ライフサイエンスコーパス: protein aggregate

1 ctional (e.g., as precursors to pathological protein aggregates).

2 normal formation and compartmentalization of protein aggregates.

3 earance of Huntington's disease-linked polyQ protein aggregates.

4 rge number of proteins, and the formation of protein aggregates.

5 well as highly oligomerized cargo that mimic protein aggregates.

6 e size, hydrophobicity, and heterogeneity of protein aggregates.

7 e endoplasmic reticulum and the clearance of protein aggregates.

8 nitiated by the internalization of exogenous protein aggregates.

9 stasis, resulting in such a critical mass of protein aggregates.

10 formation of and dissolve previously formed protein aggregates.

11 ons with a subset of morphologically defined protein aggregates.

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

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

14 l protein LC3 and clearance of ubiquitinated protein aggregates.

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

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

17 cargos, such as dysfunctional organelles and protein aggregates.

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

19 and retention of damaged material, including protein aggregates.

20 highly challenging samples as supramolecular protein aggregates.

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

22 of selective autophagy, which relocalize to protein aggregates.

23 unction of proteins like HSP70 in combatting protein aggregates.

24 -dependent autophagy allows the clearance of protein aggregates.

25 efficiency and the thermostability of prion protein aggregates.

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

27 lular responses and diseases associated with protein aggregates.

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

29 d separation and characterization of complex protein aggregates.

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

31 removal of excessive or damaged proteins and protein aggregates.

32 ing illnesses through the formation of toxic protein aggregates.

33 iding the formation of potentially cytotoxic protein aggregates.

34 r multimodal detection of disease-associated protein aggregates.

35 mediate filament system and segregation into protein aggregates.

36 mors, resulting in an abundance of misfolded protein aggregates.

37 ability of dendritic cells to process stable protein aggregates.

38 damaged organelles, pathogens, and unwanted protein aggregates.

39 ultiple myeloma cells to the accumulation of protein aggregates.

40 lecular chaperones involved in disassembling protein aggregates.

41 eraged to bolster the clearance of cytotoxic protein aggregates.

42 al functions in proteostasis by solubilizing protein aggregates.

43 oidosis and affect the cytotoxicity of these protein aggregates.

44 ively around the cytosolic cargo, that is, a protein aggregate, a mitochondrion, or a cytosolic bacte

45 tions in HD mouse striatum reduce mutant HTT protein aggregates, a biomarker of HD pathogenesis and s

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

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

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

49 In agreement with these data, protein aggregate accumulation and microglia activation

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

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

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

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

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

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

56 rvous system through phagocytic clearance of protein aggregates and cellular debris.

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

58 Protein aggregates and damaged organelles are tagged wit

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

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

61 agy, leading to the accumulation of unfolded protein aggregates and dysfunctional mitochondria, the c

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

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

64 s essential for degradation of ubiquitinated protein aggregates and homeostasis in skeletal muscle.

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

66 phagosome formation and selective removal of protein aggregates and organelles by recruiting autophag

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

68 IRE1 promotes LE-mediated microautophagy of protein aggregates and protects cells from their cytotox

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

72 re defined at post mortem by the presence of protein aggregates and the loss of specific subsets of n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 In many bacteria, including mycobacteria, protein aggregates are located at the cellular pole.

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

89 Lipid and protein aggregates are one of the fundamental materials

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

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

92 Large cytosolic protein aggregates are removed by two main cellular proc

93 Protein aggregates are situated at the boundary between

94 Protein aggregates are the hallmark of stressed and agei

95 Such protein aggregates are the root cause of numerous diseas

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

97 ransitions and the formation of amyloid-like protein aggregates as observed in neurodegenerative dise

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

99 retromer leads to increased accumulation of protein aggregates, as well as enhanced cellular neuroto

100 cificity against a wide range of peptide and protein aggregates associated with neurodegenerative dis

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

102 ence supports the hypothesis that pathogenic protein aggregates associated with neurodegenerative dis

103 tic sequestration of insoluble ubiquitinated protein aggregates associated with p62 and NBR1.

