ライフサイエンスコーパス: ER stress

1 endothelial cells suppresses miR-204-induced ER stress.

2 cies of how the UPR evaluates and alleviates ER stress.

3 cancer, activates UPR and results in chronic ER stress.

4 aviour and function in an attempt to relieve ER stress.

5 cholic acid (TUDCA), a specific inhibitor of ER stress.

6 ractions, one homeostatic and one induced by ER stress.

7 croRNAs play an important role in regulating ER stress.

8 ECM proteins in the ER of TM cells, inducing ER stress.

9 ol-requiring enzyme 1 (IRE1) under temporary ER stress.

10 percomplex assembly of the mitochondria, and ER stress.

11 ssion of mutant MYOC, resulting in relief of ER stress.

12 exposed to cytokines or thapsigargin-induced ER stress.

13 XBP1u mRNA is recruited for cleavage during ER stress.

14 for RyR1 myopathies that are associated with ER stress.

15 ein response and promotes cell survival upon ER stress.

16 proteostasis in the presence and absence of ER stress.

17 n coupled with unfolded protein response and ER stress.

18 ein response (UPR) is activated to cope with ER stress.

19 genesis and bone healing via suppressing the ER stress.

20 ith GET dysfunctions are more susceptible to ER stress.

21 itochondrial network in the absence of overt ER stress.

22 betes was also shown to induce activation of ER stress.

23 rescued by inhibition of rRNA processing or ER stress.

24 e investigated the role of Parkin in cardiac ER stress.

25 nal was administered to evaluate the role of ER stress.

26 e endoplasmic reticulum (ER), referred to as ER stress.

27 m (ER) homeostasis create a condition termed ER stress.

28 protein response, associated with sustained ER stress.

29 potent transcription factor adaptive toward ER stress.

30 survival in the face of recursive, transient ER stress.

31 tate glands indicate the presence of chronic ER stress.

32 resident ER chaperones, indicating increased ER stress.

33 lving GRP78 trimethylation in the context of ER stress.

34 ptosis and steatosis associated with hepatic ER stress.

35 rentiation induced by endoplasmic reticulum (ER) stress.

36 -factor limitation or endoplasmic reticulum (ER) stress.

37 nsitizes cells to the endoplasmic reticulum (ER) stress.

38 paired autophagy, and endoplasmic reticulum (ER) stress.

39 iR-204 expression and endoplasmic reticulum (ER) stress.

40 es (STING) to mediate endoplasmic reticulum (ER) stress.

41 nd in the response to endoplasmic reticulum (ER) stress.

42 cellular response to endoplasmic reticulum (ER) stress.

43 insults that lead to endoplasmic reticulum (ER) stress.

44 mechanism induced by endoplasmic reticulum (ER) stress.

45 manifestations is the endoplasmic reticulum (ER) stress.

46 ine (5-aza) underwent endoplasmic reticulum (ER) stress.

47 ble linkage of ischemic osteonecrosis to the ER stress, a surgery-induced animal model was employed a

48 on of both the unfolded protein response and ER stress accompanied by increased autophagic activity a

49 mutants get1 and get3 were less tolerant of ER stress agents and showed symptoms of ER stress even u

50 ron chelator ciclopirox (CPX), which reduces ER stress, alleviated the cytotoxicity of 5-aza.

51 onomous mechanisms that involve induction of ER stress also participate.

52 igation demonstrated (1) that indicators for ER stress and activation markers for fibroblasts were el

53 Here, we show that oncogenic HRas induces ER stress and activation of IRE1alpha.

54 the ameloblast secretory pathway leading to ER stress and an activated unfolded protein response (UP

55 atment with ABT-627 failed to decrease renal ER stress and apoptosis in ETB def rats.

56 ro, we showed RTN1A mediates albumin-induced ER stress and apoptosis in human podocytes.

57 the development of tunicamycin-induced renal ER stress and apoptosis.

58 o Hepa-1c1c7 cells induced oxidative stress, ER stress and apoptosis.

59 Inhibition of VCP/p97 induces proteotoxic ER stress and cell death in cancer cells, making it an a

60 (EtOH) and cigarette smoke extract (CSE) on ER stress and cell death responses in mouse and human pr

61 iosynthesis during stress, thus ameliorating ER stress and cell death.

