ライフサイエンスコーパス: UPR

1 UPR activation and development of parkinsonian signs cou

2 UPR-regulated genes associated with tamoxifen resistance

3 hway inhibition assays, we showed that the 3 UPR pathway transducers-protein kinase RNA-activated (PK

4 Although a UPR was not detected in lenses expressing K6W-Ub, they a

5 nction is sufficient to extend lifespan in a UPR(mt)-dependent manner.

6 Induction of a UPR in human lens epithelial cells (HLECs) also induced

7 abrogates protein aggregation and protects a UPR mutant against ER stress conditions.

8 ation during HSC activation occurs through a UPR-dependent mechanism that requires the transcription

9 Unfolded proteins activate UPR signaling across the ER membrane to the nucleus by p

10 verexpressed in pancreatic cancer, activates UPR and results in chronic ER stress.

11 developmental mitochondrial stress activates UPR(mt) reporters and extends lifespan.

12 e discuss the potential role of the adaptive UPR in staving off type 2 diabetes by enhancing beta-cel

13 sed Abeta phagocytosis, PERK expression, and UPR RNA signature, and decreased ER stress signature.

14 methylases potently suppresses longevity and UPR(mt) induction, while gain of function is sufficient

15 of the mammalian orthologs in longevity and UPR(mt) signaling.

16 ER stress and UPR activation partially contribute to HCV-induced NF-ka

17 lationship between HCV-induced ER stress and UPR activation with TGF-beta1 production has not been fu

18 ors block HCV up-regulation of ER stress and UPR activation.

19 study, we examined the role of ER stress and UPR in regulation of skeletal muscle mass in naive condi

20 provides initial evidence that ER stress and UPR pathways are essential for maintaining skeletal musc

21 ticulum unfolded protein response (UPR), and UPR signaling effects important changes in lipid metabol

22 ansition from "physiological" to "apoptotic" UPR, but accumulating evidence indicates that signaling

23 oping HIV/neuroAIDS therapeutics targeted at UPR/ER stress.

24 -phenylbutyric acid (4-PBA) which attenuates UPR.

25 During ER stress, transport is activated by UPR-dependent Ero1 induction, and cytosolic glutathione

26 IRE1 is the most conserved UPR sensor in eukaryotic cells.

27 t mitochondrial dysfunction and constitutive UPR(mt) activation.

28 arget, bZIP60, govern the two cytoprotective UPR signaling pathways known to date.

29 gs provide a new paradigm for XBP1-dependent UPR regulation and position MIST1 as a potential biother

30 nscription factor, AtbZIP28, and established UPR regulator, the AtBiP2 chaperone.

31 DD34 mRNA occurs and GADD34 is essential for UPR progression.

32 cytes were necessary but also sufficient for UPR/ER stress induction in Tat-expressing astrocytes and

33 chaperone BiP, leading to acute, full-geared UPR activation.

34 Treatment of cells with the non-genotoxic UPR agonist thapsigargin led to a rapid inhibition of DN

35 nt to promote longevity via ATFS-1, the host UPR(mt)-responsive transcription factor.

36 It remains unknown whether and how UPR components can be utilized to counteract chronic ER

37 However, UPR(ER) function is impaired with age, which, we propose

38 Our findings identify the cytosolic HSP70-UPR axis as an unexpected regulator of RMS pathogenesis,

39 ein degradation (ERAD) pathway, an important UPR function for destruction of aberrant proteins, media

40 otype, these cells can be further applied in UPR-targeted drug discovery towards the development of d

41 (UPR), but downregulation of PBA1 increased UPR and ERSID.

42 central regulatory role in the heat-induced UPR pathway.

43 that BAP1 represses metabolic stress-induced UPR and cell death through activating transcription fact

44 ility to dampen the metabolic stress-induced UPR transcriptional network.

45 We hypothesized that Chlamydia induces UPR and exploits it to upregulate host cell uptake and m

46 ans not only delays aging but also maintains UPR(mt) signaling, suggesting an epigenetic mechanism th

47 cell dysfunction the result of a maladaptive UPR or a failure of the UPR to adequately adapt?

48 ntire secretory pathway, whereas maladaptive UPR outputs trigger apoptosis.

