ライフサイエンスコーパス: UPR

1 UPR and DDR alterations are associated with aging and wi

2 Finally, we propose that using a UPR(mt) nuclear gene expression signature may be a more

3 IEC shedding was a UPR-dependent protective response to Glafenine that rest

4 Aberrant UPR(mt) signaling is associated with a wide spectrum of

5 work, we expressed the constitutively active UPR(ER) transcription factor, XBP-1s, in a subset of ast

6 ation of the ER ZnT8 level promotes adaptive UPR, acting as a protective mechanism that decongests th

7 strate a novel MUC1-CDA axis of the adaptive UPR that provides survival advantage upon ER stress indu

8 -phosphate levels and, consequently, affects UPR activation.

9 Altered UPR signaling, exemplified in Rnf5(-/-) mice, coincides

10 review current knowledge related to altered UPR signaling in leukemia and highlight possible strateg

11 an excess of the ER resident chaperone (and UPR target gene) BiP over u(s) is restored lead to u(s)-

12 lk between the oxidative protein folding and UPR and ERAD pathways.

13 heat tolerance, probably through the HSR and UPR and by enhancing the cell death pathway.

14 ysis revealed enhanced expression of HSR and UPR genes, as well as reduced cell death, under heat and

15 TGFbeta and UPR signaling pathways are tightly intertwined during HS

16 ER, suggesting a direct role in the UPR and UPR-mediated cell death.

17 Another UPR pathway activates the activating transcription facto

18 Here, we describe currently available UPR modulating compounds, specifically highlighting the

19 uss the emerging signaling crosstalk between UPR stress sensors and the DDR, as well as their involve

20 +) dynamics in beta cells and regulates both UPR activation and cell death, suggesting that RyR-media

21 enhanced proteotoxic stress, as evidenced by UPR induction, and resensitized tumor spheroids to prote

22 R stress resistance independent of canonical UPR(ER) pathways but dependent upon the cell-surface rec

23 These data support that one of the canonical UPR branches, through ATF4 and its target gene FAM129A,

24 Strikingly, in contrast to canonical UPR signaling, Sema3A-induced eIF2alpha phosphorylation

25 tion, results in ER stress with compensatory UPR induction.

26 erstanding of the UPR, emphasizing conserved UPR elements between plants and metazoans and highlighti

27 m for tuning ER quality control and coupling UPR activity to signals that mobilise ER calcium in secr

28 thways, revealing a new arm of the cytosolic UPR.

29 f mutant p85alpha (R649W) in vivo, decreased UPR-dependent induction of ER stress response genes.

30 degradation (ERAD) pathway, exhibit delayed UPR activation after lithium and galactose exposure beca

31 Deregulated UPR signaling, which often occurs in hematopoietic stem

32 her, these results suggest that differential UPR activation makes cells more responsive to bacterial

33 However, translational control during UPR has not been demonstrated in yeast.

34 ation-mediated translational controls during UPR.

35 ased the levels of ubiquitinated eS7A during UPR in an Ire1-independent manner.

36 h the KDEL receptor, localization in the ER, UPR activation, and subsequent TGF-beta signaling.

37 2-Dio2 polymorphism-carrying mouse exhibited UPR and hypothyroidism in distinct brain areas.

38 the fat1Delta mutant, likely accounting for UPR induction.

39 he astrocyte reactivity state resulting from UPR over-activation is a distinct pathogenic mechanism t

40 that the loss of PIGBOS leads to heightened UPR and increased cell death.

41 oderate levels of ER stress, the homeostatic UPR sets in motion transcriptional and translational cha

42 to IAN6 genes in the regulation of the HSR, UPR, and cell death, and suggest that their natural vari

43 Here, by reconstituting components of human UPR, ER stress and BiP chaperone systems, we discover th

44 Our results identify UPR(mt) as a therapeutic target for restoration of place

45 The delay in UPR activation did not occur in yeast strains in which k

46 Imbalances in UPR signaling are implicated in the pathogenesis of nume

47 to both ameliorate pathologic imbalances in UPR signaling implicated in these different diseases and

48 mycin exposure caused sustained increases in UPR target genes in adipose tissue.

49 ative phosphorylation (OXPHOS), resulting in UPR(mt) activation.

