ライフサイエンスコーパス: protein aggregate

1 nitiated by the internalization of exogenous protein aggregates.

2 efficiency and the thermostability of prion protein aggregates.

3 ogies and can therefore be used to visualize protein aggregates.

4 lular responses and diseases associated with protein aggregates.

5 s and unimpaired clearance of stress-induced protein aggregates.

6 d separation and characterization of complex protein aggregates.

7 , and dispersed protein/peptide molecules or protein aggregates.

8 removal of excessive or damaged proteins and protein aggregates.

9 ing illnesses through the formation of toxic protein aggregates.

10 iding the formation of potentially cytotoxic protein aggregates.

11 r multimodal detection of disease-associated protein aggregates.

12 l disease stages, preceding the formation of protein aggregates.

13 the proteostasis network dictate the fate of protein aggregates.

14 be beneficial to prevent the accumulation of protein aggregates.

15 ates the UPR(ER) without promoting misfolded protein aggregates.

16 y often results in the accumulation of large protein aggregates.

17 ence in patient brain of both repeat RNA and protein aggregates.

18 es associated with accumulation of misfolded protein aggregates.

19 enciphered within different conformations of protein aggregates.

20 rotein aggregation and even reverse existing protein aggregates.

21 onversion of homotypic proteins into growing protein aggregates.

22 mation of nonfunctional or potentially toxic protein aggregates.

23 formation of and dissolve previously formed protein aggregates.

24 ns can lead to the formation of pathological protein aggregates.

25 and extracellular accumulation of neurotoxic protein aggregates.

26 n short amyloidogenic peptides and denatured protein aggregates.

27 nelles, long-lived proteins and a variety of protein aggregates.

28 characterize the structure and nature of LHC protein aggregates.

29 forces powered by ATP hydrolysis to remodel protein aggregates.

30 ons with a subset of morphologically defined protein aggregates.

31 or the nuclear export of very large RNPs and protein aggregates.

32 re proteostasis and to avoid the toxicity of protein aggregates.

33 l protein LC3 and clearance of ubiquitinated protein aggregates.

34 spectra that reflect the 3D structure of the protein aggregates.

35 s for the insight into the properties of tau protein aggregates.

36 uction of the fraction of the heat denatured protein aggregates.

37 and retention of damaged material, including protein aggregates.

38 highly challenging samples as supramolecular protein aggregates.

39 ystem (UPS) to avoid a build-up of misfolded protein aggregates.

40 of selective autophagy, which relocalize to protein aggregates.

41 -dependent autophagy allows the clearance of protein aggregates.

42 es (146 S; 8200 kDa) or pentameric FMDV coat protein aggregates (12 S; 282 kDa) was detected, a modes

43 eome integrity and limit the accumulation of protein aggregates, a hallmark of aging and degenerative

44 fined subset of neurons, we demonstrate that protein aggregates accumulate at synaptic terminals and

45 re we show that autophagosomal cargo such as protein aggregates accumulate within lysosomes in aneupl

46 -spectrum kinase inhibitor dasatinib blocked protein aggregate accumulation and restored in vitro org

47 a-localized ribosomes, ultimately preventing protein aggregate accumulation within mitochondria.

48 lting in autophagy impairment, intracellular protein aggregate accumulation, unfolded protein respons

49 y monitoring neuronal function, and clearing protein aggregates across the lifespan.

50 Reactivation of intracellular protein aggregates after a severe stress is mandatory fo

51 isorders associated with the accumulation of protein aggregates; amyloid-beta (Abeta) and tau in the

52 Cross-beta fibrous protein aggregates (amyloids and amyloid-based prions) a

53 seases involve the accumulation of misfolded protein aggregates and 'prion-like' seeding and spread h

54 s, including the presence of desmin-positive protein aggregates and a concurrent disarrangement of th

55 The mutant AAT protein aggregates and accumulates in the liver leading

56 Prions are self-replicating protein aggregates and are the primary causative factor

57 plaques, enhance aggrephagy of p62-enriched protein aggregates and blunt macrophage apoptosis and pr

58 aterial state, which is reminiscent of solid protein aggregates and controlled by protein disaggregas

59 Protein aggregates and damaged organelles are tagged wit

60 ane vesicles termed autophagosomes to remove protein aggregates and damaged organelles from the cytop

61 process involved in lysosomal degradation of protein aggregates and damaged organelles.

