ライフサイエンスコーパス: endoplasmic reticulum stress

1 as they tend to aggregate and induce robust endoplasmic reticulum stress.

2 tal to the adaptation to AKI associated with endoplasmic reticulum stress.

3 rols and had decreased lung inflammation and endoplasmic reticulum stress.

4 on, decreased lipid clearance, and increased endoplasmic reticulum stress.

5 xpression, beta cell functional failure, and endoplasmic reticulum stress.

6 tion, nephrin phosphorylation and attenuated endoplasmic reticulum stress.

7 type I interferon response via induction of endoplasmic reticulum stress.

8 s regulating dynein-associated molecules and endoplasmic reticulum stress.

9 cts, e.g. lipotoxicity, oxidative stress and endoplasmic reticulum stress.

10 s through inhibition of oxidative stress and endoplasmic reticulum stress.

11 and an increase of hepatocellular injury and endoplasmic reticulum stress.

12 atic CES2 stimulates lipogenesis by inducing endoplasmic reticulum stress.

13 bolism, proliferation, and the resolution of endoplasmic reticulum stress.

14 eceptors, does protect these neurons against endoplasmic reticulum stress.

15 ated protein kinases activation and elevated endoplasmic reticulum stress.

16 e, deletion of P5-ATPase Spf1p gives rise to endoplasmic reticulum stress.

17 er for autophagy under conditions that cause endoplasmic reticulum stress.

18 al role in determining cell viability during endoplasmic reticulum stress.

19 uction of metabolic stresses, such as AAS or endoplasmic reticulum stress.

20 d microRNA, regulates TLR/Th17 signaling and endoplasmic reticulum stress.

21 beit with slower kinetics in response to the endoplasmic reticulum stress.

22 appaBalpha, and JNK, indicating induction of endoplasmic reticulum stress.

23 nally advantageous, conferring resistance to endoplasmic reticulum stress.

24 uction in VPA-induced lipid peroxidation and endoplasmic reticulum stress.

25 cts with a unique carbon skeleton that cause endoplasmic reticulum stress.

26 ibitor CFTR(inh)-172, CF BAL, or inducers of endoplasmic reticulum stress.

27 ssociated with mitochondrial dysfunction and endoplasmic reticulum stress.

28 ggestive of impaired protein degradation and endoplasmic reticulum stress.

29 , GAS delivers streptolysin toxins, creating endoplasmic reticulum stress.

30 gene was induced by either AA deprivation or endoplasmic reticulum stress.

31 inhibition, increased cytosolic calcium and endoplasmic reticulum stress.

32 ivation of the unfolded protein response and endoplasmic reticulum stress.

33 shed CHOP expression indicative of decreased endoplasmic reticulum stress.

34 axis of gene expression variation leading to endoplasmic reticulum stress.

35 ular insults, such as nutrient deficiency or endoplasmic reticulum stress.

36 escues ATF4-deficient cells from MYC-induced endoplasmic reticulum stress.

37 , leading to mitochondrial abnormalities and endoplasmic reticulum stress.

38 ng expression of specific genes to alleviate endoplasmic reticulum stress.

39 in RTV bioactivation, oxidative stress, and endoplasmic reticulum stress.

40 MEK-GSK3beta, to promote HSC survival under endoplasmic reticulum stress.

41 ivation of the unfolded protein response and endoplasmic reticulum stress.

42 d T-helper cell type 17 (Th17) signaling and endoplasmic reticulum stress.

43 tion, disordered autophagy, and pathological endoplasmic reticulum stress.

44 Chronic hypoxia also triggered mild endoplasmic reticulum stress, a conserved homeostatic re

45 hese include oxidative stress, inflammation, endoplasmic reticulum stress, aberrant insulin signaling

46 e genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-respo

47 Expression of CEL MODY increased endoplasmic reticulum stress, activated the unfolded pro

48 XNIP post-transcriptionally via induction of endoplasmic reticulum stress, activation of inositol-req

49 on of cultured mammalian beta-cells and that endoplasmic reticulum stress acts upstream of FGF1 relea

50 ed ultrastructural changes characteristic of endoplasmic reticulum stress after 8 h and were no longe

51 reduction of IL6 and IL8 release and reduced endoplasmic reticulum stress after IL1B stimulation.