49 This inhibits the IRE-1-mediated UPR(ER) and initiates the p38/SKN-1(Nrf2) antioxidant re

50 entify factors critical to the Ire1-mediated UPR and found several proteins, Dom34, Hbs1 and Ski comp

51 nse tradeoffs based on CPR5 and SA-modulated UPR signaling, whereby CPR5 acts as a positive modulator

52 be drawn, arguing that a cell-nonautonomous UPR-based regulation of heterologous cells may be phylog

53 nd potential initiator of cell-nonautonomous UPR-based regulation.

54 We showed that Spry2 is a novel UPR target and its upregulation is dependent on PERK.

55 is, but excessive or prolonged activation of UPR can lead to pathologic conditions.

56 t cells undergo cell death upon cessation of UPR protection and while attempting to restore homeostas

57 , an ER stress sensor, is a key component of UPR.

58 This elevation of UPR marker expression was also observed in the human MEC

59 nvironments, and frequently show evidence of UPR activation, this pathway could modulate the response

60 The main function of UPR is to restore homeostasis, but excessive or prolonge

61 on of glutathione prevented the induction of UPR, and AC and HQ induced structural changes in PDI.

62 Moreover, we found that the inhibition of UPR causes severe atrophy in cultured myotubes.

63 Inhibition of UPR reduced the activity of Akt/mTOR pathway and increas

64 To demonstrate the involvement of UPR in the pathobiology of these lesions, we employed ch

65 ic insights into CPR5-mediated modulation of UPR signaling.

66 To assess the therapeutic potential of UPR manipulation to axonal regeneration, we locally deli

67 udies highlight the coordinate regulation of UPR by the GADD34- and CReP-containing eIF2alpha phospha

68 The vital role of UPR pathways in Chlamydia development and pathogenesis c

69 Further, we propose a simplified view of UPR-mediated cell death after CHOP induction.

70 velopment and into adulthood under normal or UPR conditions.

71 anscriptional upregulation of ATF4 and other UPR genes.

72 do not inhibit the Golgi proteases or other UPR branches.

73 l independence of bZIP28 and bZIP60 in plant UPR, and identify an antagonizing role of BI1 in the pro

74 gain insights into the coordination of plant UPR strategies, we analyzed the functional relationship

75 The plant UPR transducers are the kinase and ribonuclease IRE1 and

76 It is the activation of this proapoptotic UPR in pancreatic beta-cells that has been implicated in

77 Progestins, UPR activation and perhaps reduced ICI-stimulated ERalph

78 Prolonged UPR activation, and in particular the PERK branch, can r

79 Severe or chronic/prolonged UPR can breach the threshold for survival and lead to ce

80 llagen I retention in the ER, which promotes UPR-mediated HSC apoptosis.

81 ptionally active ATF6, improving prosurvival UPR function in striatal neurons.

82 ATF5 expression can rescue UPR(mt) signaling in atfs-1-deficient worms requiring th

83 The most conserved ER-resident UPR regulator, the kinase/endoribonuclease inositol-requ

84 by initiating the unfolded protein response (UPR(ER)).

85 the mitochondrial unfolded protein response (UPR(MT)) and mitophagy, are active may predict severity

86 The mitochondrial unfolded protein response (UPR(mt)) has been associated with long lifespan across m

87 rial dynamics and unfolded protein response (UPR(mt)) in the host.

88 the mitochondrial unfolded protein response (UPR(mt)) to promote cell survival along with the repair

89 tion activates an unfolded protein response (UPR(mt)), a stress signaling mechanism designed to ensur

90 the mitochondrial unfolded protein response (UPR(mt)), a transcriptional response mediated by the tra

91 hondrial-specific unfolded protein response (UPR(mt)), affecting whole-animal physiology.

92 the mitochondrial unfolded protein response (UPR(mt)).

93 the mitochondrial unfolded protein response (UPR(MT)).

94 the mitochondrial unfolded protein response (UPR(mt)).

95 The unfolded protein response (UPR) adjusts the cell's protein folding capacity in the

96 three branches of unfolded protein response (UPR) and apoptotic genes.

97 ocesses including unfolded protein response (UPR) and autophagy in response to stress.

98 /XBP1 axis of the unfolded protein response (UPR) and culminating in terminal UPR activation.

99 induction of the unfolded protein response (UPR) and disruption of autophagic flux.

