta sandwich fold with two transthyretin-like repeats that polymerize into a pilus
146 nts included urinary protein 1 (m/z=15,835), transthyretin (m/z=13,880), and a component at m/z=13,35
149 TTR production, in patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy.
150 e safety profile in patients with hereditary transthyretin-mediated amyloidosis with polyneuropathy.
151 rtitioning of destabilized retroaldolase and transthyretin mutants between the aforementioned conform
153 ly variable and influenced by the underlying transthyretin mutation, age of the affected individual,
155 arterial pressure, but not the presence of a transthyretin mutation, were independently associated wi
156 c failure and is due to dominantly inherited transthyretin mutations causing accelerated amyloid depo
157 opathy caused by extracellular deposition of transthyretin, normally involved in the transportation o
158 in amyloidosis without typical signs, senile transthyretin, or hereditary amyloidosis with a concomit
159 wing targets will be specifically discussed: transthyretin, p53, superoxide dismutase 1, lysozyme, se
160 titrypsin, complement factor B, haptoglobin, transthyretin, plasma retinol binding protein, albumin,
161 hat the murine protein interacted with human transthyretin, preventing the dissociation and partial u
163 underrecognized systemic disease whereby the transthyretin protein misfolds to form fibrils that depo
164 arallel phagocytic pathway that includes the transthyretin protein TTR-52, as well as CED-7, NRF-5 an
165 ne-to-isoleucine substitution (V122I) in the transthyretin protein, which has been associated with la
166 tiating immunoglobulin light-chain (AL) from transthyretin-related cardiac amyloidoses (ATTR) is impe
168 monomer unfolding of the human serum protein transthyretin, resulting in aggregation and extracellula
169 ement, recombinant thyroid transport protein transthyretin (rTTR), and dedicated modes of liquid chro
170 e to aggregation and deposition of wild-type transthyretin (senile systemic amyloidosis, SSA) or mono
171 C, prenylcysteine oxidase 1, paraoxonase 1, transthyretin, serum amyloid A4, and fibrinogen alpha ch
172 w in immunized mice that the carrier protein transthyretin simultaneously optimizes three factors: ef
173 ar transthyretin deposition with anakinra or transthyretin siRNA, Pcdh10 protein levels were reduced,
175 rs otherwise composed of human amyloid-prone transthyretin subunits imposes kinetic stability, preven
177 s of two protein complexes, source-activated transthyretin tetramer and nativelike serum amyloid P de
178 chemical or mutational stabilization of the transthyretin tetramer does not hinder amyloid seeding.
179 tion approach was applied to generate intact transthyretin tetramers with charge states ranging from
180 enta, they may also be delivering aggregated transthyretin to specific maternal organs, contributing
183 sion of the human systemic amyloid precursor transthyretin (TTR) ameliorates Alzheimer's disease (AD)
185 It is well established that the formation of transthyretin (TTR) amyloid fibrils is linked to the des
186 ulfated GAGs, especially heparin, accelerate transthyretin (TTR) amyloidogenesis by quaternary struct
195 g transcriptional profiling, we now identify transthyretin (TTR) and Klotho as APP/APLP2-dependent ge
196 g retinol levels, which are located near the transthyretin (TTR) and retinol binding protein 4 (RBP4)
197 gating oligomerization and ligand binding of transthyretin (TTR) and the chaperone domain from prosur
200 th retinoids for RBP4 binding, disrupts RBP4-transthyretin (TTR) complexes, and results in urinary se
201 on studies were carried out as a function of transthyretin (TTR) concentration to quantify the thermo
204 ommon familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily affecti
205 Five groups of patients were studied: (1) transthyretin (TTR) familial amyloidotic polyneuropathy
