ライフサイエンスコーパス: aggresome

1 nate NO production via formation of the iNOS aggresome.

2 oteasome as well as its sequestration to the aggresome.

3 a centrosome-associated structure, called an aggresome.

4 edes CHIP-mediated iNOS sequestration to the aggresome.

5 l inclusions instead of a single perinuclear aggresome.

6 conductance regulator (CFTRDeltaF508) to the aggresome.

7 NOS preaggresome structures to form a mature aggresome.

8 ions and may not allow them to traffic to an aggresome.

9 ated nonspecifically into a vimentin-encaged aggresome.

10 ssociated deacetylase, is a component of the aggresome.

11 interact with HDCAC6 and are degraded in the aggresome.

12 e, and the aggregates are transported to the aggresome.

13 ables HDAC6 recognition and transport to the aggresome.

14 evealed alpha-B crystallin in subsarcolemmal aggresomes.

15 ess NO as compared with cells not expressing aggresomes.

16 e-targeting signal promoted its transport to aggresomes.

17 ink between RB function and the formation of aggresomes.

18 hat target aggregation-prone polypeptides to aggresomes.

19 or misfolded intracellular proteins known as aggresomes.

20 bodies suggests them to be E1B55K containing aggresomes.

21 inked to the dynein motor and transported to aggresomes.

22 play deficits in targeting misfolded DJ-1 to aggresomes.

23 devoid of Lewy bodies, which are similar to aggresomes.

24 the multiprotein aggregates have features of aggresomes.

25 ttle information on the long term effects of aggresomes.

26 oligomer without a significant reduction in aggresomes.

27 on of large aggregates, resembling mammalian aggresomes.

28 er ways do not fully meet the description of aggresomes.

29 s into specialized "holding stations" called aggresomes.

30 ctories are generally distinct from cellular aggresomes.

31 bodies and suggest that they are related to aggresomes.

32 tein cargo to dynein motors for transport to aggresomes.

33 appear to be ubiquitinated and localized to aggresomes.

34 al morphologic and molecular similarities to aggresomes.

35 via histone deacetylase 6 (HDAC6) toward the aggresomes.

36 t present as perinuclear aggregates known as aggresomes.

37 aracterized by the constitutive formation of aggresomes.

38 R and causes internalized CFTR to reroute to aggresomes.

39 llular GFP-Tau aggregates with attributes of aggresomes.

40 f aggregates of misfolded proteins, known as aggresomes.

41 eins in the form of preamyloid oligomers and aggresomes.

42 efficiently induced the formation of nuclear aggresomes.

43 or viral proteins were recruited to nuclear aggresomes.

44 oteins that may lead to formation of nuclear aggresomes.

45 ead, they are frequently concentrated to the aggresome, a perinuclear inclusion body, and subsequentl

46 iant was fully processed but retained in the aggresome, a perinuclear structure, where misfolded prot

47 iNOS, progressively sequestered iNOS to the aggresome, a process that correlated with marked reducti

48 ol can be transported via microtubules to an aggresome, a recently discovered organelle where aggrega

49 tein vimentin, that the inclusion bodies are aggresomes, a cellular response to misfolded protein.

50 We present evidence that, as perinuclear aggresomes accumulate, they are associated with abnormal

51 One type of aggregate, the aggresome, accumulates misfolded proteins destined for d

52 nhibitor of histone deacetylase 6 and blocks aggresome activity.

53 The p62 depletion impaired aggresome and autophagosome formation, exacerbated cell

54 ulation as a result of the uncoupling of the aggresome and autophagy pathways.