62 in secretion and ER/Golgi morphology, causes ER stress and defects in cell shape.

63 A miR-204 mimic leads to ER stress and downregulates Sirt1 in endothelial cells.

64 In summary, CIRP induces lung ER stress and downstream responses to cause sepsis-assoc

65 in wild type isolated islets stimulated with ER stress and in ob/ob isolated islets at baseline.

66 inar Sec23b deletion results in induction of ER stress and increased apoptosis in the pancreas, poten

67 PBA-dosed mice exhibited the lower levels of ER stress and M2 macrophage markers than those from cGVH

68 a previously unappreciated link between the ER stress and oxidative stress gene programs, supporting

69 Here Cao et al. show that LPS induces ER stress and P300 activity via the XBP1/IRE1 pathway.

70 ssion was inducible by paracrine transfer of ER stress and pro-inflammation between different pancrea

71 esistance in pancreatic cancer by regulating ER stress and stemness.

72 However, the relationship between ER stress and the integrity of BSCB in diabetic rats aft

73 the hypothalamus was sufficient to alleviate ER stress and to revert the obese and metabolic phenotyp

74 onship between ORMDL3 and rhinovirus-induced ER stress and type I IFN in human leucocytes.

75 It induced endoplasmic reticulum (ER) stress and activated the protective inositol-requiri

76 vel led to attenuated endoplasmic reticulum (ER) stress and cell death.

77 relationship between endoplasmic reticulum (ER) stress and cGVHD, and aimed to create effective trea

78 d that ORMDL3 induces endoplasmic reticulum (ER) stress and production of the type I interferon (IFN)

79 The role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in re

80 notypes and endocrine dysregulation, but not ER-stress and p53-phosphorylation changes.Harmful chemic

81 its nuclear translocation were prevented by ER-stress and PERK inhibitors, suggesting that PERK axis

82 ur findings demonstrate that AGR2 induced in ER-stressed and inflammatory pre-neoplastic pancreas is

83 h sequesters stressed ER membranes, resolves ER stress, and curtails phagocyte death.

84 lures in the secretion of nonbulky proteins, ER stress, and defective cell morphology are secondary c

85 he disruption of BSCB after SCI via inducing ER stress, and inhibition of ER stress by 4-PBA may play

86 reatitis, mitochondrial function, autophagy, ER stress, and lipid metabolism were measured in pancrea

87 d ECs to restore protein synthesis, suppress ER stress, and reactivate mTOR signaling.

88 mic reticulum (ER) dilatation, suggestive of ER stress, and smaller insulin crystal diameters in beta

89 nstream target genes, even in the absence of ER stress; and class 3 ATF6 mutants have complete loss o

90 ization, activation, and inactivation during ER stress are regulated by Sec61.

91 Oxidative and endoplasmic reticulum (ER) stresses are hallmarks of the pathophysiology of ALS

92 Endoplasmic reticulum (ER) stress arises from accumulation of misfolded/unfolde

93 g evidence implicates endoplasmic reticulum (ER) stress as a mediator of impaired lipid metabolism, t

94 nst tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependen

95 e required to elicit apoptosis by activating ER stress-associated caspase 4/12.

96 protein homologous protein (CHOP), the major ER stress-associated proapoptotic transcription factor,

97 In response to endoplasmic reticulum (ER) stress, ATF6 migrates from the ER to Golgi to underg

98 olic inflammation and endoplasmic reticulum (ER) stress, both of which promote metabolic disease prog

99 eta-galactosidase reporters, and survival of ER stress, but it had no effect on clustering of Ire1.

100 justing BiP's activity to changing levels of ER stress, but the underlying molecular details are unex

101 CI via inducing ER stress, and inhibition of ER stress by 4-PBA may play a beneficial role on the int

102 however completely rescued on activation of ER stress by additional deletion of Grp78.

103 mutations in type X collagen, which increase ER stress by inducing misfolding of the mutant protein a

104 ein response (UPR) to endoplasmic reticulum (ER) stress by Mvarphis in a longitudinal study of fish-d

105 pathway that relieves endoplasmic reticulum (ER) stress by promoting ER-associated degradation (ERAD)

106 hat metformin induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent u

107 We show here that ER stress causes the aggregation of proteins, most of wh

108 RATIONALE: Endoplasmic reticulum (ER) stress causes the accumulation of misfolded proteins

109 Ribosome profiling in ER-stressed cells lacking these factors revealed that Ir

110 hepatic zinc uptake in Zip14 KO mice during ER stress coincides with greater expression of proapopto

111 c61 translocon interaction as well as severe ER stress conditions causes IRE1alpha to form higher-ord

112 and may determine cell fate decisions during ER stress conditions.