206 The tetrameric thyroxine transport protein transthyretin (TTR) forms amyloid fibrils upon dissociat
208 of valine for isoleucine at codon 122 of the transthyretin (TTR) gene (V122I), present in 3.43% of Af
209 The siRNAs were designed to silence the transthyretin (Ttr) gene and were conjugated to a trival
211 caused by aggregation of Ig light chains or transthyretin (TTR) in the cardiac interstitium and cond
212 ion of retinol-binding protein 4 (RBP4) with transthyretin (TTR) in the serum may decrease the uptake
214 of a GalNAc conjugate duplex targeting mouse transthyretin (TTR) indicated that GNA is well tolerated
215 he proposed mechanism of fibril formation of transthyretin (TTR) involves self-assembly of partially
228 nt of l-thyroxine (T4) from binding sites on transthyretin (TTR) is considered a significant contribu
232 The human systemic amyloid precursor protein transthyretin (TTR) is known to inhibit amyloid-beta (Ab
241 The amyloidogenic homotetrameric protein transthyretin (TTR) must undergo rate-limiting dissociat
244 ramer dissociation and monomer misfolding of transthyretin (TTR) occur before its aggregation into cr
246 ntaining amyloid deposits composed of either transthyretin (TTR) or Ig light chain from nine patients
249 s with familial amyloidosis, mutation in the transthyretin (TTR) protein is the most common type.
253 In turn, holo-RBP associates in plasma with transthyretin (TTR) to form a ternary RBP-retinol-TTR co
255 ection in vivo, overexpression of a WT human transthyretin (TTR) transgene was ameliorative in the AP
256 y for the inner thyroxine binding subsite of transthyretin (TTR) was conceived of by structure-based
257 sis is caused by an amyloidogenic variant of transthyretin (TTR) with a substitution of methionine fo
261 pete with thyroxin (T4) for binding sites on transthyretin (TTR), a T4 transport protein found in pla
262 roid hormone disrupting chemicals (THDCs) is transthyretin (TTR), a thyroid hormone transporter in ve
263 itive genes, alpha1-antitrypsin (alpha1-AT), transthyretin (TTR), and apolipoprotein B (ApoB) after i
266 protein-protein interaction between RBP4 and transthyretin (TTR), another serum protein that protects
267 ng the binding of 2,4-dinitrophenol (DNP) to transthyretin (TTR), as well as preliminary measurements
268 the conformation of model proteins, namely, transthyretin (TTR), avidin, concanavalin A (conA), and
269 ic amyloidoses caused by mutant or wild-type transthyretin (TTR), deposition occurs at a distance fro
272 yloid fibril formation by the plasma protein transthyretin (TTR), requiring rate-limiting tetramer di
275 mice were crossbred with the liver-specific transthyretin (TTR)-IGF-I transgenic mice to assess the
284 ) prion, and a short polypeptide fragment of transthyretin, TTR (105-115), directly correlates to the
285 ted Phase II/III trials for the treatment of Transthyretin Type Familial Amyloid Polyneuropathy (TTR-
286 d in 76 patients, including 56 with the wild transthyretin type, 17 with the mutant transthyretin typ
289 nuclein associated with Parkinson's disease, transthyretin V30M mutant associated with familial amylo
290 sgenic for few copies of amyloid-prone human transthyretin variants, including the aggressive L55P mu
291 of knockdown of the clinically relevant gene transthyretin was observed at doses as low as 0.03 mg/kg
295 ins (all except BSA) and an impurity (bovine transthyretin) were confidently identified by database s
296 s, two peptides (serum amyloid A protein and transthyretin) were identified and quantitated by immuno
297 euritogenesis with a decreased expression of transthyretin, which is known to be downregulated by oxi
298 cedure, which replaces the patient's variant transthyretin with the WT protein, can fail to stop subs
299 of 1.0 mg per kilogram, ALN-TTR01 suppressed transthyretin, with a mean reduction at day 7 of 38%, as
300 amyloid polyneuropathy (FAP) due to mutated transthyretin, with sudomotor failure as a common manife