100 ould activate the unfolded protein response (UPR) and drive HSC apoptosis.

101 and induction of unfolded protein response (UPR) and endoplasmic reticulum (ER) stress in astrocytes

102 IN2 modulates the unfolded protein response (UPR) and ER stress in pancreatic beta cells.

103 culum (ER) stress/unfolded protein response (UPR) and mitochondrial ROS production.

104 ability to induce unfolded protein response (UPR) and their effects on the structure and function of

105 Autophagy and the unfolded protein response (UPR) both promote activation of hepatic stellate cells (

106 Activation of the unfolded protein response (UPR) can be either adaptive or pathological.

107 BP1 branch of the unfolded protein response (UPR) has been implicated in multiple types of human canc

108 ) stress response/unfolded protein response (UPR) has been thought to influence tumorigenesis mainly

109 l effector of the unfolded protein response (UPR) in budding yeast.

110 um stress and the unfolded protein response (UPR) in GCs.

111 complexity of the unfolded protein response (UPR) in plants.

112 R) stress and the unfolded protein response (UPR) in regulating these two cellular outcomes is poorly

113 ns that elicit an unfolded-protein response (UPR) in vivo accumulate p27(Cdkn1b), show cyclin-depende

114 ticulum (ER), the unfolded protein response (UPR) increases ER-protein-folding capacity to restore pr

115 The unfolded protein response (UPR) is a cytoprotective pathway that relieves endoplasm

116 The unfolded protein response (UPR) is a shared pathway utilized by cells to cope with

117 The unfolded protein response (UPR) is activated by various stresses during vegetative

118 The unfolded protein response (UPR) is activated to cope with ER stress.

119 The unfolded protein response (UPR) is an ancient signaling pathway that commits to lif

120 The unfolded protein response (UPR) is essential for physiological growth as well as ma

121 K) pathway of the unfolded protein response (UPR) is protective against toxic accumulations of misfol

122 The unfolded protein response (UPR) maintains protein homeostasis by governing the proc

123 on, and apoptotic unfolded protein response (UPR) markers, CHOP and Caspase 12, were also increased i

124 (Ire1p)-mediated unfolded protein response (UPR) modulated Arl1p activation at late Golgi.

125 The unfolded protein response (UPR) monitors and adjusts the protein folding capacity o

126 ein levels of the unfolded protein response (UPR) negative master regulator Grp78 and an increase in

127 activation of the unfolded protein response (UPR) pathway.

128 anslation and the unfolded protein response (UPR) pathways at the protein level.

129 Although the unfolded protein response (UPR) plays a major role in certain microbial infectivity

130 own about how the unfolded protein response (UPR) responds to persistent ER stress in vivo.

131 een DREAM and the unfolded protein response (UPR) sensor activating transcription factor 6 (ATF6).

132 ytokines, ROS and unfolded protein response (UPR) signaling activation.

133 by triggering an unfolded protein response (UPR) that induced PRKR-like endoplasmic reticulum kinase

134 hway known as the unfolded protein response (UPR) that signals between the endoplasmic reticulum (ER)

135 investigated the unfolded protein response (UPR) to endoplasmic reticulum (ER) stress by Mvarphis in

136 isms known as the unfolded protein response (UPR) to increase the folding capacity of the ER.

137 ich activates the unfolded protein response (UPR) to restore ER homeostasis.

138 ER) activates the unfolded protein response (UPR) to restore homeostasis.

139 and activate the Unfolded Protein Response (UPR) to trigger adaptive responses through the effectors

140 m for the primary unfolded protein response (UPR) transducer inositol-requiring enzyme 1 (IRE1alpha)

141 components of the unfolded protein response (UPR) was observed.

142 sponse termed the unfolded protein response (UPR) whose function is to resolve ER stress.

143 activation of the unfolded protein response (UPR), a conserved pathway that transmits signals to rest

144 Activation of the unfolded protein response (UPR), a homeostatic regulatory network that responds to

145 transducer of the Unfolded Protein Response (UPR), a surveillance mechanism that ensures homeostasis

146 induction of the unfolded protein response (UPR), an adaptive ER stress response and signalling netw

147 plasmic reticulum unfolded protein response (UPR), and UPR signaling effects important changes in lip

148 induction of the unfolded protein response (UPR), but downregulation of PBA1 increased UPR and ERSID

149 significantly the unfolded protein response (UPR), p53, hypoxia-related transcription factors, and me

150 activation of the unfolded protein response (UPR), rapid translation of GADD34 mRNA occurs and GADD34

151 ctive role in the unfolded protein response (UPR), required for cells to survive ER stress.