55 ISC1 protein aggregates are recruited to the aggresome and degraded there by the autophagic pathway.

56 at E4orf3 can target the Mre11 complex to an aggresome and may explain how the cellular repair comple

57 nergizes with bortezomib to inhibit both the aggresome and proteasome pathways in preclinical studies

58 perinuclear cytoplasmic body resembling the aggresome and was excluded from the nucleus of the infec

59 e formation and targeting, we purified 103QP aggresomes and 103Q aggregates and identified the associ

60 ls in response to protein aggregation, where aggresomes and autophagosomes are produced to facilitate

61 review the evidence that some viruses induce aggresomes and autophagosomes to generate sites of repli

62 The mice developed aggresomes and contained high concentrations of amyloid

63 lation of MAP1S enhanced autophagy to remove aggresomes and dysfunctional organelles that trigger DNA

64 ically, proteasomes are also concentrated at aggresomes and other related inclusion bodies prevalent

65 es show that endogenous AT3 colocalizes with aggresomes and preaggresome particles of the misfolded c

66 PC2 that is not bound to PC1 is directed to aggresomes and subsequently degraded via autophagy, a co

67 e is a compromised exchange between DISC1 in aggresomes and the cytosolic DISC1 pool, and that the la

68 The similarity between aggresomes and virus inclusions raises the possibility t

69 The iNOS aggresome represents a "physiologic aggresome" and thus defines a new paradigm for cellular

70 pidly triggered their translocation into the aggresome, and surprisingly, this response was independe

71 ed into a perinuclear aggregate, known as an aggresome, and that ubiquitin was also associated with t

72 Mammalian RuvbL associated with the aggresome, and the aggresome substrate synphilin-1 inter

73 have been linked to the formation of nuclear aggresomes, and colocalization studies suggested that vi

74 ator in the recruitment of misfolded DJ-1 to aggresomes, and have important implications regarding th

75 quitinylation and accumulation in the ER and aggresomes, and that abnormal intracellular processing o

76 ion of the degradation of bortezomib-induced aggresomes; and consistent with this possibility, we als

77 gates resembling a protein aggregate-induced aggresome are formed.

78 Aggresomes are cytoplasmic inclusion bodies, observed in

79 Aggresomes are cytoprotective proteinaceous inclusions f

80 indings demonstrate that, in dividing cells, aggresomes are detrimental over the long term, rather th

81 Aggresomes are engulfed by autophagosomes, which then fu

82 gradative capacity is exceeded, juxtanuclear aggresomes are formed to sequester misfolded proteins.

83 the first reported instance in which nuclear aggresomes are induced by single missense mutations in a

84 Aggresomes are transient microtubule-dependent inclusion

85 characteristics, we hypothesized that PMP22 aggresomes are transitory, linking the proteasomal and l

86 This cytoplasmic body is distinct from aggresome associated with overexpression of some protein

87 Among the aggresome-associated proteins we identified, Cdc48 (VCP/

88 was not coupled with increased prevalence of aggresome-bearing cells.

89 vimentin is invariably collapsed around the aggresome but that the detection of ubiquitin is variabl

90 in targeting preaggresomal structures to the aggresome by promoting an iNOS interaction with histone

91 Schwann cells have the ability to eliminate aggresomes by a mechanism that is enhanced when autophag

92 genetic evidence for the protective role of aggresomes by demonstrating genetically that aggresome t

93 Further analysis reveals that aggresomes can have a detrimental effect on mitosis by s

94 In Poh1-deficient cells, aggresome clearance is blocked.

95 Here we present evidence that during aggresome clearance, 20S proteasomes dissociate from pro

96 , unanchored ubiquitin chain production, and aggresome clearance.

97 w that proteasomes are crucial components in aggresome clearance.

98 the autophagy pathway as the main route for aggresomes clearance, CCHE-45 cells displayed increased

99 These structures are similar in nature to aggresomes, colocalize with the aggresome marker GFP-250

100 Aggresomes containing Cav1-GFP are encased within viment

101 n (CryAB) causes DRM and is characterized by aggresomes containing CryAB(R120G) and amyloid oligomer.

102 oduction colocalized with cytosolic iNOS but aggresomes containing iNOS were distinctly devoid of NO

103 The incidence of apoptosis also increased in aggresome-containing cells.

104 sine (K) 63-linked ubiquitin chains restores aggresome degradation.