104 led accumulations of insoluble ubiquitinated protein aggregates associated with the adaptors sequesto

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

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

107 in neurodegeneration-by clearing neurotoxic protein aggregates, but also providing an opportunity fo

108 criptional remodeling with the appearance of protein aggregates, but whether these responses are indu

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

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

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

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

113 biosynthesis can result in the formation of protein aggregates capable of disrupting essential cellu

114 lyglutamine (polyQ) tract misfolds and forms protein aggregates characteristic of Huntington's diseas

115 asis, ISCs coordinate cell cycle arrest with protein aggregate clearance by Atg8-mediated activation

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

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

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

119 The protein aggregates composition was investigated by HPLC-

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

121 myloid fibrils are highly ordered nanoscopic protein aggregates comprising a cross-beta amyloid core

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

123 These protein aggregates contain Ltn1-dependent polyubiquitin

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

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

126 Protein aggregates containing ubiquitin (Ub) are commonl

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

128 bring new insight, to our knowledge, on how protein aggregates could induce DC and T cell activation

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

130 The failure to remove protein aggregates, damaged organelles, or intracellular

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

132 denaturation perturb the structure of prion protein aggregates differently.

133 similarities to neurodegeneration-associated protein aggregate diseases.

134 Protein aggregates disrupt cellular homeostasis, causing

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

136 The spread of protein aggregates during disease progression is a commo

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

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

139 ther than merely reflecting association with protein aggregate end-points.

140 that nuclear senescence factors - including protein aggregates, extrachromosomal ribosomal DNA circl

141 The precise mechanisms by which protein aggregates first arise in the majority of sporad

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

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

144 ells was found associated with robust global protein aggregate formation and captured stable proteins

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

146 Ube2v1 plays an important role in protein aggregate formation, partially by enhancing K63

147 ntributed to Ube2v1's function in regulating protein aggregate formation.

148 Protein aggregates formed at 75 degrees C were much more

149 Stress granules (SGs) are cytoplasmic RNA-protein aggregates formed in response to inhibition of t

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

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

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

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

154 se, is the sequential transfer of pathogenic protein aggregates from cell-to-cell within affected tis

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

156 The molecular weight distribution of protein aggregates from raw meat and cooked pork product

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

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

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

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

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

162 ntracellular stability and proteotoxicity of protein aggregates implicated in neurodegenerative disea

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

164 d by the sequential spread and deposition of protein aggregates in a predictable pattern that correla

165 ak (peak 1) of the cooked products contained protein aggregates in addition to high molecular weight

166 es both the size and number of ubiquitinated protein aggregates in aged flies, and increases longevit

167 The tau protein aggregates in aging and Alzheimer disease and ma

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

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

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

171 ninvasive analytical tool for characterizing protein aggregates in biopharmaceutical formulations.

172 ators can drive formation and disassembly of protein aggregates in both conformational states.

173 A commonly used approach for studying protein aggregates in cells is number and brightness (N&

174 ro called AggreCount to identify and measure protein aggregates in cells.

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

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

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

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

179 arkinson's disease (PD), and alpha-synuclein protein aggregates in Lewy bodies and Lewy neurites in s

180 ep deprivation accelerates the spread of tau protein aggregates in neural networks.

181 d be used to enhance autophagic clearance of protein aggregates in neurodegenerative disorders.

182 ed levels of certain metal ions are found in protein aggregates in neurons of people suffering from P

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

184 ah1-Pih1 (R2TP) complex and the formation of protein aggregates in response to thermal stress.

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

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

187 logy, regional deposition of misfolded prion protein aggregates in the brain, and size of their prote

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

189 etion of LTN1 results in the accumulation of protein aggregates in the presence of oxidizing and alky

190 wNMR was sensitive to an increase in soluble protein aggregates in the range of <1.0%.