52 Endoplasmic reticulum stress alone, however, did not ind

53 We detected prolonged, severe endoplasmic reticulum stress already at 20 weeks of age

54 reast epithelial cells to agents that induce endoplasmic reticulum stress, altering the unfolded prot

55 nstrate that the depletion of eIF5A leads to endoplasmic reticulum stress, an unfolded protein respon

56 54Arg) mutation showed evidence of increased endoplasmic reticulum stress and a reduction in Golgi vo

57 High-fat diet in sedentary mice led to endoplasmic reticulum stress and aberrant mitochondrial

58 dividuals with AATD by a mechanism involving endoplasmic reticulum stress and aberrant TNF-alpha sign

59 Induction of endoplasmic reticulum stress and activation of the intri

60 Endoplasmic reticulum stress and activation of the unfol

61 ons promote protein misfolding, resulting in endoplasmic reticulum stress and activation of the unfol

62 were dispensable for house dust mite-induced endoplasmic reticulum stress and airways fibrosis.

63 feration of pancreatic cancer cells, induced endoplasmic reticulum stress and apoptosis, and reduced

64 y in a vast array of human cancers, inducing endoplasmic reticulum stress and apoptosis, toxic autoph

65 s monoclonal protein trafficking, leading to endoplasmic reticulum stress and apoptosis.

66 coordinated stress pathways that coalesce on endoplasmic reticulum stress and autophagy programs to m

67 ," misfolding during assembly and leading to endoplasmic reticulum stress and autophagy responses.

68 igates osteoarthritis symptoms by regulating endoplasmic reticulum stress and autophagy.

69 ecially caspase-mediated apoptosis marked by endoplasmic reticulum stress and calreticulin exposure a

70 ol level, which was associated with elevated endoplasmic reticulum stress and caused apoptosis.

71 response in islet beta cells with subsequent endoplasmic reticulum stress and cellular death.

72 p1), a transcription factor activated during endoplasmic reticulum stress and critically involved in

73 bolished N-Ras(G12D)-mediated survival under endoplasmic reticulum stress and diminished the competit

74 egenerating livers, XBP1 deficiency leads to endoplasmic reticulum stress and DNA damage.

75 rkinson's iPSC-derived DAns showed increased endoplasmic reticulum stress and impairments in choleste

76 light-chain dimers, significantly increasing endoplasmic reticulum stress and inducing cytotoxicity b

77 Endoplasmic reticulum stress and induction of autophagy

78 nesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation.

79 nduce polymer formation, prime the cells for endoplasmic reticulum stress and initiate nuclear factor

80 mulation of Y437H myocilin in the TM induced endoplasmic reticulum stress and led to a 45% loss of sm

81 y, increased levels of p62, and increases in endoplasmic reticulum stress and mitochondrial damage, c

82 of reactive oxygen species and induction of endoplasmic reticulum stress and mitochondrial dysfuncti

83 (apoptosis or toxic autophagy) by promoting endoplasmic reticulum stress and modulating multiple sig

84 Although palmitate-induced endoplasmic reticulum stress and nuclear factor kappaB p

85 Dysregulated endoplasmic reticulum stress and phosphorylation of euka

86 (UPR) is activated in plants in response to endoplasmic reticulum stress and plays an important role

87 Therefore, PP-IX leads to endoplasmic reticulum stress and proteasome inhibition i

88 In vivo, endoplasmic reticulum stress and SREBP-1-dependent effec

89 response in COVID-19 infection by modulating endoplasmic reticulum stress and stimulating the resolut

90 one loss reflects reversible calorie-induced endoplasmic reticulum stress and the associated unfolded

91 tifies L. pneumophila infection as a form of endoplasmic reticulum stress and the sensor pATF6 is pro