62 n chains are attached as selective labels on protein aggregates and dysfunctional organelles, thus pr

63 ion, leading to accumulation of p62-mediated protein aggregates and enhanced oxidative and ER stress

64 ere the larger diameter peak was ascribed to protein aggregates and entrapped oil droplets.

65 S editing efficacy resulted in ubiquitinated protein aggregates and mitochondrial defects in cardiomy

66 eration characterized by the accumulation of protein aggregates and mitochondrial dysfunction.

67 ed vesicles called exophers that can contain protein aggregates and organelles.

68 roaches based on blocking neuronal uptake of protein aggregates and promoting their clearance.

69 and ClpB/Hsp104 collaboratively disaggregate protein aggregates and reactivate inactive proteins.

70 flow-based fractionation of highly purified protein aggregates and simultaneous measurement of their

71 pretation of tests based on the detection of protein aggregates and suggest that de novo formation of

72 before observed structural motif for ordered protein aggregates and suggests a possible mechanism for

73 ong prodromal phase between the formation of protein aggregates and the appearance of the first clini

74 for characterizing the interactions between protein aggregates and the membranes of live neuronal ce

75 ithout disturbing selective interaction with protein aggregates and the oligothiophene-aggregate inte

76 olved in neurodegenerative diseases can form protein aggregates and their aggregation process may be

77 erstanding of the structures of pathological protein aggregates and their associated disease mechanis

78 the capture of heat stress-induced cytosolic protein aggregates and their retention in the mother cel

79 that compromise molecular chaperones, these proteins aggregate and become cytotoxic.

80 g recycling of long-lived proteins, abnormal protein aggregates, and damaged organelles under cellula

81 ent levels of C-terminal truncation, soluble protein aggregates, and glycation that all likely have a

82 of microbes, dead cells, redundant synapses, protein aggregates, and other particulate and soluble an

83 in soluble preamyloid oligomers, disordered protein aggregates, and stable amyloid or prion conforme

84 sion pathology, in addition to the classical protein aggregates, and suggested that structures previo

85 the dividing yeast cell on the diffusion of protein aggregates, and the possibility of aggregate bin

86 ng of nascent proteins, breakup of misfolded protein aggregates, and translocation of proteins across

87 Protein aggregates are a common feature of neurodegenera

88 mpartments as insoluble amyloid or amorphous protein aggregates are a hallmark feature of many debili

89 In aggresomes, protein aggregates are actively degraded by the autophag

90 Protein aggregates are also formed within the endoplasmi

91 Amyloid protein aggregates are associated with dozens of devasta

92 tion; however, a large number of non-amyloid protein aggregates are considered "amorphous," and in mo

93 way in which cytosol, damaged organelles and protein aggregates are engulfed in autophagosomes and de

94 embly or promote the destabilization of such protein aggregates are in clinical testing.

95 modifications on the molecular properties of protein aggregates are largely unknown.

96 Ligands for identifying protein aggregates are of great interest as such deposit

97 Lipid and protein aggregates are one of the fundamental materials

98 rs investigated whether amyloid beta (Abeta) protein aggregates are present in the hearts of patients

99 iques currently used for characterization of protein aggregates are prone to a number of limitations

100 Thus, whereas cytoplasmic protein aggregates are retained in the mother cell to pr

101 Protein aggregates are situated at the boundary between

102 Protein aggregates are the hallmark of stressed and agei

103 Such protein aggregates are the root cause of numerous diseas

104 These protein aggregates are thought to cause neuronal dysfunc

105 For therapeutic proteins, aggregates are a significant risk factor for d

106 mitotic potential, and display intracellular protein aggregates as compared to cells from unaffected

107 s successfully modified from the analysis of protein aggregates, as found in simple protein mixtures,

108 taining to the formation and interactions of protein aggregates associated with neurodegenerative dis

109 ntify and characterize the potentially toxic protein aggregates associated with neurodegenerative dis

