ライフサイエンスコーパス: ER

1 ER calcium depletion robustly activates the unfolded pro

2 ER tubules formed by Drp1 promote mitochondrial division

3 ER-PB contact and PB biogenesis were modulated by alteri

4 pective study with the collected data of 171 ER patients.

5 Thus, [Ca(2+)](ER) is a major regulator of InsP(3)R channel activity an

6 ectomy, and in the remaining 36 patients, 70 ERs and 111 ablations were performed.

7 n but also controls cellular defense against ER and oxidative stress.

8 ry role in macrophages by protecting against ER stress and promoting anti-inflammatory polarization.

9 est that an insulin sensitizer may alleviate ER stress associated with YIPF5 disruption by decreasing

10 is located within the Golgi, where it allows ER-escaped glycoproteins to bypass the classical N-glyco

11 e to two classes of estrogen receptor-alpha (ER) antagonists.

12 shomeostasis and apoptosis, and iii) altered ER Ca(2+) homeostasis in kidney disease, including podoc

13 ibitor tauroursodeoxycholic acid ameliorates ER stress and fibrosis in Grp78 KO mouse and IPF lung sl

14 hown that the helices align TANGO1 around an ER exit site.

15 howed that this ERAD branch is defined by an ER membrane complex consisting of the ubiquitin ligase R

16 result in full hospitalization following an ER visit.

17 IRE1beta is an ER stress sensor uniquely expressed in epithelial cells

18 ocyte-derived neurotrophic factor (MANF), an ER-resident protein with no known structural homologs an

19 increased autophagy and up-regulation of an ER stress-responsive chaperone.

20 on of genes predicted to be regulated via an ER-2 motif.

21 for extraction of mislocalized tail-anchored ER proteins from the mitochondrial outer membrane.

22 Neither GES nor NPC learned that HER2 and ER are direct risk factors.

23 lular stresses, such as viral infections and ER stress, leads to the regulation of mRNA stability and

24 lls from old mice and patients with IPF, and ER stress inhibitor tauroursodeoxycholic acid ameliorate

25 y mediate the independent effects of OSE and ER on food intake.

26 ependent and simultaneous effects of OSE and ER on satiation and associated endocrine responses.

27 te tubular injury is mediated by oxidant and ER stress.

28 Therefore, IL6/STAT3 and ER oncogenic pathways are functionally decoupled, highli

29 these enhancers are shared by both STAT3 and ER, IL6/STAT3 activity is refractory to standard ER-targ

30 tegrated unfolded protein response (UPR) and ER-associated degradation (ERAD) are the primary mechani

31 d by the unfolded protein response (UPR) and ER-associated degradation (ERAD).

32 By choosing an appropriate ER signal sequence and expression vector, this simple te

33 and significance of using metal complexes as ER stress-inducing agents for the treatment of cancer is

34 Diverse forms of cell stress, such as ER stress or mitochondrial stress, can also promote infl

35 Ca(2+) uptake pump, sarco/ER Ca(2+) ATPase, ER Ca(2+) release channels, inositol 1,4,5-trisphosphate

36 mechanism to prevent membrane mixing between ER and the retrograde membrane.

37 r obstacle that hinders their utility beyond ER(+) breast cancer.

38 When we blocked ER motility using a dominant negative approach against m

39 We conclude that the brief ER visits to active spines have the important function o

40 ng at the majority of loci normally bound by ER.

41 ression is induced in hepatic macrophages by ER stress, and VDR plays a dual regulatory role in macro

42 on metal-based anticancer agents that cause ER stress.

43 , disturbed the epigenetic state, and caused ER stress, while melatonin reduced this damage.

44 suggest that PI3K pathway dysfunction causes ER stress that may drive the pathogenesis of several dis

45 ce the understanding of poorly characterized ER stress-dependent RIP.

46 s were modulated by altering PB composition, ER shape, or ER translational capacity.