113 ggregation and protects a UPR mutant against ER stress conditions.

114 he activation of caspase 12, suggesting that ER stress contributes to cell death.

115 In acute/transient ER stress, decreased global protein synthesis and increa

116 anagement of the tradeoff between growth and ER stress defense by the stress response hormone salicyl

117 tical surveillance strategy for plant growth-ER stress defense tradeoffs based on CPR5 and SA-modulat

118 overexpression of dimeric ERdj3 exacerbates ER stress-dependent reductions in the secretion of a des

119 rmine whether the ET-1 system promotes renal ER stress development in response to tunicamycin.

120 l factors, Atf6 and Ire1alpha during chronic ER stress due to presence of ERG in prostate epithelium

121 to limit the amino acid response and prevent ER stress during amino acid depletion by asparaginase.

122 play an important role in the development of ER stress during hyperglycemia.

123 Surprisingly, cells undergoing ER stress during inflammatory stimulation showed reduced

124 for how sustained activation of PERK axis of ER-stress during chronic HCV infection activates oncogen

125 that the PERK axis of endoplasmic reticulum (ER) stress elicited prominent nuclear translocation of N

126 Endoplasmic reticulum (ER) stress elicits EC dysregulation in metabolic syndrom

127 iver fibrosis by promoting nitroxidative and ER stress, endotoxemia, inflammation, IR, and low TEE.

128 rs orchestrating metabolic inflammation, and ER stress enhances macrophage activation.

129 t of ER stress agents and showed symptoms of ER stress even under unstressed conditions.

130 ce to overt diabetes; endoplasmic reticulum (ER) stress expedites beta cell failure in this situation

131 f Plin2 in Akita mice leads to mitigation of ER stress, forestalling beta cell apoptosis, partially r

132 TM cells were more prone to ER stress from ECM accumulation compared to other ocular

133 that IRE1 inhibitors uncouple lipid-induced ER stress from inflammasome activation in both mouse and

134 al function of BAP1 in the regulation of the ER stress gene-regulatory network.

135 Silencing of PECAM-1 or key ER stress genes abrogated SS regulation of VCAM-1 transc

136 ETA receptor activation induces renal ER stress genes and apoptosis, while functional activati

137 otype on the expression of ORMDL3, IFNB1 and ER stress genes were assessed.

138 Endoplasmic reticulum (ER) stress has been recognized to play an important role

139 Chronic endoplasmic reticulum (ER) stress has recently emerged as a mechanism for neuro

140 Mitochondrial dysfunction caused pancreatic ER stress, impaired autophagy, and deregulation of lipid

141 l activation, indicating that the UPR senses ER stress in a ratiometric fashion.

142 these chemokines was partially controlled by ER stress in a signal transducer and activator of transc

143 diet, exposure to cigarette smoke increased ER stress in acinar cells and sensitized the pancreas to

144 the UPR in the first 48 h and benefits from ER stress in an amino acid-dependent manner.

145 tumorigenic and immunoregulatory effects of ER stress in cancer, and we explore the concept of targe

146 ER-Golgi contacts fail to form during ER stress in cells lacking Nvj2p.

147 major regulator of ECM structure, prevented ER stress in Dex-treated TM cells.

148 nt of cGVHD, we investigated cGVHD-triggered ER stress in fibroblasts and macrophages.

149 We report a novel role for ER stress in mechanoregulation at arterial regions of at

150 ia the ER stress pathway and amelioration of ER stress in mice completely abolishes high fat diet-ind

151 ates the unfolded protein response (UPR) and ER stress in pancreatic beta cells.

152 Here, we determined the roles of RTN1A and ER stress in podocyte injury and DN.

153 in DN and RTN1A might be a key regulator of ER stress in podocytes.

154 1A and CHOP was found leading to an enhanced ER stress in podocytes.

155 th cellular fibronectin also induced chronic ER stress in primary human TM cells.