105 egraded not only by proteasomes, but also by aggresomes, dependent on histone deacetylase 6 (HDAC6) a

106 Insights into the possible roles played by aggresomes during virus assembly are emerging from an un

107 ls and are transported along microtubules to aggresomes for immobilization and subsequent degradation

108 Juxtanuclear aggresomes form in cells when levels of aggregation-pron

109 Similar inclusions called aggresomes form in response to protein aggregation.

110 This accelerated aggresome formation also relies on the stress-induced co

111 re, the treatment of cells with PIs leads to aggresome formation and accumulation of polyubiquitinate

112 ggest a connection between HDAC activity and aggresome formation and also lay the groundwork for a di

113 The p62 promotes aggresome formation and autophagy activation and protect

114 Depletion of RuvbL1 or RuvbL2 suppressed aggresome formation and caused buildup of multiple cytop

115 d mechanistic bases for the role of HDAC6 in aggresome formation and further suggest a novel ubiquiti

116 med an siRNA screen for proteins involved in aggresome formation and identified novel mammalian AAA+

117 required in addition to E1B-55K for E1B-55K aggresome formation and MRE11 export to aggresomes in ad

118 sequence to human Hook proteins, involved in aggresome formation and other transport activities.

119 Expression of HDAC6 improves aggresome formation and protects IBMPFD mutant cells fro

120 h Rheb activity in TSC mutant cells inhibits aggresome formation and sensitizes cell death in respons

121 To identify additional factors involved in aggresome formation and targeting, we purified 103QP agg

122 activation of Myc was sufficient to provoke aggresome formation and thus sensitivity to BZ + SAHA, a

123 cetylase 6 and dynein, proteins required for aggresome formation and transport of misfolded protein.

124 cells, the TSC mutant cells are defective in aggresome formation and undergo apoptosis upon misfolded

125 fects developed gradually after juxtanuclear aggresome formation and were not associated with small c

126 sfolded protein cargos, and therefore blocks aggresome formation by inhibiting dynein-dependent trans

127 Finally, we show that the prevention of aggresome formation by over-expression of wild-type park

128 together, our study shows that inhibition of aggresome formation can strongly potentiate the efficacy

129 Aggresome formation contributes to the protection of vir

130 iNOS aggresome formation depends on a functional dynein motor

131 synphilin 1, indicating that aggregation and aggresome formation determinants can be separated geneti

132 groundwork for a direct test of the role of aggresome formation in ALS etiology.

133 ubiquitin interacting motifs cannot restore aggresome formation in AT3 knockdown cells.

134 acilitates the ability of ataxin-3 to induce aggresome formation in cells.

135 f-life values in rabbit reticulocyte lysate, aggresome formation in COS-1 cells, and protein aggregat

136 ed a screen for small molecules that disrupt aggresome formation in cultured cells.

137 ic activity functions to attenuate aggregate/aggresome formation in heart.

138 indings suggest that parkin is important for aggresome formation in human neuronal cells and may lead

139 Interestingly, bortezomib did not induce aggresome formation in immortalized normal human pancrea

140 estigate the molecular mechanisms underlying aggresome formation in mammalian cells.

141 This study indicates that aggresome formation in response to misfolded proteins ma

142 Perinuclear aggresome formation is a key mechanism to dispose of mis

143 Recent evidence suggests that aggresome formation is a physiologic stress response not

144 Recent evidence suggests that aggresome formation is a physiologic stress response not

145 Aggresome formation is an active cellular response that

146 ss for specific proteins whose regulation by aggresome formation is deemed necessary by the cell.

147 They also raise the possibility that aggresome formation may contribute to some of reported p

148 d "physiologic aggresome," is exemplified by aggresome formation of inducible nitric oxide synthase (

149 d "physiologic aggresome," is exemplified by aggresome formation of iNOS, an important host defense p

150 with the huntingtin fragment and its role in aggresome formation required the huntingtin N-terminal N

151 Blocking aggresome formation results in increased levels of toxic

152 ng signal from huntingtin was sufficient for aggresome formation upon inhibition of the proteasome.

153 Bortezomib-induced aggresome formation was determined to be cytoprotective

154 Aggresome formation was observed in the presence of bort

155 diomyocytes promoted accumulation of p62 and aggresome formation, accompanied by the disappearance of

156 Therefore, aggresome formation, but not aggregation of synphilin 1,

157 synthesis, increases in HDAC6 expression and aggresome formation, induction of Noxa, and sensitivity

158 argo, and the cellular factors that regulate aggresome formation, remain unknown.