110 s a limited capacity to self-protect against protein aggregate-associated pathology, and mounting evi

111 Tetrameric full-length protein aggregated at similar rates and kinetics to isol

112 Prior work indicates that prion protein aggregates bind heparan sulfate proteoglycans (H

113 olesterol, significantly decreased preformed protein aggregates both in vitro and in cell-transfectio

114 ollaborate with Hsp70 to dissolve disordered protein aggregates but employ distinct mechanisms of int

115 underlying such asymmetrical segregation of protein aggregates by mother and daughter cells remains

116 s, which are distinct from the classical MFM protein aggregates by their morphology and filamentous a

117 uently results in the formation of insoluble protein aggregates called inclusion bodies (IBs).

118 Accumulation of protein aggregates can also be induced from a variety of

119 Here we demonstrate that cytosolic protein aggregates can also behave as infectious entitie

120 The resulting protein aggregates can be resolved or degraded by molecu

121 nder conditions of normal ER inheritance, ER protein aggregates can enter the daughter cell.

122 Stress induced by cytoplasmic protein aggregates can have deleterious consequences for

123 Protein aggregates cannot be processed by the proteasome

124 Misfolded protein aggregates, characterized by a canonical amyloid

125 appears as a central and major regulator of protein aggregate clearance by modulating autophagic act

126 possible connections among glucosylceramide, protein aggregate clearance, and autophagy.

127 nt K63-deubiquitinating enzyme to facilitate protein aggregate clearance.

128 isorder characterized by the accumulation of protein aggregates comprised of alpha-synuclein (alpha-s

129 rotein disaggregase from yeast, can dissolve protein aggregates connected to neurodegenerative diseas

130 Mallory-Denk bodies (MDBs) are protein aggregates consisting of ubiquitinated keratins

131 These protein aggregates contain Ltn1-dependent polyubiquitin

132 are characterized by formation of peptide or protein aggregates containing a cross-beta structure.

133 species were comparable, detergent-insoluble protein aggregates containing phosphorylated c-Src accum

134 s of ALS include the presence of cytoplasmic protein aggregates containing TDP-43 and an associated l

135 Protein aggregates containing ubiquitin (Ub) are commonl

136 Myh6-sTNF mice develop protein aggregates containing ubiquitin-tagged proteins

137 topathological features, including different protein aggregates, continues to be evaluated.

138 hnique, used for fast amplification of prion protein aggregates, could be adapted for growing alpha-s

139 Selective autophagy eliminates protein aggregates, damaged organelles, and other target

140 d represent non-living membrane vesicles and protein aggregates derived from blood.

141 When expressed in the mammalian cytosol, protein aggregates derived from the prion domain NM of y

142 denaturation perturb the structure of prion protein aggregates differently.

143 that transcellular propagation of fibrillar protein aggregates drives the progression of neurodegene

144 tudy, we show that yeast mother cells form a protein aggregate during early replicative aging that is

145 bsence of significant mother/bud exchange of protein aggregates during the budded phase of the cell c

146 In this study, we exposed abnormal prion protein aggregates encompassing the spectrum of human pr

147 We suggest that the quaternary structure of protein aggregates, especially soluble oligomers, may al

148 athematical modeling, we find that fusion of protein aggregates facilitates asymmetric segregation.

149 biomolecular orientational distributions in protein aggregates, fibrillar structures of cells, and c

150 rn, promote a metabolic shift that mobilizes protein aggregates for degradation, and reset proteostas

151 ugh they share common pathological features, protein aggregates form in different subcellular locatio

152 ing an absence of normal protein production, protein aggregate formation, enhanced proteasomal degrad

153 Protein aggregates formed on ER are frequently also asso

154 channels (Cav2.1) and is characterized by CT protein aggregates found in cerebellar Purkinje cells (P

155 Amyloids are ordered protein aggregates, found in all kingdoms of life, and a

156 ed by the productive spreading of prion-like protein aggregates from a "donor cell" that is the sourc

157 ition, prion-like encompasses the release of protein aggregates from brain cells and their uptake by

158 s that distinguish infectious and pathogenic protein aggregates from more innocuous ones are poorly u

159 afely clear large and otherwise pathological protein aggregates from the body.