152 activation of the unfolded protein response (UPR), suggesting that specific TG6 mutants elicit an end

153 ulum (ER)-induced unfolded protein response (UPR), the ubiquitin-proteasome system (UPS) and autophag

154 tively termed the unfolded protein response (UPR), to maintain a productive ER protein-folding enviro

155 his activates the unfolded protein response (UPR), which alters the expression of many genes involved

156 tress elicits the unfolded protein response (UPR), which enhances the operation in plant cells of the

157 the activation of unfolded protein response (UPR), which is instructed by multiple transcriptional re

158 induction of the unfolded protein response (UPR), which profoundly reduces FGF signaling in cardiac

159 The unfolded protein response (UPR), which protects cells against accumulation of misfo

160 activation of the Unfolded Protein Response (UPR)-associated transcription factor ATF6 attenuates sec

161 inhibited by the unfolded protein response (UPR)-induced eIF-2alpha phosphorylation to protect again

162 rvival, named the unfolded protein response (UPR).

163 hway known as the unfolded protein response (UPR).

164 activation of the unfolded protein response (UPR).

165 and an activated unfolded protein response (UPR).

166 activation of the unfolded protein response (UPR).

167 uring an enhanced unfolded protein response (UPR).

168 m (ER) elicit the unfolded protein response (UPR).

169 and a heightened unfolded protein response (UPR).

170 etween HD and the unfolded protein response (UPR).

171 followed by the unfolding protein response (UPR).

172 nly known as the unfolding protein response (UPR).

173 tein provokes the unfolded protein response (UPR).

174 activated by the unfolded protein response (UPR).

175 ess that leads to unfolded protein response (UPR).

176 ess response, the unfolded protein response (UPR).

177 traffic, and the unfolded protein response (UPR).

178 he ability of the unfolded protein response, UPR, to regulate cell homeostasis through both gene expr

179 otein response of the endoplasmic reticulum (UPR(ER)).

180 in atfs-1-deficient worms requiring the same UPR(mt) promoter element identified in C. elegans.

181 lants subjected to severe or chronic stress, UPR promotes programmed cell death (PCD).

182 m 4-phenylbutyrate (4PBA), reduces ER stress/UPR and improves muscle function, but does not restore S

183 hypoglycosylation is a mechanism of stressed UPR induction intrappc11mutants.

184 However, sustained UPR activation has negative effects on cellular function

185 s generated widespread interest in targeting UPR as therapeutic strategies.

186 n response (UPR) and culminating in terminal UPR activation.

187 We found that UPR signaling is responsible for up-regulating TANGO1 in

188 Here, we show that UPR induces Sestrin2 via ATF4 and NRF2 transcription fac

189 The UPR also reduces protein folding demands in the ER by de

190 The UPR has long been known to regulate phospholipid metabol

191 The UPR is largely dependent on transcription factors (TFs)

192 The UPR is relayed to the cell through the activation of PER

193 The UPR marker sp-XBP1 was constitutively activated in ERalp

194 The UPR(mt) promotes a complex transcription program ultimat

195 ATFS-1 transcription factor to activate the UPR(MT) After short-term acute stress has been mitigated

196 ty of selected mtDNA species to activate the UPR(mt) is a process that is exploited by cancer cells t

197 ect in ER-to-Golgi trafficking activated the UPR pathway in ULK-deficient cells; both processes were

198 extended the lifespan without affecting the UPR gene expression network.

199 Once BiP is in excess again, the UPR transitions to chronic, submaximal activation, indic

200 he interdependence between autophagy and the UPR during HSC activation.

201 HCV infection induces ER stress and the UPR in a JNK-dependent manner.

202 ork reveals a unique role for TANGO1 and the UPR in facilitating collagen I secretion and fibrogenesi

203 In wild-type (WT) HSCs, both TANGO1 and the UPR were induced by transforming growth factor beta (TGF

204 Of note, induction of IBTKalpha and the UPR, along with inhibition of autophagic flux, was assoc

205 response hormone salicylic acid (SA) and the UPR, which is modulated by SA via unknown mechanisms.