156 rs from thapsigargin- or tunicamycin-induced ER stress in promoting GADD34 transcription and the pref

157 ell types, we hypothesized that ARV-mediated ER stress in the central nervous system resulted in chro

158 ation, exhibit elevated PLIN2 expression and ER stress in their beta cells.

159 henylbutyrate, uncovering the involvement of ER stress in this response.

160 tamine-dependent survival and sensitivity to ER stress in USF3-deficient cells provide avenues for th

161 y tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells,

162 (RTN) 1A in mediating endoplasmic reticulum (ER) stress in kidney tubular cells and the expression of

163 accumulation leads to endoplasmic reticulum (ER) stress in the TM.

164 isfolding, leading to endoplasmic reticulum (ER) stress in the trabecular meshwork (TM), the tissue t

165 well as management of endoplasmic reticulum (ER) stress in unfavorable growth conditions.

166 eir ability to induce endoplasmic reticulum (ER) stress in various cell types, we hypothesized that A

167 his coincided with reduced cytokine-mediated ER stress, indicated by measurements of CCAAT/enhancer-b

168 Real-time PCR and ELISA analyses showed that ER stress induced a pro-inflammatory phenotype in pancre

169 ER stress-induced apoptosis is regulated by the highly l

170 , deficient in Trpc3 are less susceptible to ER stress-induced apoptosis than Trpc3 expressing cells.

171 h in stress conditions through repression of ER stress-induced bZIP28/IRE1-bZIP60 arms.

172 blunt excessive CHOP to prevent maladaptive ER stress-induced cell death and adverse cardiac ventric

173 Loss of ER stress-induced CMA activation sensitizes cells to ER

174 s-induced CMA activation sensitizes cells to ER stress-induced death.

175 ive 13d markedly protects beta-cells against ER stress-induced dysfunction and death with near 100% m

176 class of beta-cell protective agents against ER stress-induced dysfunction and death.

177 he transcription regulator TRIP-Br2 mediates ER stress-induced inhibition of lipolysis and thermogene

178 e show that ablation of TRIP-Br2 ameliorates ER stress-induced inhibition on lipolysis, fatty acid ox

179 A receptor as a therapeutic approach against ER stress-induced kidney injury.

180 e-associated BAX inhibitor 1 (BI1) modulates ER stress-induced programmed cell death through yet-unkn

181 dy by Shan et al. (2017), which demonstrated ER stress-induced rewiring of adipose tissue macrophage

182 atty acid synthesis, which are suppressed in ER stress-induced WT mice.

183 ER stress-induced Zip14 KO mice show greater levels of h

184 gate the function of cathepsin B and PBA1 in ER-stress-induced PCD (ERSID).

185 s are exposed to a lipid load or to chemical ER stress inducers.

186 We hypothesize that unresolved ER stress induces the inflammatory responses observed in

187 ER stress induction led to a reduced ECD protein level,

188 such as oxidative and endoplasmic reticulum (ER) stress, inflammation, and insulin resistance (IR) we

189 cription 3 (STAT3)-dependent manner, whereby ER stress inhibited STAT3 activation.

190 4-phenylbutyric acid (4-PBA), an ER stress inhibitor lowered the adverse effect of diabet

191 By contrast, treatment of PCOS mice with an ER stress inhibitor, tauroursodeoxycholic acid or BGP-15

192 Endoplasmic reticulum (ER) stress initiates an important mechanism for cell ada

193 and the contribution of excess CHOP to this ER stress injury was confirmed by reduction in TM-induce

194 o-survival factor, with yet unknown roles in ER stress, interacts with active IRE1alpha, inhibits bot

195 This suggests that ER stress interferes with Wnt signalling downstream of n

196 In conclusion, our data demonstrated that ER stress is a novel target to ameliorate OI phenotype;

197 By 72 h, ER stress is alleviated and ERAD proceeds unhindered.

198 ely, the results support the notion that the ER stress is an important pathological outcome in the su

199 luenza A virus (IAV) are expressed in cells, ER stress is induced, resulting in rapid HA degradation

200 The onset of ER stress is known to correlate with various disease pro

201 However, a role for zinc during hepatic ER stress is largely unknown despite important roles in

202 vascular reactive oxygen species induced by ER stress is mitigated by by miR-204 inhibition.