160 We explore how autophagy eliminates protein aggregates from within mitochondria and the role

161 pathies are only detected after irreversible protein aggregates have formed.

162 The stereotypical spread of pathological tau protein aggregates have recently been attributed to the

163 The in vitro digestion of heated whey protein aggregates having different structure and physic

164 uses produce cytoplasmic inclusion bodies or protein aggregates; however, a hallmark of viruses of th

165 ysfunction occurs before the accumulation of protein aggregates (i.e., alpha-syn) and neurodegenerati

166 Amyloid fibrils are self-assembled protein aggregates implicated in a number of human disea

167 gelatin was the continuous phase whilst whey protein aggregated in discontinuous inclusions within th

168 des that are derived from alpha-synuclein, a protein aggregated in Parkinson's disease, act as antige

169 In fact, intracellular toxic protein aggregates in Alzheimer's disease form within th

170 nhibition and PLEKHM1 regulates clearance of protein aggregates in an autophagy- and LIR-dependent ma

171 e for phagocytosis in transfer of pathogenic protein aggregates in an intact brain.

172 mice developed fewer beta-amyloid precursor protein aggregates in axons of the corpus callosum after

173 findings also support a role for prion-like protein aggregates in cellular defense and adaptation.

174 isaggregase that solubilizes and reactivates protein aggregates in cooperation with the DnaK/Hsp70 ch

175 in both the transmission and propagation of protein aggregates in disease.

176 n of 43 kDa (TDP-43) characterizes insoluble protein aggregates in distinct subtypes of frontotempora

177 Accumulation of mutated AAT protein aggregates in hepatocytes leads to endoplasmic r

178 ocalizes from a ribosome-associated state to protein aggregates in its role as a chaperone.

179 erative disease has been that the pathologic protein aggregates in live tissue are not amenable to st

180 model predicts a key role for extracellular protein aggregates in mediating progression of disease.

181 B(R120G), ubiquitin conjugates, and aberrant protein aggregates in mice with CryAB(R120G)-based desmi

182 f intracellular or extracellular deposits of protein aggregates in nervous tissues.

183 ology to track the formation of heat-induced protein aggregates in otherwise unperturbed dividing cel

184 highlighted the transcellular propagation of protein aggregates in several major neurodegenerative di

185 ement of Lsb proteins in the partitioning of protein aggregates in stressed cells.

186 molecular chaperone can be used to overcome protein aggregates in the absence of external energy inp

187 terized by the formation of pathological tau protein aggregates in the brain and progressive neurodeg

188 The deposition of tau protein aggregates in the brain is a pathological hallma

189 roteostasis and transcellular propagation of protein aggregates in the nervous system.

190 coherent networks with reduced size of whey protein aggregates in the presence of high levels of glu

191 is specifically mislocalized to pathological protein aggregates in these cases.

192 tif fused to NEFH caused prominent and toxic protein aggregates in transfected cells and disrupted mo

193 characterized by the appearance of nonnative protein aggregates in various tissues.

194 nherent in tracking the dynamics and fate of protein aggregates in vivo.

195 aracterized by the accumulation of insoluble protein aggregates, including neurofibrillary tangles co

196 ce exhibit many AATD symptoms, including AAT protein aggregates, increased hepatocyte death, and live

197 an cells effectively eliminate intracellular protein aggregates, indicating that efficient disaggrega

198 Our capacity for tracking how misfolded proteins aggregate inside a cell and how different aggre

199 Here we show that amorphous protein aggregates interact with tissue-type plasminogen

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

201 nd animal models and involves the release of protein aggregates into the extracellular space.

202 us medical conditions where normally soluble proteins aggregate into fibers [3, 4].