206 As the UPR is essential for successful ER homeostatic readjustm

207 As the UPR up-regulates proteins involved in secretion, we stud

208 s have far-reaching consequences because the UPR is activated by a myriad of environmental or pathoph

209 olic adaptations or rewiring mediated by the UPR(mt) and how this may contribute to the resolution of

210 g rapid transcriptional induction during the UPR.

211 ns for interventions that seek to engage the UPR(mt) to improve metabolic health and longevity.

212 through diverse mechanisms and highlight the UPR as a potential therapeutic target for patient treatm

213 Yet, how the UPR achieves ER homeostatic readjustment is poorly inves

214 em for dissecting the intricacies of how the UPR evaluates and alleviates ER stress.

215 Thus, these findings clarify how the UPR influences the roles of Syt1p, Arl1p, and Imh1p in G

216 ere, we discuss recent advances into how the UPR integrates information about the intensity and durat

217 ve been described in mammals [3, 4], how the UPR(mt) is regulated remains unclear.

218 in, we tackle the biggest controversy in the UPR literature: the function of the transcription factor

219 Augmented genes in the UPR signature included chaperones, lectins, foldases, an

220 aster regulator Grp78 and an increase in the UPR.

221 ase variants have the capacity to induce the UPR(MT), but also that coexpression of alphaS and ATFS-1

222 hibition of only cytosolic HSP70 induced the UPR, suggesting that the essential activity of HSP70 in

223 on of nutrient transporters, and induced the UPR.

224 VPA-mediated inositol depletion induces the UPR by increasing the de novo synthesis of ceramide.

225 ment (UPRE), suggesting that VPA induces the UPR pathway.

226 e, we show that O. tsutsugamushi invokes the UPR in the first 48 h and benefits from ER stress in an

227 rt-term acute stress has been mitigated, the UPR(MT) is eventually suppressed to restore homeostasis

228 esigned to relieve ER stress or modulate the UPR during enamel development to ameliorate the clinical

229 Initially, with the support of the UPR acting in pro-survival mode, Enamp.S55I heterozygous

230 er, here we show that the PERK branch of the UPR also controls DNA replication.

231 Mutations associated with activation of the UPR caused death of primary neurons and reduced the surv

232 ; OMIM 122860), we propose activation of the UPR could be part of the disease mechanism for CDD patie

233 To understand the role of the UPR during reproductive development, we analyzed a doubl

234 Homeostatic activation of the UPR enforces adaptive programs that modulate and augment

235 Despite the significance of the UPR for cell homeostasis, in plants the regulatory circu

236 r regulators and downstream effectors of the UPR have distinct roles in mediating cellular processes

237 w, we discuss the evidence for a role of the UPR in beta-cell dysfunction and death in the developmen

238 M proteome associated with activation of the UPR in diabetes, which may serve as novel benchmarks for

239 a transgenic mouse model, activation of the UPR in early differentiating osteocytes delays maturatio

240 ibition of PERK, but not the IRE1 arm of the UPR in satellite cells inhibits myofiber regeneration in

241 haracterize a newly identified branch of the UPR initiated by the ER-localized co-chaperone from Arab

242 Induction of the UPR is linked to decreased ATG16L1 stabilization in Ikka

243 ed, MIST1 functions as a co-regulator of the UPR master transcription factor XBP1 for a portion of ta

244 analyzed the functional relationship of the UPR modulators through the analysis of single and higher

245 our results suggest that the PERK arm of the UPR plays a pivotal role in the regulation of satellite

246 Activation of the UPR sensor PERK (EIFAK3/PEK) results in the phosphorylat

247 utant knocks out the RNA-splicing arm of the UPR signaling pathway.

248 repression of Blimp-1 and inhibition of the UPR that prepares cells to become professional secretors

249 ined during pharmacological induction of the UPR through a mechanism suggested to involve GADD34-medi

250 ult of a maladaptive UPR or a failure of the UPR to adequately adapt?

251 field that support a strong relevance of the UPR to many areas of plant life.