203 ge on the molecular mechanism of how chronic ER stress is stimulated and leads to cell death in pancr

204 We hypothesize that ER stress is the aetiological factor in this case of hum

205 Endoplasmic reticulum (ER) stress is a local factor that affects various cellul

206 eath (PCD) induced by endoplasmic reticulum (ER) stress is implicated in various plant physiological

207 ry control of cardiac endoplasmic reticulum (ER) stress is incompletely characterized.

208 ween the ER and other organelles, but during ER stress, it relocalizes to and increases ER-Golgi cont

209 (PI) class ARVs induced neuronal damage and ER stress, leading to PKR-like ER kinase-dependent phosp

210 ER stress leads to de novo biosynthesis of non-trimethyl

211 t inhibition of Sp1, as well as induction of ER stress, leads to lysosomal membrane permeabilization

212 , is a master regulator of the UPR, reducing ER stress levels and apoptosis due to an enhancement of

213 were associated with reduction of RTN1A and ER stress marker expression in the podocytes of TUDCA-tr

214 Lung ER stress markers (BiP, pIRE1alpha, sXBP1, CHOP, cleaved

215 LIX and ALG-2 levels are detected along with ER stress markers and associated caspases in transgenic

216 mycin treatment similarly increased cortical ER stress markers in both rat genotypes; however, only E

217 We found increased expression of RTN1A and ER stress markers in the kidney of db/db-Unx mice.

218 phic zone, attenuated enhanced expression of ER stress markers such as Bip and Atf4, increased bone g

219 creased co-localization of ECM proteins with ER stress markers was observed in human post-mortem glau

220 ER stress markers were increased in the lungs of healthy

221 ma2-AMPK led to increases in pre-rRNA level, ER stress markers, and cell death during glucose depriva

222 CM derived from Dex-treated TM cells induced ER stress markers.

223 such as cystic fibrosis (CF), and targeting ER stress may be useful for alleviating damaging neutrop

224 lcium homeostasis can mitigate cytokine- and ER stress-mediated beta cell death.

225 AS) meta-analysis to determine modulators of ER stress-mediated inflammation.

226 apoptosis due to increased expression of the ER stress mediator tribbles-3.

227 The endoplasmic reticulum (ER) stress occurs frequently in cancers.

228 Endoplasmic reticulum (ER) stress occurs in the early stages of SCI and affects

229 the existence of two independent effects of ER stress on PCSK9 expression and secretion.

230 maceutical interventions designed to relieve ER stress or modulate the UPR during enamel development

231 Paradoxically, reduced ER stress or Xbp1 splicing promotes growth arrest and pr

232 Reduction of ER stress or Xbp1 splicing using pharmacological, geneti

233 brown adipocytes TRIP-Br2 expression via the ER stress pathway and amelioration of ER stress in mice

234 te antiviral response through activating the ER stress pathway during viral infection.

235 Thus, the ER stress pathway senses influenza HA as "nonself" or mi

236 viral innate immunity is triggered after the ER stress pathway senses viral glycoproteins.

237 It also activates ER stress pathways that promote acinar cell death.

238 However, whether ER stress pathways underlie ATM regulation of energy hom

239 nal derivatives from these iPSCs revealed an ER stress phenotype, marked by induction of the IRE1alph

240 Our data suggest that ER stress plays a major role in podocyte injury in DN an

241 Therefore, ER stress poses a promising target in colorectal cancers

242 ic zinc uptake is critical for adaptation to ER stress, preventing sustained apoptosis and steatosis.

243 phy and heart failure.Endoplasmic reticulum (ER) stress promotes cardiac dysfunction.

244 sitive Hsp40 whose degradation during severe ER stress provides a mechanism to promote BOK accumulati

245 beta-cell-protective small molecules against ER stress provides a new promising modality for the trea

246 erization of IRE1, a conserved transmembrane ER stress receptor.

247 However, conditions that cause ER stress regardless of their ability to dysregulate ER

248 his by generating mice in which both Apc and ER stress repressor chaperone Grp78 can be conditionally

249 s by bacteria-induced endoplasmic reticulum (ER) stress, required extrinsic signals from innate lymph

250 uates the pro-survival function of bZIP28 in ER stress resolution and, differently to animal cells, i

251 cial role for PLIN2 in modulating autophagy, ER stress resolution, and beta cell apoptosis and surviv

252 with genetic mutations that affect both the ER stress response and autophagy.