50 rature and plant growth regulators increased UPR activation, as assessed by an increase in splicing o

51 CTB-KDEL's capacity to induce UPR and epithelial restitution or wound healing was corr

52 hese results suggest that B. abortus-induced UPR is triggered by bacterial cyclic dimeric GMP, in a S

53 Furthermore, the Brucella-induced UPR is crucial for induction of multiple molecules linke

54 CXL146-induced UPR activation led to a series of downstream events, inc

55 Initially, UPR signaling aims at cytoprotection and restoration of

56 While young cells initiated UPR-related translational and transcriptional regulatory

57 rein, we explored the role of the integrated UPR and ERAD in oligodendrocytes in regulating myelin pr

58 nted in this study imply that the integrated UPR and ERAD in oligodendrocytes maintain myelin thickne

59 required for cell non-autonomous intestinal UPR(ER) activation, including the biogenic amine tyramin

60 RIM and RIC interneurons, induced intestinal UPR(ER) activation and extended longevity, and exposure

61 The key UPR sensor IRE1alpha resides in the ER and deploys a cyt

62 the first time detect and quantify all major UPR receptors, transducers and effectors that are not re

63 asize the significance of virulence-mediated UPR(mt) repression and the potency of the UPR(mt) as an

64 thereby reestablishing galactose metabolism, UPR activation, and cellular adaption to lithium-galacto

65 implications for the control of the metazoan UPR.

66 fore investigating evidence of mitochondrial UPR (UPR(mt)) in placentas of PE < 34 wk patients.

67 o found that robust, perpetual mitochondrial UPR activation effectively reduces muscle weakness cause

68 In this study, we used the small molecule UPR modulator Integrated Stress Response InhiBitor (ISRI

69 cytoplasmic tau aggregates but exhibited no UPR activation.

70 nce processing induce an early activation of UPR(mt) that, in turn, modulates cytosolic quality contr

71 llicular B cells up-regulate a wide array of UPR-affiliated genes before initiating antibody secretio

72 1 distinctly regulates different branches of UPR pathway to promote plasma cell development and funct

73 n the identification and characterization of UPR modulating compounds, providing new opportunities to

74 In general, the density of UPR protein-positive cells was found to decrease signifi

75 teraction of BiP with the luminal domains of UPR proteins IRE1 and PERK switch BiP from its chaperone

76 one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essent

77 with heat, chemicals, or virus elicitors of UPR.

78 with aortic stenosis also showed evidence of UPR(mt) activation, which correlated with reduced tissue

79 significantly linked with the expression of UPR genes, and in particular ERN1 (IRE1) and ATF4.

80 results by revealing the basal expression of UPR-affiliated mRNA networks without detectable Xbp1 act

81 and potentially therapeutic implications of UPR signaling in human disease.

82 l agonist given BPTPE's delayed induction of UPR and apoptosis, with a higher probability of tumor cl

83 649W(+/-) mice revealed reduced induction of UPR target genes in adipose tissue, whereas chronic tuni

84 Prolonged induction of UPR(ER) signaling activated the survival branch of the U

85 estine showed significantly higher levels of UPR activation than female intestine, as well as higher

86 , ATF5, has been identified as a mediator of UPR(mt) MNRR1 knockout cells display an ~40% reduction i

87 tant role upstream of this known mediator of UPR(mt).

88 hese findings suggest an abnormal pattern of UPR activity in SCZ, with specific dysregulation of the

89 Partial reduction of UPR signaling at the level of phosphorylated eIF2alpha i

90 is case a microprotein, in the regulation of UPR originating in the ER.

91 es in the understanding of the regulation of UPR signalling and its implications in the pathophysiolo

92 translation is central to the regulation of UPR, quantification and determination of protein copy nu

93 we provide evidence of a protective role of UPR(mt) and mitochondrial clearance against impaired mit

94 ein expression and phosphorylation states of UPR sensor pathway proteins in the dorsolateral prefront

95 d knockdown of GGDPS induces upregulation of UPR markers and disrupts MUC1 trafficking in PDAC cells.

96 le to targeted interventions against ongoing UPR signaling.

97 affecting cell proliferation, cell death, or UPR induction in murine myeloblast 32D and human promyel

98 he endoplasmic reticulum (ER), but not other UPR sensors, such as protein kinase R-like ER kinase (PE

99 ucing the unfolded protein response pathway (UPR) and apoptosis.