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 ntitative mass-spectrometry of mycobacterial protein aggregates in wild-type, hspX-deleted and hspX-o

196 Moreover, the three main proteins aggregating in ALS/FTD, including in sporadic c

197 out as a powerful noninvasive tool to detect protein aggregates, including subvisible particles in bi

198 sed to m-Tyr contained large, electron-dense protein aggregates, indicating that m-Tyr destabilized a

199 titioning could be used to confine cytotoxic protein aggregates inside droplet-like compartments but

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

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

202 about the assembly pathways by which soluble proteins aggregate into dense microdroplets.

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

204 Amyloidogenic peptides and proteins aggregate into fibrillary structures that are u

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

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

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

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

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

210 The formation of misfolded protein aggregates is a hallmark of neurodegenerative di

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

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 protein aggresome-a collection of endogenous protein aggregates-is an important indicator of bacteria

215 hallmark, the accumulation of characteristic protein aggregates, known as Lewy bodies (LB) in PD, and

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

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

218 in brain mass reduction or mutant huntingtin protein aggregate levels.

219 multiple cytoplasmic cargo (e.g., proteins, protein aggregates, lipid droplets or organelles) to the

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

221 vast array of cellular substrates, including protein aggregates, macromolecular complexes and polymer

222 work reveals that wtf parasites can exploit protein aggregate management pathways to selectively des

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

224 amyotrophic lateral sclerosis-characteristic protein aggregates observed in autophagy-deficient neuro

225 an amyloid-like structure resembling that of protein aggregates observed in disease.

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

227 mine the relative impact of lipoproteins and protein aggregates on the isolated EV population.

228 the presence of high-molecular-weight (HMW) protein aggregates or disruption of the lens microarchit

229 ad of conformationally distinct pathological protein aggregates, or strains.

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

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

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

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

234 duction of metal-induced and prion-dependent protein aggregate production.

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

236 These protein aggregates reduce visual acuity by scattering or

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

238 rgeting to aggresomes, and the processing of protein aggregates, respectively.

239 ome system, and defective clearance of these protein aggregates results in proteotoxicity and cell de

240 he mechanisms by which these locally ordered protein aggregates self-assemble in solution.

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

242 Protein aggregates significantly contribute to the devel

243 re, we demonstrate that for validated native protein aggregates, sorting to the cellular pole followi

244 mulating fragments is delayed within natural protein aggregates such as postsynaptic densities (PSDs)

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

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

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

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

249 disease (AD), including the accumulation of protein aggregates, tau pathology, and neuronal cell dea

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

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

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

253 Prions are infectious, self-propagating protein aggregates that are notorious for causing devast

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

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

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

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

258 Prions are infectious protein aggregates that cause several fatal neurodegener

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

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

261 e autophagy results in accumulation of toxic protein aggregates that detrimentally affect cellular fu

262 Protein aggregates that form under heat shock contain bo

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

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

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

266 , are essential in the reactivation of toxic protein aggregates that occur during translation or peri

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

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

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

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

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

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

273 ith MLN4924 causes accumulation of misfolded protein aggregates, ultimately inducing immunogenic cell

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

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

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

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

278 ed before any significant increase in global protein aggregate was detectable.

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

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

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

282 isulfide and non-disulfide bond formation in protein aggregates, was markedly enhanced by 60 umol GA

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

284 f protein glycation and reduced formation of protein aggregates were also observed with millet phenol

285 triatal delivery, pathological mHTT-positive protein aggregates were distributed widely among cogniti

286 However, neither cell death nor protein aggregates were observed in 2D iPSC-derived cort

287 at HRI controls autophagy to clear cytosolic protein aggregates when the ubiquitin-proteasome system

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

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

290 e filled with dysfunctional mitochondria and protein aggregates, which are autophagy targets, this au

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

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

293 or decades on several biomarkers of myofibre protein aggregates, which are present in <1% of myofibre

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

295 tivity and the accumulation of ubiquitinated protein aggregates, whose efficient degradation required

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

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

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

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

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