159 cological interventions were used to disrupt aggresome formation, revealing their cytoprotective func

160 RNA (siRNA) screen for proteins involved in aggresome formation, we defined the pathway that regulat

161 srupting Hsp70-CHIP interaction prevents the aggresome formation, whereas a dominant-negative CHIP mu

162 ther degradative system leads to an enhanced aggresome formation.

163 g misfolded protein metabolism by modulating aggresome formation.

164 rylation of RB and the inhibition of nuclear aggresome formation.

165 n disease, as a model to study mechanisms of aggresome formation.

166 tor bortezomib (BZ) by disrupting BZ-induced aggresome formation.

167 , were shown genetically to be essential for aggresome formation.

168 eased cytoplasmic localization, coupled with aggresome formation.

169 , an important host defense protein, through aggresome formation.

170 of proteasome inhibitor strikingly increased aggresome formation.

171 s well play essential roles in CFTRDeltaF508 aggresome formation.

172 nd the influence of proteasome inhibition on aggresome formation.

173 ups of compounds that specifically prevented aggresome formation.

174 d sufficiency of CryAB(R120G) expression for aggresome formation.

175 nd this turnover was slowed by inhibition of aggresome formation.

176 f heat shock protein 70 (Hsp70) in promoting aggresome formation.

177 Wild-type AT3 restores aggresome formation; however, AT3 with mutations in the

178 rfering RNA knockdown of AT3 greatly reduces aggresomes formed by CFTRDeltaF508, demonstrating a crit

179 Furthermore, endogenous Cav1 accumulated in aggresomes formed in response to proteosomal inhibition.

180 Aggresome-forming proteins were found to have an acceler

181 It is widely believed that aggresomes have a protective function, sequestering pote

182 -55K aggresome formation and MRE11 export to aggresomes in adenovirus-infected cells.

183 We discuss the role of aggresomes in cancer and the potential to target this pa

184 In this report, the role of aggresomes in cell viability was addressed in the contex

185 We observed that TPMT*3A forms aggresomes in cultured cells and that it aggregates in v

186 acking a polyQ tract may also induce nuclear aggresomes in cultured cells.

187 0 promoted localization of RIP1 to insoluble aggresomes in murine vascular allografts and in human ce

188 ggregates of ubiquitin-conjugated proteins ("aggresomes") in vitro and in vivo.

189 tanuclear aggregates with characteristics of aggresomes including immunoreactivity for vimentin, gamm

190 accumulations meet the criteria defined for aggresomes, including gamma-tubulin colocalization and f

191 in deacetylase that is also known to promote aggresome inclusion of the misfolded polyubiquitylated p

192 observe that endogenous parkin is present in aggresomes induced by a variety of stresses including do

193 Nuclear aggresomes induced by proteins containing an expanded po

194 lt in imbalanced protein homeostasis through aggresome-induced autophagy.

195 Our finding that Cav1 is both an aggresome-inducing and aggresome-localized protein provi

196 Co-transfection of WT ZEBRA with aggresome-inducing mutants Z(R183E) and Z(R179E) inhibit

197 nto an aggresome through association with an aggresome-inducing protein has implications for the pote

198 Interestingly, aggresome induction was cell-type dependent and was obse

199 The aggresome is an organelle that recruits aggregated prote

200 ure, targeting of aggregated proteins of the aggresome is coordinated with lysosome positioning aroun

201 The distribution of AGS3 to the aggresome is dependent upon the TPR domain, and it is ac

202 gnificance of cellular formation of the iNOS aggresome is hitherto unknown.

203 oteins into pericentriolar inclusions called aggresomes is a means that cells use to minimize misfold

204 That stress response, termed "physiologic aggresome," is exemplified by aggresome formation of ind

205 That stress response, termed "physiologic aggresome," is exemplified by aggresome formation of iNO

206 In this study, we show that aggresome levels do not correlate with disease.

207 nse, resulting in accumulation of the large "aggresome"-like aggregates that promote de novo prion ge

208 an internalize PHFs, leading to formation of aggresome-like bodies, opens new therapeutic avenues to

209 logs in yeast suppressed the formation of an aggresome-like body and enhanced the aggregate toxicity.