92 We hypothesized that IFN-gamma induces endoplasmic reticulum stress and the unfolded protein re

93 ssion through calorie-dependent induction of endoplasmic reticulum stress and the unfolded protein re

94 egulated the expression of genes involved in endoplasmic reticulum stress and Toll-like receptor (TLR

95 th intracellular accumulation of uromodulin, endoplasmic reticulum-stress and signs of tubular damage

96 of misfolded or unfolded proteins - known as endoplasmic reticulum stress - and the activation of the

97 of the rough endoplasmic reticulum (without endoplasmic reticulum stress) and Golgi apparatus, incre

98 vironmental stressors, including heat shock, endoplasmic reticulum stress, and arsenic.

99 icked gammaTE in upregulating A20, enhancing endoplasmic reticulum stress, and attenuating TNF-trigge

100 except for genes associated with apoptosis, endoplasmic reticulum stress, and autophagy (P < 0.05).

101 ion of islet amyloid, signs of oxidative and endoplasmic reticulum stress, and beta-cell death.

102 nuclear factor-kappaB inflammatory response, endoplasmic reticulum stress, and cell death.

103 s associated with cytoplasmic vacuolization, endoplasmic reticulum stress, and dysregulated autophagy

104 somal protein degradation are enhanced, with endoplasmic reticulum stress, and energy depletion, lead

105 stance to hyperthermia, oxidative stress and endoplasmic reticulum stress, and fecundity enhancement

106 -kappaB activation, proinflammatory markers, endoplasmic reticulum stress, and insoluble phosphorylat

107 nounced potentiation of cellular heat shock, endoplasmic reticulum stress, and oxidative stress respo

108 ilencing, Wnt signaling, neuronatin-mediated endoplasmic reticulum stress, and the laforin glycogen p

109 cancer cells induces mitochondrial defects, endoplasmic-reticulum stress, and the release of damage-

110 ted receptor-alpha, and Nrf-1; inhibition of endoplasmic reticulum stress; and inhibition of enhanced

111 ir functions are diverse, including roles in endoplasmic reticulum stress, apoptosis and retinal dege

112 as markedly down-regulated, genes related to endoplasmic reticulum stress, apoptosis, and inflammatio

113 proliferation and hypertrophy, angiogenesis, endoplasmic reticulum stress, apoptosis, and senescence.

114 and colleagues identify chemotherapy-induced endoplasmic reticulum stress as a novel strategy to targ

115 21 expression attenuated tunicamycin-induced endoplasmic reticulum stress, as demonstrated by using a

116 free fatty acid-induced oxidative stress and endoplasmic reticulum stress, as denoted by a reduction

117 ion of reactive oxygen species and increased endoplasmic reticulum stress, as revealed by biochemical

118 rease in post-ischemic proton production and endoplasmic reticulum stress, as well as an activation o

119 es the xCT promoter in synergy with the ATF4 endoplasmic reticulum stress-associated transcription fa

120 tein response at 8 weeks and overt beta cell endoplasmic reticulum stress at 12-16 weeks.

121 PERK activation in response to endoplasmic reticulum stress attenuates eIF2B activity b

122 HFpEF-specific downregulated genes engaged endoplasmic reticulum stress, autophagy, and angiogenesi

123 cluding activation of inflammatory cascades, endoplasmic reticulum stress, autophagy, and mitochondri

124 oes not interfere with the production of NP: endoplasmic reticulum stress, autophagy, or production o

125 orylation site mutants survive low levels of endoplasmic reticulum stress better than IRE1 deletions

126 mechanisms, including reduced oxidative and endoplasmic reticulum stress both in vivo and in vitro.