203 Discovering the mechanisms by which proteins aggregate into fibrils is an essential first st

204 sms by which disease-associated peptides and proteins aggregate into fibrils, and of structural prope

205 elevant for the intercellular trafficking of protein aggregates involved in prion, Alzheimer's, Hunti

206 The accumulation of protein aggregates is a common pathological hallmark of

207 Accumulation of fibrillar protein aggregates is a hallmark of many diseases.

208 Deposition of insoluble protein aggregates is a hallmark of neurodegenerative di

209 The aberrant accumulation of toxic protein aggregates is a key feature of many neurodegener

210 l capacity of daughter cells, the fate of ER protein aggregates is determined by whether or not they

211 of NAC from polysomes and re-localisation to protein aggregates is observed during ageing, in respons

212 c underpinnings of how the recovery of toxic protein aggregates is promoted and how this potent unfol

213 The formation and deposition of tau protein aggregates is proposed to contribute to cognitiv

214 An alternative system to disassemble large protein aggregates is provided by the 38-kDa subunit of

215 (AxD), which is characterized by cytoplasmic protein aggregates known as Rosenthal fibers along with

216 tment of neurodegenerative diseases with tau protein aggregates known as tauopathies.

217 P hydrolysis to unfold and solubilize stable protein aggregates, leading to their native refolding.

218 Formation of these protein aggregates leads to AD-like neurodegeneration.

219 uding gliosis, accumulation of ubiquitinated protein aggregates, lipofuscinosis, and endolysosomal ab

220 cumulation of oxidized proteins, deposits of protein aggregates, loss of podocytes, and glomeruloscle

221 t2, Ssa1/2, and Hsp82, suggesting that these protein aggregates may be addressed to aggresome-like st

222 or the recycling of nutrients and removal of protein aggregates, misfolded proteins, and pathogens, c

223 dence implicating soluble oligomers, smaller protein aggregates not detectable by conventional micros

224 Ubiquitinated protein aggregates, of which TDP-43 is a major component

225 nical blockade of the trabecular meshwork by protein aggregates or contaminant particles associated w

226 en proposed to assemble by forming solid RNA/protein aggregates or through phase separation into a li

227 Transcellular propagation of protein aggregates, or proteopathic seeds, may drive the

228 er of a wide variety of substrates including proteins, aggregates, organelles, and pathogens via a gr

229 , Parkinson's, and diabetes by forming toxic protein aggregates, our findings show that cells can uti

230 thways that target misfolded plasma membrane proteins, aggregated polypeptides and cytosolic heat-ind

231 that enable histochemical differentiation of protein aggregates post-mortem would be advantageous for

232 Yeast self-perpetuating protein aggregates (prions) provide a convenient model f

233 Our work shows that fusion of protein aggregates promotes the formation of damage-free

234 nderstanding the structure and energetics of protein aggregates provides insights into the mechanism

235 Misfolded prion protein aggregates (PrP(Sc)) show remarkable structural

236 These effects strongly enhance protein aggregate reactivation by the DnaK-ClpB network,

237 These protein aggregates reduce visual acuity by scattering or

238 by which phagocytic glia contribute to both protein aggregate-related neuroprotection and pathogenes

239 tween cells via two nonexclusive mechanisms: protein aggregates released from dying cells and taken u

240 Misfolded protein aggregates represent a continuum with overlappin

241 Processing (P)-bodies are cytoplasmic RNA protein aggregates responsible for the storage, degradat

242 in loaded nanodiscs from empty nanodiscs and protein aggregates results in monodisperse nanodisc prep

243 ur data show a weak repulsive barrier before proteins aggregate reversibly, unless a favorable contac

244 nsitive to heat-stress and do not accumulate protein aggregates showing that ClpXP is dispensable for

245 smic reticulum (ER), although the fate of ER protein aggregates, specifically during cell division, i

246 rds Abeta aggregates compared to other toxic protein aggregates such as tau, alpha-synuclein (alpha-S

247 We further observed that clozapine clears protein aggregates, such as alpha-synuclein, PolyQ prote

248 struggle to yield reliable results for large protein aggregates, such as amyloid oligomers.