210 membrane and causes it to be deposited into aggresome-like compartments.

211 om the aggresome, whereas mInsc augments the aggresome-like distribution of AGS3.

212 plications for the potential cytotoxicity of aggresome-like inclusion bodies in degenerative diseases

213 ogressive muscular weakness characterized by aggresome-like inclusions in the myofibrils.

214 ls with mutant FHL1 induced the formation of aggresome-like inclusions that incorporated both mutant

215 h prosaposin localized to large juxtanuclear aggresome-like inclusions, which is indicative of its mi

216 Aggresome-like induced structures (ALIS) have been descr

217 biquitinated proteins in structures known as aggresome-like induced structures (ALIS).

218 agy, which we show as selective autophagy of aggresome-like induced structures (ALIS).

219 in contributes to the formation of dendritic aggresome-like induced structures (DALIS) through a uniq

220 oplasm and showed a filamentous and punctate aggresome-like pattern compared with diffuse cytoplasmic

221 In ALS animal models, mutant SOD1 forms aggresome-like structures in motor neurons and astrocyte

222 s, PMP22 has an extended half-life and forms aggresome-like structures that are surrounded by molecul

223 these protein aggregates may be addressed to aggresome-like structures when the RQC complex fails to

224 umulates in the endoplasmic reticulum and in aggresome-like structures where it is ubiquitinylated.

225 egates in the left ventricle, development of aggresome-like structures, and a corresponding induction

226 LC3 II expression and promoted formation of aggresome-like structures, suggesting that synphilin-1 a

227 le and ubiquitinated, and are accumulated in aggresome-like structures.

228 US complexes that become precursors of large aggresome-like structures.

229 e related to the localization of pM140 to an aggresome-like, microtubule organizing center-associated

230 esting that CS induced CFTR movement into an aggresome-like, perinuclear compartment.

231 that Cav1 is both an aggresome-inducing and aggresome-localized protein provides new insights into h

232 in nature to aggresomes, colocalize with the aggresome marker GFP-250, and are highly enriched in ubi

233 Alternatively, aggresomes may be part of an innate cellular response th

234 nchial epithelial cells used the physiologic aggresome mechanism for iNOS inactivation.

235 es and the p53 nuclear export to cytoplasmic aggresomes observed in E1A-E1B-transformed cells.

236 We report that AGS3 enters into the aggresome pathway and that distribution of the protein i

237 ZEBRA mutants directly induced the nuclear aggresome pathway in cells with and without EBV.

238 The aggresome pathway is activated when proteasomal clearanc

239 ere is emerging evidence that inhibiting the aggresome pathway leads to accumulation of misfolded pro

240 tudy reveals a critical role for CHIP in the aggresome pathway.

241 a previously unexpected critical role in the aggresome pathway.

242 ions raises the possibility that viruses use aggresome pathways to concentrate cellular and viral pro

243 , protein synthesis rates, the percentage of aggresome-positive cells, and the sensitivity to BZ + SA

244 cells, it had no impact on the percentage of aggresome-positive cells.

245 ulates actinomyosin- and autophagy-dependent aggresome processing.

246 Further, cells expressing iNOS aggresomes produced significantly less NO as compared wi

247 hagy-lysosome pathway, but why targeting the aggresome promotes degradation of aggregated species is

248 n aggregates from the cytoplasm, cannot form aggresomes properly, and are hypersensitive to the accum

249 In aggresomes, protein aggregates are actively degraded by

250 Aggresomes recruit motor proteins that transport misfold

251 The concept of Lewy bodies as aggresome-related inclusions fits well with ongoing disc

252 by which misfolded proteins are recruited to aggresomes remains unclear.