127 Skin fibroblasts showed signs of increased endoplasmic reticulum stress, but despite the reported i

128 autoimmune attack against beta-cells causes endoplasmic reticulum stress by forcing the remaining be

129 These changes are concomitant with endoplasmic reticulum stress, calcium handling defects,

130 Elevated markers of oxidative stress, endoplasmic reticulum stress, caspase activation, and ne

131 Endoplasmic reticulum stress, caused by the presence of

132 Endoplasmic reticulum stress causes unfolded proteins to

133 IGF2 led to beta-cell dedifferentiation and endoplasmic reticulum stress causing islet dysfunction i

134 ncreatic acinar cells, supporting a role for endoplasmic reticulum stress/cell death pathways in thes

135 Glucose-regulated protein 78 (GRP78) is an endoplasmic reticulum stress chaperone that regulates th

136 esterol (FC) in macrophages, which can cause endoplasmic reticulum stress, cholesterol crystal format

137 entify cell type-specific pathways involving endoplasmic reticulum-stress, circadian signaling, ion c

138 mTORC1 activation caused endoplasmic reticulum stress, columnar cell lesions, and

139 crease in autophagic flux, and a decrease in endoplasmic reticulum stress compared to Wt mice.

140 Under endoplasmic reticulum stress conditions, induction of CS

141 he Ire1 kinase-endonuclease, activated under endoplasmic reticulum stress conditions, relieves the in

142 Furthermore, endoplasmic reticulum stress contributes to the aetiolog

143 dverse effects on mitochondrial function and endoplasmic reticulum stress, could have contributed to

144 XBP1, we observed of liver tissue persistent endoplasmic reticulum stress, defects in acute-phase res

145 t-TUCB consistently reduced endoplasmic reticulum stress demonstrated by the attenua

146 pression may contribute to the oxidative and endoplasmic reticulum stress described in PE, as well as

147 3R activity, apoptosis, phosphorylation, and endoplasmic reticulum stress did not trigger the dissoci

148 vated GCN2 kinase, whereas mitochondrial and endoplasmic reticulum stress did not.

149 ly response genes, oxidative, heat shock and endoplasmic reticulum stress, DNA damage responses, indu

150 Cytokine-induced endoplasmic reticulum stress enhanced exosome secretion

151 Moreover, subthreshold endoplasmic reticulum stress (ER stress) drove insulin d

152 1) and TRP vanilloid-3 (TRPV3) in regulating endoplasmic reticulum stress (ERS) and cytotoxicity in h

153 tic proteins BIM and BAX, JNK signaling, and endoplasmic reticulum stress, explaining why SRp55 deple

154 Cells undergoing endoplasmic reticulum stress express spliced X-box bindi

155 e R992C mutant collagen II molecules endured endoplasmic reticulum stress, had atypical polarization,

156 binding of ABA to GRP78, a key regulator of endoplasmic reticulum stress, has also been proposed.

157 ene ontology and pathway analysis identified endoplasmic reticulum stress, HIF-1 signaling, and Toll-

158 resses transcription factors associated with endoplasmic reticulum stress, human T-cell lymphotrophic

159 iant is retained intracellularly and induces endoplasmic reticulum stress identified with an XBP1-bas

160 We found that loss of ubiquilins leads to endoplasmic reticulum stress, impairs mTORC1 activity, p

161 mechanism for activation of autophagy during endoplasmic reticulum stress in Arabidopsis thaliana.

162 reticulum homeostasis and prevent cytotoxic endoplasmic reticulum stress in ccRCC.

163 vestigated whether mutant OA protein induces endoplasmic reticulum stress in D2J osteoblasts.

164 hondrial biogenesis, collagen deposition and endoplasmic reticulum stress in db/db mice.

165 uences of this variant on brain T3 activity, endoplasmic reticulum stress in glial cells, and cogniti

166 ory stress induced both oxidative stress and endoplasmic reticulum stress in HFD-fed mice livers.

167 Induction of endoplasmic reticulum stress in knockout macrophages inc

168 Reduced endoplasmic reticulum stress in response to CS exposure

169 c role, possibly by mediating the effects of endoplasmic reticulum stress in the activation of pro-at

170 ndrogen receptor, induces AR aggregation and endoplasmic reticulum stress in the prostate glands of E

171 damage, apoptosis, and DNAJC3 (a marker for endoplasmic reticulum stress) in pancreatic islets.