252 Regulation of the UPR transducers entails changes in their oligomeric stat

253 protein stress-sensing luminal domain of the UPR transducers PERK and IRE1alpha does not abolish thei

254 lar resistance to chronic malfunction of the UPR(MT) Given the increasingly recognized role of mitoch

255 prolonged, cell-autonomous activation of the UPR(MT) in C. elegans dopaminergic neurons.

256 uch of the focus has been on the role of the UPR(mt) in maintaining or re-establishing protein homeos

257 d, these data suggest that regulation of the UPR(mt) is conserved from worms to mammals.

258 S and ATFS-1-associated dysregulation of the UPR(MT) synergistically potentiate dopaminergic neurotox

259 Using SOD2 as a surrogate marker of the UPR(mt), we found that in primary breast cancers, SOD2 i

260 nces of prolonged cellular activation of the UPR(MT), we provide evidence that this pathway is not a

261 As such, plants make special use of the UPR, and evidence indicates that the master regulators a

262 I retention within the ER, induction of the UPR, and HSC apoptosis.

263 ed cells to pharmacological induction of the UPR, and the observed decrease in cell viability was res

264 oribonuclease (RNase), a key mediator of the UPR, cleaves Xbp1 mRNA to generate a potent transcriptio

265 IRE1 immediately following engagement of the UPR, in order to limit prolonged IRE1 RNAse activity tha

266 ion of genes directed by the PERK arm of the UPR, including genes involved in amino acid metabolism,

267 lso called BiP, is a master regulator of the UPR, reducing ER stress levels and apoptosis due to an e

268 rosine kinase (IBTKalpha) as a member of the UPR, whose expression is preferentially translated durin

269 ticulum calcium levels, and induction of the UPR.

270 c1 protein and concomitant activation of the UPR.

271 e studied whether TANGO1 was a target of the UPR.

272 omain co-chaperones as key regulators of the UPR.

273 that links autophagy with activation of the UPR.

274 NA synthesis inhibition was dependent on the UPR effector PERK and was associated with phosphorylatio

275 c agents ameliorating protein folding or the UPR can be considered as a potential therapeutic treatme

276 TF1A causes an imbalance that overwhelms the UPR, induces cellular injury, and provokes acinar metapl

277 During ER stress, the UPR-activated transcription factors ATF4 and ATF6alpha t

278 Our results reveal that the UPR in S. pombe executes RIDD in an intricate interplay

279 r, new evidence has emerged showing that the UPR is also the source of cell-extrinsic effects, partic

280 , submaximal activation, indicating that the UPR senses ER stress in a ratiometric fashion.

281 in Caenorhabditis elegans has shown that the UPR(mt) is regulated by the transcription factor ATFS-1,

282 structurally abnormal; presumably due to the UPR modulating ameloblast behaviour and function in an a

283 accumulation of p27, whether related to the UPR or not, prevents the phosphorylation of lamin A/C an

284 Understanding age-related changes to the UPR(ER) will provide new avenues for therapeutic interve

285 If unsuccessful, the UPR initiates a proapoptotic program to eliminate the ma

286 When the UPR is inactive, HAC1 mRNA is stored as an unspliced iso

287 s well as in identifying scenarios where the UPR(mt) plays a protective role, such as during bacteria

288 pect of mitochondrial signaling in which the UPR(MT) pathway, under disease-associated, context-speci

289 nt loads; however, key regulators within the UPR remain to be identified.

290 enables pharmacological modulation all three UPR branches either singly or in combination.

291 abeling we confirmed the activation of three UPR branches and increased ERp29 and calreticulin in dia

292 X-box binding protein 1 (XBP1), one of three UPR effector pathways and sought to establish the interd

293 izing SA-dependent growth inhibition through UPR modulation.

294 cells adapt to mitochondrial stress through UPR(mt) regulation.

295 Thus, UPR activation during human pregnancy might be a common

296 ein folding homeostasis likely contribute to UPR activation, but deletion of the unfolded protein str

297 e is pharmacological chaperoning, leading to UPR suppression.

298 ults show that HIV-1 Tat expression leads to UPR/ER stress in astrocytes, which in turn contributes t

299 regulation of tumor growth, including tumor UPR-based cell-nonautonomous signaling as a mechanism of

300 flies expressing these three mutant variants.UPR and parkinsonian signs could be partially rescued by