253 The iNOS aggresome represents a "physiologic aggresome" and thus

254 Importantly, translocation to aggresomes required a special aggresome-targeting signal

255 The disassembly and disposal of aggresomes requires Poh1, a proteasomal deubiquitinating

256 cate that adenovirus 5 exploits the cellular aggresome response to accelerate inactivation of MRE11-R

257 Here we present evidence that aggresomes serve a cytoprotective function and are assoc

258 Our results show that aggresomes significantly accelerate protein degradation

259 istribution of the receptors to juxtanuclear aggresomes, significantly more so for TPbeta than beta2A

260 tophagic activity dramatically enhanced both aggresome size and abundance, consistent with a role for

261 acetylated alpha-tubulin but with diminished aggresome size and apoptotic nuclei.

262 Notably, HDIs did not modify aggresome structures but instead rescued newly synthesiz

263 to localize to the Mre11 complex and p53 to aggresome structures; together with the viral E4orf6 pro

264 The formation of these "mito-aggresome" structures requires microtubule motor-depende

265 RuvbL associated with the aggresome, and the aggresome substrate synphilin-1 interacted directly with

266 ormation of hetero-oligomers, indicating the aggresome targeting in trans.

267 aggresomes by demonstrating genetically that aggresome targeting of polyglutamine polypeptides reliev

268 cued newly synthesized protein and prevented aggresome targeting, suggesting that HDIs disturbed traf

269 ein, Bmh1, was also found to be critical for aggresome targeting.

270 in, along with the P-region, plays a role in aggresome targeting.

271 e ankyrin-like repeat in synphilin 1 with an aggresome-targeting signal from huntingtin was sufficien

272 repeat to a huntingtin fragment lacking its aggresome-targeting signal promoted its transport to agg

273 anslocation to aggresomes required a special aggresome-targeting signal within the sequence of synphi

274 ot form aggresomes, this domain serves as an aggresome-targeting signal.

275 tamine domain (103QP) represents a bona fide aggresome that colocalizes with the spindle pole body (t

276 Viral E1B-55K protein forms aggresomes that sequester p53 and MRN in transformed cel

277 rt of a system, reminiscent of the mammalian aggresome, that collects aggregates preventing their eff

278 As expected from the properties of aggresomes, the microtubule disrupting agents, vinblasti

279 (P-region) of huntingtin (103Q) cannot form aggresomes, this domain serves as an aggresome-targeting

280 tein is inactivated when sequestered into an aggresome through association with an aggresome-inducing

281 inated signaling intermediaries in insoluble aggresomes, thus reducing their bioavailability for down

282 nduce relocalization of the variant from the aggresome to the cell surface.

283 ted than its wild-type counterpart and forms aggresomes upon proteasome impairment.

284 rocess is clustering of lysosomes around the aggresome via a novel mechanism.

285 egion, led to the recruitment of 103Q to the aggresome via formation of hetero-oligomers, indicating

286 regates are recruited and transported to the aggresome via the microtubule network by a protein compl

287 tophagic pathway and leads to the failure of aggresome vimentin cage degradation.

288 tive autophagosmes and the disruption of the aggresomes' vimentin cage independent of MAP1LC3B positi

289 t-lived Schwann cell (SC) protein that forms aggresomes when the proteasome is inhibited or the prote

290 CML cells, resulting in its accumulation in aggresomes, where is it unable to conduct signal transdu

291 Gialpha rescues AGS3 from the aggresome, whereas mInsc augments the aggresome-like dis

292 he transport of the HDAC6-PC2 complex toward aggresomes, whereas expression of the R4227X mutant fail

293 munodetected in the gamma-tubulin-associated aggresomes, which also contained Abeta, p-tau, ubiquitin

294 tic of the DRMs and identify these bodies as aggresomes, which are characteristic of the neurodegener

295 ocate to the cytoplasm and are prone to form aggresomes while losing their binding ability to heteroc

296 st protein Mre11: E4 11k sequesters Mre11 in aggresomes, while the E4 34k/E1b 55k complex participate

297 , therefore, show that DISC1 is recruited to aggresomes with negative effects on neuronal function, a

298 The commonality of these aggresomes with oligomeric protein aggregates found in t

299 PQ83 protein accumulated within aggresomes with PAO-specific staining.

300 (K48/K63-linked) proteins into juxtanuclear aggresomes, without affecting 20S proteasome activity.