172 conditions such as heat or agents that cause endoplasmic reticulum stress, including tunicamycin and

173 Transforming growth factor-beta1, but not endoplasmic reticulum stress, induced FKBP10 expression

174 binding and inhibiting p53, but its role in endoplasmic reticulum stress-induced apoptosis remains u

175 SF10 expression were far more susceptible to endoplasmic reticulum stress-induced apoptosis than cont

176 plasmic reticulum stress signaling and block endoplasmic reticulum stress-induced apoptosis, cardiac

177 criptionally downregulates CHOP and inhibits endoplasmic reticulum stress-induced apoptosis.

178 response, IRE1alpha-XBP1, protects HSCs from endoplasmic reticulum stress-induced apoptosis.

179 Furthermore, P12 inhibited endoplasmic reticulum stress-induced c-Jun N-terminal ki

180 pUL38 also plays a role in blocking endoplasmic reticulum stress-induced cell death during H

181 A twofold to threefold enhancement in endoplasmic reticulum stress-induced IL-10 expression wa

182 with high kinome selectivity that prevented endoplasmic reticulum stress-induced IRE1alpha oligomeri

183 rotein metabolism and adaptive activation of endoplasmic-reticulum-stress-induced survival pathways.

184 ts for rapid adaptive response to subsequent endoplasmic reticulum-stress inducing conditions.

185 f ribonucleotide reductase (RNR) inhibition, endoplasmic reticulum stress induction, and regulation o

186 es consistent with facets of T2DM, including endoplasmic reticulum stress, inflammation, and hyperpro

187 tions include histone deacetylase inhibitor, endoplasmic reticulum stress inhibitor, ammonia sink, an

188 Using this system, we found that hypoxia and endoplasmic reticulum stress, insults commonly present i

189 We examined whether endoplasmic reticulum stress is also involved in the pat

190 Endoplasmic reticulum stress is an evolutionarily conser

191 Endoplasmic reticulum stress is defined as the accumulat

192 In mouse OIR, adipose endoplasmic reticulum stress is increased, and APN produ

193 COMP in growth plate chondrocytes activates endoplasmic reticulum stress, leading to inflammation an

194 ted on PCs demonstrated that LCDD LC induces endoplasmic reticulum stress, likely accounting for the

195 ve stress, calcium and phosphate signalling, endoplasmic reticulum stress, lipid and mineral metaboli

196 es IL-18 and IL-6 and phosphorylation of the endoplasmic reticulum stress marker inositol-requiring e

197 (AECs), which correlated with expression of endoplasmic reticulum stress markers in AECs.

198 ished the overexpression of inflammatory and endoplasmic reticulum stress markers induced by cerulein

199 Neither endoplasmic reticulum stress markers nor endoplasmic ret

200 ein 2) protein expression and activation and endoplasmic reticulum stress markers were studied.

201 increases APN production by reducing adipose endoplasmic reticulum stress markers.

202 In vitro, fumarate stimulated endoplasmic reticulum stress, matrix gene expression, an

203 tations in the WFS1 gene predispose cells to endoplasmic reticulum stress-mediated apoptosis and may

204 In addition, acrolein induced endoplasmic reticulum stress-mediated death of epithelia

205 edistribution of tight junction proteins and endoplasmic reticulum stress-mediated epithelial cell de

206 Mechanoregulation of p38 activity enhances endoplasmic reticulum stress-mediated inflammation by ar

207 on of inflammatory response, oxidative load, endoplasmic reticulum stress, mitochondrial damage, and

208 ipotoxicity with impaired membrane function, endoplasmic reticulum stress, mitochondrial dysfunction,

209 Here, we describe a crosstalk between endoplasmic reticulum stress, mTOR signalling and autoph

210 rther validated by demonstrating increase in endoplasmic reticulum stress of MDA-MB-468 cells with ti

211 of Akt-SREBP-1 activation, and inhibition of endoplasmic reticulum stress or SREBP-1 prevented angiot

212 tion of FKBP10, as well as its regulation by endoplasmic reticulum stress or transforming growth fact

213 lammation, ceramide or diglyceride contents, endoplasmic reticulum stress, or autophagy.