100 whereas VDR knockout mice undergo persistent UPR activation and apoptosis in response to chemical ER

101 s of primary bone marrow revealing perturbed UPR in myeloid precursors and in vitro differentiation o

102 ZnT8 to protect beta-cells from proapoptotic UPR during chronic low-grade inflammation.

103 sadvantages in their application for probing UPR function.

104 s implicate IEC delamination as a protective UPR-mediated response to chemical injury, and uncover an

105 d immunoglobulin heavy chain binding protein UPR-response genes.

106 ession in LTED BC through triggering a rapid UPR and apoptosis.

107 54-amino acid microprotein PIGBOS regulates UPR.

108 ced mitochondrial unfolded protein response (UPR(mt)) and enhanced mitochondrial clearance in iPSC-de

109 The mitochondrial unfolded protein response (UPR(mt)) is a mitochondrial-to-nuclear signaling pathway

110 the mitochondrial unfolded protein response (UPR(mt)), autophagy, and mitochondrial biogenesis, there

111 pithelial damage, unfolded protein response (UPR) activation, and inflammation.

112 sphorylation, and unfolded protein response (UPR) activation.

113 148 activates the unfolded protein response (UPR) and causes large-scale reorganization of the ER.

114 ed involvement of unfolded protein response (UPR) and endoplasmic reticulum (ER) stress pathways, but

115 activation of the unfolded protein response (UPR) and ER stress response via a genetically intact MYC

116 The integrated unfold protein response (UPR) and ER-associated degradation (ERAD) are the primar

117 The integrated unfolded protein response (UPR) and ER-associated degradation (ERAD) are the primar

118 regulated by the unfolded protein response (UPR) and ER-associated degradation (ERAD).

119 R, activating the unfolded protein response (UPR) and restoring the ER to its normal physiological st

120 activation of the unfolded protein response (UPR) and subsequent adaptation of cellular physiology in

121 n particular, the unfolded protein response (UPR) and the DNA damage response (DDR).

122 The unfolded protein response (UPR) and the heat shock response (HSR) are two evolution

123 th activating the unfolded protein response (UPR) and the proinflammatory response associated with vi

124 between different unfolded protein response (UPR) branches in stressed senescent cells.

125 ions activate the unfolded protein response (UPR) by inhibiting phosphoglucomutase activity and causi

126 I3K modulates the unfolded protein response (UPR) by interacting with and regulating the nuclear tran

127 activation of the unfolded protein response (UPR) components, which coincides with increased expressi

128 ) stress, and the unfolded protein response (UPR) consistent with elevated secretory activity.

129 e ATF6 arm of the unfolded protein response (UPR) during reperfusion, a typical clinical intervention

130 hat activates the unfolded protein response (UPR) exclusively when normal ER membrane lipid compositi

131 ntitative PCR for unfolded protein response (UPR) genes, and single-cell RNA sequencing on whole bone

132 The unfolded protein response (UPR) has been shown to be active in both models of depre

133 s, as well as the unfolded protein response (UPR) in the endoplasmic reticulum (ER), are two mechanis

134 ealed an adaptive unfolded protein response (UPR) including a marked immunoproteasome activation that

135 The unfolded protein response (UPR) is a cellular homeostatic circuit regulating protei

136 The unfolded protein response (UPR) is a conserved adaptive signaling pathway that gove

137 The unfolded protein response (UPR) is activated in plants in response to endoplasmic r

138 etwork termed the unfolded protein response (UPR) is activated.

139 The unfolded protein response (UPR) is emerging as the possible origin of these events.

140 Unfolded protein response (UPR) of the endoplasmic reticulum (UPR(ER)) helps mainta

141 (ER) stress, the unfolded protein response (UPR) orchestrates adaptive cellular changes to reestabli

142 ependent upon the unfolded protein response (UPR) pathway, a pathway previously shown to associate wi

143 ant activation of unfolded protein response (UPR) pathway, which was partially rescued by the additio

144 m (ER) stress and unfolded protein response (UPR) pathways are increased in skeletal muscle under mul

145 The unfolded protein response (UPR) plays a central role in regulating endoplasmic reti

146 activation of the unfolded protein response (UPR) promote growth and invasion in cancer.