47 s for defects in the degradation of cortical ER following treatment with rapamycin, a drug that mimic

48 nsgenic mice with ubiquitously expressed Cre/ER and the Cre-inducible fluorescent reporter YFP.

49 This study demonstrates ER has comparable long-term outcomes for clinical T1aN0

50 Because I/R impairs oxygen-dependent ER protein disulfide formation and such impairment can b

51 nthases Lro1 and Dga1 are formed at discrete ER subdomains defined by seipin (Fld1), and a regulator

52 Treatment of mice with disseminated ER+ human breast cancer showed that D9 plus MK-2206 bloc

53 While some dSTACs elicit ER subtype-selectivity in the presence of hormone, most

54 on and activation of estrogen receptor (ESR1/ER) and its target genes (PGR, KRT8/CK8, BCL2), which ar

55 The C-terminal domain facilitates ER export of proSP-B.

56 ranscription factor XBP1s, which facilitates ER-mediated protein folding.

57 omote mitochondrial division by facilitating ER-mitochondria interactions.

58 ve the ER on microtubules to generate a fine ER network.

59 sting of ductal carcinoma in situ (DCIS) for ER is recommended to determine potential benefit of endo

60 al during gametogenesis and are required for ER-localized phospholipid metabolism in vegetative and r

61 r, these results support a critical role for ER Ca(2+) depletion-activated Ca(2+) current in mediatin

62 ons: These results support a causal role for ER stress and resulting epithelial dysfunction in PF and

63 ed over a decade ago in a genetic screen for ER protein homeostasis.

64 The corresponding 5-year survival for ER and esophagectomy were 53% versus 61% (P = 0.3), resp

65 Furthermore, ER contact sites defined the position where PB and stres

66 S) based on clinical T/N stage, tumor grade, ER, PR, HER2, number of metastatic sites, and presence o

67 f VDR in macrophages are critical in hepatic ER stress resolution in mice.

68 sed on: i) Ca(2+) homeostasis in the ER, ii) ER Ca(2+) dyshomeostasis and apoptosis, and iii) altered

69 We identified patients with stage I-III ER+/HER2- breast cancer.

70 nct membrane network, while breaks appear in ER-like, pore-free regions.

71 variety of cis-regulatory elements (CREs) in ER stress-responsive gene promoters.

72 ha gene (ESR1) mutations occur frequently in ER-positive metastatic breast cancer, and confer clinica

73 ects of the pure antiestrogen fulvestrant in ER(+) breast cancer and evaluate its effects under physi

74 PREX1 levels are significantly increased in ER+ tumors and associated with invasive disease and dist

75 ker of resistance to PI3Kalpha inhibition in ER(+) breast cancer.

76 IC cohort revealed that higher PREX1 mRNA in ER(+ve)/luminal tumors was associated with poor outcome

77 Human VKOR needs to be preserved in ER-enriched microsomes to exhibit warfarin sensitivity,

78 al an unexpected role for TRAIL receptors in ER-stress-induced inflammation.

79 mechanism underlying endocrine resistance in ER+ breast cancer.

80 ular changes during infection that result in ER stress.

81 potential of IL6/STAT3-targeted therapies in ER(+) breast cancer.

82 nd dafachronic acid respectively to increase ER and DAF-12 coactivation by the sirtuins.

83 e expressed a low affinity Ca(2+) indicator (ER-GCaMP6-150) in the ER, and measured its fluorescence

84 a novel ER stress suppressor, in As-induced ER stress response and cytotoxicity in neural cells.

85 s with concomitant suppression of As-induced ER stress.

86 that deoxyuridine could abrogate ROS-induced ER stress to promote cancer cell survival.

87 Inhibiting ER stress with 4-PBA decreased the effect of albumin on

88 bules in the formation of the interconnected ER network.

89 l N-glycosylation trimming pathway involving ER glucosidases I and II.

90 irmed by elevated expression levels of known ER stress markers.