214 lysis in mice without evidence of autophagy, endoplasmic reticulum stress, or necroptosis.

215 d hepatic metabolic disorders, which trigger endoplasmic reticulum stress, oxidative stress, and fina

216 Our results therefore indicate that the endoplasmic reticulum stress pathway could potentially b

217 The unfolded protein response is an endoplasmic reticulum stress pathway mediated by the pro

218 previously predicted a role for CHAC1 in the endoplasmic reticulum stress pathway, linked functionall

219 he NF-kappaB-inducible nitric oxide synthase-endoplasmic reticulum stress pathway.

220 Endocrine disrupting chemicals induce endoplasmic reticulum stress, perturb NF-kappaB, and p53

221 g accumulation of ubiquitinated proteins and endoplasmic reticulum stress-related apoptosis in variou

222 Endoplasmic reticulum stress-related dysfunction in Wolf

223 ticulum stress identified with an XBP1-based endoplasmic reticulum stress reporter.

224 ne CASP3 is likely governed by an integrated endoplasmic reticulum stress response (ERSR) and is cons

225 lpha/ATF4 signaling branch of the integrated endoplasmic reticulum stress response (IERSR) is activat

226 signs of immunogenic cell death including an endoplasmic reticulum stress response and exposure of ca

227 ion causes tissue damage, which triggers the endoplasmic reticulum stress response and subsequent eic

228 l, we confirmed that podocyte injury induces endoplasmic reticulum stress response and upregulated un

229 T1 blockage does not alter mTOR signaling or endoplasmic reticulum stress response but can be modulat

230 cal functions in triglycerides transport and endoplasmic reticulum stress response due to its unique

231 ous GWAS findings in the HLA region; and (3) endoplasmic reticulum stress response genes.

232 The endoplasmic reticulum stress response in the TLR9/RP105-

233 itochondrial respiration, as a result of the endoplasmic reticulum stress response induced by high pr

234 The integrated endoplasmic reticulum stress response inLeishmania amazo

235 vidence suggests that after podocyte injury, endoplasmic reticulum stress response is activated, but

236 Our studies illuminate how the adaptive endoplasmic reticulum stress response is advantageous in

237 stimulate protein synthesis, resulting in an endoplasmic reticulum stress response mediated by Perk.

238 have illustrated detrimental changes in the endoplasmic reticulum stress response or unfolded protei

239 endritic cells resulted in activation of the endoplasmic reticulum stress response pathway and marker

240 The unfolded protein response (UPR), an endoplasmic reticulum stress response pathway, has been

241 ing phagocytosis through an unfolded protein/endoplasmic reticulum stress response pathway, resulting

242 d activation of the proapoptotic arms of the endoplasmic reticulum stress response that is probably s

243 testing of small-molecule modulators of the endoplasmic reticulum stress response, which improved bo

244 ggesting that specific TG6 mutants elicit an endoplasmic reticulum stress response.

245 effect due to the latter's ability to induce endoplasmic reticulum stress response.

246 ls was TNFalpha independent but involved the endoplasmic reticulum stress response.

247 tro and in vivo, and subsequent induction of endoplasmic reticulum stress response.

248 critical tumor suppressor by augmenting the endoplasmic reticulum stress response.

249 uroplasticity and deployment of a successful endoplasmic reticulum stress response.

250 iption factor DDIT3 which is associated with endoplasmic reticulum-stress response.

251 ced proliferation, increased metabolism, and endoplasmic reticulum stress-response activation in trop

252 machinery and the IRE1-alpha-MKK4 arm of the endoplasmic-reticulum-stress-response pathway.