147 e PERK arm of the unfolded protein response (UPR) regulates cellular proteostasis and survival in res

148 y an unresolvable unfolded protein response (UPR) represents a potential new therapeutic strategy.

149 imulations, human unfolded protein response (UPR) RT(2) PCR profiler arrays, live cell microscopic im

150 The unfolded protein response (UPR) senses defects in the endoplasmic reticulum (ER) an

151 ally triggers the unfolded protein response (UPR) sensor IRE1alpha in the endoplasmic reticulum (ER),

152 er cells enhanced unfolded protein response (UPR) signaling and cell death upon ER stress induction.

153 cells exploit the unfolded protein response (UPR) to mitigate endoplasmic reticulum (ER) stress cause

154 by activating the unfolded protein response (UPR) under the control of the transcription factor Xbp1.

155 activation of the unfolded protein response (UPR) with downstream inflammatory and pro-thrombotic res

156 induction of the unfolded protein response (UPR), a common response to viral infection.

157 s buffered by the unfolded protein response (UPR), a set of signaling pathways designed to either rec

158 s mediated by the unfolded protein response (UPR), a signal transduction pathway that senses the fide

159 o proteins of the unfolded protein response (UPR), a signaling pathway of great clinical importance,

160 auses a sustained Unfolded Protein Response (UPR), a significant attenuation of the pro-tumorigenic E

161 The unfolded protein response (UPR), an endoplasmic reticulum stress response pathway,

162 activation of the unfolded protein response (UPR), and we hypothesized this may affect mitochondrial

163 activation of the unfolded protein response (UPR), decreased protein synthesis, and enhanced vulnerab

164 regulators of the unfolded protein response (UPR), IRE1alpha and PERK, promote adaptation or apoptosi

165 protein mediating unfolded protein response (UPR), is required for transducing the signal for activat

166 and, in turn, the unfolded protein response (UPR), leading to a distinct transcriptomic signature wit

167 of ER stress and unfolded protein response (UPR), leading to T cell death by apoptosis in the Sting(

168 activation of the unfolded protein response (UPR), notably the branch comprising the kinase PERK and

169 activation of the unfolded protein response (UPR), specifically phosphorylated protein kinase R-like

170 In the unfolded protein response (UPR), stress in the endoplasmic reticulum (ER) activates

171 activation of the unfolded protein response (UPR), triggering death of neutrophil precursors and resu

172 es, including the unfolded protein response (UPR), which acts to attenuate endoplasmic reticulum (ER)

173 vely known as the unfolded protein response (UPR), which are designed to restore biosynthetic capacit

174 (ER) activate the unfolded protein response (UPR), which enhances protein folding to restore homeosta

175 ER) activates the unfolded protein response (UPR)-a signaling network that ultimately determines cell

176 and bZIP28 in the unfolded protein response (UPR).

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

178 work known as the unfolded protein response (UPR).

179 activation of the unfolded protein response (UPR).

180 tly activates the unfolded protein response (UPR).

181 nses, such as the unfolded protein response (UPR).

182 1 mRNA during the unfolded protein response (UPR).

183 e resolved by the unfolded protein response (UPR).

184 es, including the unfolded protein response (UPR).

185 teins through the unfolded protein response (UPR).

186 the mitochondrial unfolded protein response (UPR).

187 hen activates the unfolded protein response (UPR).

188 work known as the unfolded protein response (UPR).

189 ent activated the unfolded protein response (UPR); as evidenced by the activation of inositol-requiri

190 K-eIF2alpha arm of the endoplasmic reticulum UPR pathway, independent of ATF4.

191 lpha/HSPA5 axis of the endoplasmic reticulum UPR.

192 response (UPR) of the endoplasmic reticulum (UPR(ER)) helps maintain proteostasis in the cell.

193 otein response of the endoplasmic reticulum (UPR(ER)) is a crucial mediator of secretory pathway home

194 otein response of the endoplasmic reticulum (UPR(ER)), become defunct with age.

195 rther translational development of selective UPR modulators for human disease.