253 We show that Liraglutide modulates the ER stress response and elicits ER proteostasis and autop

254 Sp1 results in its decreased binding to the ER stress response element present in the promoter regio

255 transcription factor 6 alpha), which induces ER stress response genes.

256 icamycin injection significantly reduced the ER stress response in cortex and medulla, and also inhib

257 amplification of the amino acid response and ER stress response transcriptional signatures.

258 Myocardial ischemia induces the ER stress response; however, neither the function of thi

259 hat ECD regulates the endoplasmic reticulum (ER) stress response.

260 restores cell morphology and attenuates the ER-stress response.

261 cer, and we explore the concept of targeting ER stress responses to enhance the efficacy of standard

262 We found that IAV HA glycoproteins induce ER stress, resulting in HA degradation via ERAD and cons

263 an and yeast IRE1 use a common mechanism for ER stress sensing.

264 ivates the transcription factor XBP1 via the ER stress sensor IRE1, resulting in the induction of P30

265 by unfolded protein response.IRE1alpha is an ER stress sensor, whose activity induces apoptosis.

266 phological alterations and the expression of ER stress sensors Atf6, Ire1alpha, Perk, their downstrea

267 tate of "ER stress." Sustained activation of ER stress sensors endows malignant cells with greater tu

268 ted well with the differential regulation of ER stress sensors, in particular Perk.

269 increases in response to tunicamycin-induced ER stress, serum deprivation or reduced levels of mitofu

270 ed a role of CYP450 and consequent oxidative ER stress signaling in these effects.

271 As ER stress signaling upregulates the E3-ubiquitin ligase

272 In conclusion, our findings indicate that ER stress signalling results in loss of Apc mutated inte

273 ession, and UPR RNA signature, and decreased ER stress signature.

274 (ER), thereby provoking a cellular state of "ER stress." Sustained activation of ER stress sensors en

275 poorly investigated, as in most studies the ER stress that is elicited cannot be overcome.

276 t due to induction of endoplasmic reticulum (ER) stress that resulted in apoptosis.

277 During ER stress, the inositol requiring enzyme 1alpha (IRE1alp

278 During ER stress, the UPR-activated transcription factors ATF4

279 ter region of Grp78, the master regulator of ER stress, thereby preventing homeostasis.

280 the form of a Western diet promotes vascular ER stress through miR-204.

281 ded protein response and thus directly links ER stress to ER-phagy.

282 However, the coupling of ER stress to IRE1 oligomerization and activation has rem

283 During ER stress, transport is activated by UPR-dependent Ero1

284 Endoplasmic reticulum (ER) stress, triggered by unfolded protein accumulation i

285 Pharmacological inducers of ER stress, tunicamycin and thapsigargin, were found to i

286 one, sodium 4-phenylbutyrate (4PBA), reduces ER stress/UPR and improves muscle function, but does not

287 pharmacologically and high-fat diet-induced ER stress using Zip14(-/-) (KO) mice, which exhibit impa

288 y, this study suggests that the reduction of ER stress utilizing PBA can be a clinically translatable

289 spatial metric of EC orientation, markers of ER stress, VCAM-1 and ICAM-1 expression, and monocyte re

290 This suggests CIRP directly induces ER stress via TLR4 activation.

291 etion of endothelial Sirt1 in mice, promotes ER stress via upregulation of miR-204, whereas overexpre

292 In the present study, we showed that ER stress was activated in granulosa cells of PCOS patie

293 The results indicated that the ER stress was associated with ONFH and salubrinal signif

294 ER stress was monitored by measuring HSPA5, CHOP and spl

295 nistered thapsigargin displayed hypothalamic ER stress, whereas genetic overexpression of GRP78 speci

296 effects of fatty acid- and chemical-induced ER stress, whereas PLIN2 overexpression exacerbates them

297 Its activation serves as a key sensor of ER stress, which has been implicated in traumatic brain

298 the Sec61 translocon that is activated upon ER stress with little change in the complex.

299 Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav

300 gulated by triggering endoplasmic reticulum (ER) stress with thapsigargin and in islets of ob/ob mice