253 er, treatment with adropin(34-76) alleviated endoplasmic reticulum stress responses and reduced activ

254 Both inflammation and endoplasmic reticulum stress responses are significantly

255 e incidence of inflammation and induction of endoplasmic reticulum stress responses during an extende

256 Recent findings have linked endoplasmic reticulum stress responses mediated by inosi

257 ticulum-mitochondria cross-talk, or reducing endoplasmic reticulum stress, restore the mitochondria m

258 T protein aggregates in hepatocytes leads to endoplasmic reticulum stress, resulting in impairment of

259 enzyme-1 alpha (IRE1alpha) protein caused by endoplasmic reticulum stress results in the homodimeriza

260 lular stress, including oxidative stress and endoplasmic reticulum stress, secondary to increased dem

261 Here, we demonstrate that the endoplasmic reticulum stress sensor inositol-requiring e

262 pathway causing cardiac hypertrophy involves endoplasmic reticulum stress sensor PERK (protein kinase

263 ough augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring

264 w that during Brucella abortus infection, an endoplasmic reticulum stress sensor, IRE1alpha, initiate

265 master stress regulator-detaches from three endoplasmic reticulum stress sensors (IRE1alpha, PERK, a

266 GGF1 protein therapy and miR-183-5p regulate endoplasmic reticulum stress signaling and block endopla

267 onical, AGGF1-mediated regulatory system for endoplasmic reticulum stress signaling associated with i

268 Mechanistically, AGGF1 regulates endoplasmic reticulum stress signaling by inhibiting ERK

269 ence of alpha-synuclein expression, specific endoplasmic reticulum stress signaling events were signi

270 el consistently associated with induction of endoplasmic reticulum stress signaling in mouse models a

271 This protein complex is also essential for endoplasmic reticulum stress signaling induction, possib

272 The major endoplasmic reticulum stress signaling pathway causing c

273 CM-P), phosphorylation of stress kinases and endoplasmic reticulum stress signaling was increased, in

274 adipokines and macrophage infiltration), the endoplasmic reticulum stress signaling, and decrease of

275 tes to antiapoptotic-like cell death via the endoplasmic reticulum stress-signaling pathway rather th

276 ndidate genes at the beta-cell level and the endoplasmic reticulum stress signalling that contributes

277 f glioma proliferation rate, malignancy, and endoplasmic reticulum stress statuses.

278 100 only) exhibited only subtle increases in endoplasmic reticulum stress, suggesting that an altered

279 RCN1 mutant cell lines were revealed to have endoplasmic reticulum stress, suggesting the involvement

280 endoplasmic reticulum (ER) is ensured by the endoplasmic reticulum stress surveillance (ERSU) pathway

281 in 1 (Pdx1) regulates beta-cell survival and endoplasmic reticulum stress susceptibility, in part thr

282 osphatase, are healthy and more resistant to endoplasmic reticulum stress than wild type controls.

283 els a novel link between innate immunity and endoplasmic reticulum stress that is crucial for bacteri

284 Accumulation of misfolded proteins triggers endoplasmic reticulum stress that leads to unfolded prot

285 veolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the

286 resulting in the induction of oxidative and endoplasmic reticulum stress, the formation of the infla

287 breast cancer cells 1 induces DNA damage and endoplasmic reticulum stress, the latter being responsib

288 tokine and microbial stimulation to suppress endoplasmic reticulum stress, thereby assuring antiinfla

289 Cells are protected from endoplasmic reticulum stress through the unfolded protei

290 SREBP-1 and endoplasmic reticulum stress thus provide potential nove

291 entiation, linking unfolded protein response/endoplasmic reticulum stress to secretory optimization,

292 ere, we report an unexpected function of the endoplasmic reticulum stress transducer IRE1alpha as a s

293 CN results from mutant ELANE, which triggers endoplasmic reticulum stress, UPR, and apoptosis.

294 Notably, angiotensin II-induced endoplasmic reticulum stress was identified as a key med

295 Endoplasmic reticulum stress was not found to be a major

296 iptional and translational analyses revealed endoplasmic reticulum stress was not the etiology of our

297 8), and C/EBP-homologous protein, markers of endoplasmic reticulum stress, was more prominent in the

298 rkers of inflammation, oxidative stress, and endoplasmic reticulum stress were assessed in healthy pi

299 Myocardial markers of endoplasmic reticulum stress were expressed higher in ES

300 myeloid cells, polyploidization can trigger endoplasmic reticulum stress with consequent exposure of