249 f proteins, and proteases that degrade toxic protein aggregates, suggest that Brucella protects itsel

250 es of J-proteins, which expands the range of protein aggregates targeted by metazoan Hsp70 for disagg

251 Highly ordered protein aggregates, termed amyloid fibrils, are associat

252 Prions are self-propagating protein aggregates that act as protein-based elements of

253 rmation of potentially insoluble and harmful protein aggregates that also may serve as storage compar

254 Amyloid fibrils are ordered, insoluble protein aggregates that are associated with neurodegener

255 Prions are self-propagating protein aggregates that are characteristically transmiss

256 alysis, Psd1(ts) beta subunits accumulate in protein aggregates that are resolved by Yme1p acting alo

257 Amyloid fibrils are beta-sheet-rich protein aggregates that are strongly associated with a v

258 or environmental changes, which may lead to protein aggregates that are toxic for the cell.

259 Amyloids are ordered protein aggregates that are typically associated with ne

260 Amyloids are highly organized protein aggregates that arise from inappropriately folde

261 ed properties, in contrast to many amorphous protein aggregates that arise when proteins misfold.

262 which results in the formation of non-native protein aggregates that challenge the capacity of the pr

263 contrast, the refringent particles represent protein aggregates that contain several blood proteins.

264 Protein aggregates that form under heat shock contain bo

265 In dividing yeast cells, protein aggregates that form under stress or during agei

266 mproves autophagy-mediated disposal of toxic protein aggregates that form within the secretory pathwa

267 and ER protein aggregates, we found that ER protein aggregates that induce ER stress are retained in

268 Prions are self-templating protein aggregates that stably perpetuate distinct biolo

269 ems for sensitive and selective detection of protein aggregates, the pathological hallmarks of severa

270 build-up of potentially toxic intracellular protein aggregates, the timing and location of the inter

271 multisubunit complex comprising constitutive protein aggregates, their autophagy receptor, and a scaf

272 re ATP-powered chaperones that restore toxic protein aggregates to a native folded state.

273 ngs show that cells can utilize amyloid-like protein aggregates to function as central regulators of

274 by alpha2-antiplasmin and degrades amorphous protein aggregates to release smaller, soluble but relat

275 yeast cells confine aging factors, including protein aggregates, to the aging mother cell.

276 net gels, but not acid gels, to form compact protein aggregates under acidic conditions of the stomac

277 amic characteristics of transiently evolving protein aggregates under ambient conditions by directly

278 We further show that formation of other protein aggregates upon carbon depletion also is trigger

279 stablishment of asymmetrical partitioning of protein aggregates upon division is driven by the large

280 Ubiquitinated proteins aggregate upon proteasome failure, and the aggr

281 HSP70-HSP110 disaggregase machinery to clear protein aggregates via the 26S proteasome.

282 ellular accumulation of extended beta-folded protein aggregates was detected after 40 min up to 2 h.

283 The accumulation of GABARAP-containing protein aggregates was observed in the vicinity of sperm

284 A progression in the mechanical strength of protein aggregates was observed resulting from enhanced

285 Finally, disassembly of protein aggregates was promoted by RuvbL.

286 s visualization of both the ER itself and ER protein aggregates, we found that ER protein aggregates

287 Prions are self-perpetuating amyloid protein aggregates which underlie various neurodegenerat

288 proteostasis can lead to the accumulation of protein aggregates, which are associated with aging and

289 vels predisposes neurons to develop abnormal protein aggregates, which are hallmarks of AD and its as

290 a PET radiotracer developed for imaging tau protein aggregates, which are implicated in neurologic d

291 activity and the formation of metastable DNA-protein aggregates, which were easily detected in our sm

292 eins, which target the AAA+ disaggregases to protein aggregates while concurrently stimulating their

293 e clearance, 20S proteasomes dissociate from protein aggregates, while Poh1 and selective subunits of

294 Amyloids, protein aggregates with a cross beta-sheet structure, co

295 conventional techniques for the analysis of protein aggregates with a novel approach that employs th

296 lso defective in the ability to disaggregate protein aggregates with ClpB, DnaJ and GrpE, although th

297 ral properties that differ when they bind to protein aggregates with different morphologies and can t

298 concentrations allowing to form networks of protein aggregates with different structures.

299 n budding yeast, identifying >170 endogenous proteins aggregating within minutes of heat shock in mul

300 rotein is structurally perturbed and the apo-protein aggregates without reattainment of the monomer-d