196 Since UPR can serve as a lever between survival and death, reg

197 Using 23 promoter fragments of six UPR marker genes in a high-throughput enhanced yeast one

198 The role of MNRR1 in stimulating UPR(mt), which is blunted in MELAS cells, was surprising

199 which triggers endoplasmic reticulum stress, UPR, and apoptosis.

200 d bone marrow-derived macrophages suppresses UPR target genes in primary hepatocytes treated with ER

201 Sustained UPR activation leads to cell death and inflammatory resp

202 uccessful at resolving ER stress, a terminal UPR program dominates and actively signals cell suicide.

203 -Tag2) mouse models of PanNETs revealed that UPR signaling was optimized for adaptation and that inhi

204 The UPR and HSR occur in different cellular compartments and

205 The UPR enforces adaptive or cell death programs by integrat

206 The UPR is comprised of three signaling pathways activated d

207 The UPR is the cellular response to stress which results in

208 The UPR is triggered by unfolded protein stress and leads to

209 The UPR transmits information about protein folding status t

210 to: 1) identify conditions that activate the UPR(mt) in the heart; and 2) study the relationship amon

211 revealed that GGDPSi treatment activates the UPR and triggers apoptosis in a variety of human and mou

212 neurons cell non-autonomously activates the UPR(ER) in the intestine, leading to enhanced proteostas

213 ived membranous structures and activates the UPR, a set of signaling pathways involved in adaptation

214 art; and 2) study the relationship among the UPR(mt), mitochondrial function, and cardiac contractile

215 in EOC suggests a role for ER stress and the UPR in EOC.

216 s in the ER membrane induce the UPR, and the UPR in turn controls the expression of some lipid metabo

217 Here we characterize how ER stress and the UPR inhibit insulin signaling.

218 lationship between lipid homeostasis and the UPR.

219 Although oxidative protein folding and the UPR/ERAD pathways each are well-understood, very little

220 However, other stress pathways besides the UPR converge on phosphorylated eIF2alpha in the integrat

221 and discuss emerging connections between the UPR(mt) signaling and a translational regulation program

222 rotein whose expression is controlled by the UPR through the IRE1-bZIP60 pathway in Arabidopsis.

223 dback loop that differentially channeled the UPR output.

224 of non-conventional mRNA splicing during the UPR.

225 light possible strategies for exploiting the UPR as treatment for this disease.

226 If stress resolution fails, the UPR commits the cell to apoptotic death.

227 1s, a transcription factor essential for the UPR.

228 a prototypic beta-herpesvirus, harnesses the UPR to regulate its own life cycle.

229 However, how the UPR and its components affect autophagic activity has no

230 oligodendrocytes caused ERAD impairment, the UPR activation, and attenuation of myelin protein biosyn

231 d to the ER, suggesting a direct role in the UPR and UPR-mediated cell death.

232 on (ERAD), and reduces IRE1 signaling in the UPR pathway.

233 d a lipid bilayer stress (LBS) sensor in the UPR transducer protein Ire1, located at the interface of

234 Hence, signaling events in the UPR, such as activation of the JNK mitogen-activated pro

235 Defects in the ER membrane induce the UPR, and the UPR in turn controls the expression of some

236 tochondrial stresses transiently induced the UPR(mt) in cultured cardiomyocytes.

237 Ceapins specifically inhibit the UPR sensor ATF6alpha, an ER-tethered transcription facto

238 epurinated ribosomes, thereby inhibiting the UPR.

239 ganisms evolved into multicellular life, the UPR complexity has increased to suit their growth and de

240 t of intracellular pathogens manipulates the UPR to promote survival and replication in host cells.

241 An inhibitor of the UPR antagonized PV expansion in macrophages, indicating

242 n evaluating the implied significance of the UPR as a critical determinant across major neurodegenera

243 nbred for differences in the activity of the UPR between permissive and elevated temperature in conju

244 that different components downstream of the UPR contribute to NOD1 activation.

245 he pancreatic ER kinase (PERK) branch of the UPR functions as the master regulator of protein transla

246 nt diseases and define the importance of the UPR in diverse cellular and organismal contexts.

247 ing transcription factor 6 (ATF6) arm of the UPR in mitigating adverse outcomes associated with ische

248 attenuates the LLC-induced activation of the UPR in skeletal muscle of mice.

249 doplasmic reticulum kinase (PERK) arm of the UPR in the regulation of skeletal muscle mass and functi

250 This mutant allowed separation of the UPR inhibition by RTA from cytotoxicity because it reduc

251 requiring enzyme 1 (IRE1alpha) branch of the UPR is directly involved in the polarization of macropha

252 ur findings suggest that the PERK arm of the UPR is essential for the maintenance of skeletal muscle

253 nscription factor, a pivotal response of the UPR to heat stress.

254 Despite the biological significance of the UPR to the life of the organism, the regulatory transcri

255 d depurination activity on inhibition of the UPR using mRTA mutants.

256 ed glial cell nonautonomous induction of the UPR(ER) and life-span extension.

257 robust cell nonautonomous activation of the UPR(ER) in distal cells and rendered animals more resist

258 However, both ATF6 and PERK branches of the UPR(ER) participate in amelioration of tauopathy by cons

259 gnaling activated the survival branch of the UPR(ER) pathway, in which cells had elevated expression

260 In C. elegans, expression of the UPR(ER) transcription factor xbp-1s in neurons cell non-

261 ed UPR(mt) repression and the potency of the UPR(mt) as an antibacterial response.

262 Furthermore, the role of the UPR(mt) in maintaining cancer cells in the mitohormetic

263 These results identify the induction of the UPR(mt) in the mammalian (including human) heart exposed

264 Further study of the UPR(mt) will potentially enable development of new thera

265 Induction of the UPR(mt) with methacycline reduced OXPHOS capacity, while

266 r activities intersect upon induction of the UPR, and how decisions are made to dispose of misfolded

267 lecules to target distinct components of the UPR, and their possible applications in treating human d

268 recent advances in the understanding of the UPR, emphasizing conserved UPR elements between plants a

269 ER-associated degradation (ERAD), or of the UPR, in particular the ATF6alpha branch.

270 y between PERK and the XBP1-ATF6 arms of the UPR, whereby PERK attenuates the expression of a specifi

271 NK signaling promoted phosphorylation of the UPR-associated transcription factor CCAAT/enhancer bindi

272 ction on activation of the three arms of the UPR.

273 ivity is required for full activation of the UPR.

274 gment stress resistance independently of the UPR.

275 wnstream targets of the IRE1alpha arm of the UPR.

276 C61A1 cause SCN through dysregulation of the UPR.

277 clease Xrn1 to enact opposing effects on the UPR.

278 in immunoprecipitation analyses pinpoint the UPR as a broad-spectrum compensatory response wherein LB

279 ated by three ER transmembrane proteins, the UPR constantly surveils protein folding conditions withi

280 Together, these findings reveal the UPR program as the sum of two independent stress respons

281 igating combinations of agents targeting the UPR and autophagy in SMARCB1-deficient MRTs.

282 Our results suggest that the UPR is implicated in noise-induced cochlear synaptopathy

283 These results suggest that the UPR is not induced as a response to tau misfolding and a

284 These findings demonstrate that the UPR, which is associated with stress responses in plants

285 Thus, the UPR, an endoplasmic-reticulum-associated response, quite

286 In this review, we aim to tie the UPR-TLR response and depression, and describe the implic

287 iological traits and 831 PDIs underlying the UPR.

288 ibiotic, has been reported to upregulate the UPR in prostate cancer cell lines and to slow their grow

289 t or ER stresses lead to cell death when the UPR cannot repair stress damage, but the means by which

290 While the UPR and HSR appear to operate independently, we have fou

291 or Rpn4 and show that it cooperates with the UPR.

292 associated with a CRE that may contribute to UPR management.

293 oxic stress deploy divergent transcriptional UPR programs.

294 ensing; however, they were unable to trigger UPR-related transcriptional responses.

295 cent research into the mechanisms underlying UPR(mt) signaling in Caenorhabditis elegans and discuss

296 poor response to drugs inducing unresolvable UPR and possibly other forms of chemotherapy helping in

297 investigating evidence of mitochondrial UPR (UPR(mt)) in placentas of PE < 34 wk patients.

298 ion of ATF4, CHOP, and XBP-1 and upregulates UPR target genes.

299 of RNA-based regulation in the budding yeast UPR and have implications for the control of the metazoa

300 During the budding yeast UPR, Ire1 excises an intron from the HAC1 mRNA and the e