91 to investigate the importance of early life ER stress in the nutritional programming of this metabol

92 Maintaining ER lipid homeostasis despite these fluctuations is cruci

93 AD) are the primary mechanism that maintains ER protein homeostasis.

94 The first crystal structure of mammalian ER Glu I will constitute the basis for the development o

95 Thus, Protrudin-mediated ER-endosome contact sites promote cell invasion by facil

96 Methods: ER+, PR+ T47D breast cancer cells expressing wild-type (

97 resulting increase in deoxyuridine mitigated ER stress-induced cytotoxicity.

98 e replacement using 29-mm Sapien-3 and 34-mm ER is safe and feasible.

99 Moreover, in cells, MANF bound to a model ER protein exhibiting improper disulfide bond formation

100 first diagnosis, family history, morphology, ER status, PR status, and HER2 status, and (neo)adjuvant

101 not bind to this protein during nonreductive ER stress.

102 a novel mechanism that is crucial for normal ER lipid metabolism and protects the ER from dysfunction

103 gate the roles of microRNA(miR)-124, a novel ER stress suppressor, in As-induced ER stress response a

104 is coincident with enhanced accumulation of ER-derived ATZ inclusion bodies.

105 proteins blunted the selective advantage of ER-mutant tumor cells to survive estrogen deprivation, a

106 for in vitro bioactivities (e.g., agonism of ER, GR, and PPARgamma) and BC concentrations; fathead mi

107 Pharmacological blockade of ER stress in vitro using dexamethasone or the chemical c

108 es lacking the Sel1L-Hrd1 protein complex of ER-associated protein degradation (ERAD).

109 the HFD group showed increased expression of ER stress and apoptotic markers and increased expression

110 +) homeostasis or increase the expression of ER stress-associated genes in HEK-293 cells.

111 in EOC, here we determined the expression of ER stress-associated proteins (GRP78, ATF6 and PERK) and

112 Albumin induced features of ER stress in renal tubular cells with ATF3/ATF4 activati

113 us, regulating the production and feeding of ER membranes into NE holes together with ESCRT-mediated

114 ments in preclinical and clinical imaging of ER and PR in breast cancer.

115 Increase of ER stress in Tsc1 loss-of-function cells upon foxo knock

116 We propose that the induction of ER constrictions contributes to the BMB2-dependent incre

117 Under mild or moderate levels of ER stress, the homeostatic UPR sets in motion transcript

118 were used to assess the expression levels of ER-associated proteins using immunohistochemistry (IHC).

119 he R330fs mutant can disrupt localization of ER-alpha and FOXA1.

120 However, the downstream mediators of ER stress pathway in promoting lipid accumulation remain

121 ese data to construct mathematical models of ER agonist and antagonist pathways to prioritize chemica

122 Recognition of ER proteins by the KDEL receptor is pH dependent, with b

123 at ITPR3 in CCA cells was also in regions of ER in close association with mitochondria.

124 ese findings reveal TRIM25 as a regulator of ER homeostasis and a potential target for tumor therapy.

125 recent studies have highlighted the role of ER Ca(2+) imbalance caused by dysfunction of sarco/ER Ca

126 Despite the potential role of ER stress for As-induced neurotoxicity, the underlying m

127 s of these six ERalpha genotypes to a set of ER agonists showed that both steric and electrostatic fa

128 NBAS and UPF1 coregulate the stability of ER-associated transcripts, in particular those associate

129 STAT3 hijacks a subset of ER enhancers to drive a distinct transcriptional program

130 genes after 3 months' endocrine treatment of ER+ patients (n = 68) predicted poor prognosis.

131 The influence of ERs on binge drinking in female mice suggests that treat

132 The inositol-requiring enzyme (IRE1) is one ER stress sensor that is activated to splice the bZIP60

133 ted by altering PB composition, ER shape, or ER translational capacity.

134 es demonstrate that activation of pancreatic ER kinase (PERK) protects oligodendrocytes against infla

135 ellular physiology in response to pathologic ER stress.

136 report that Drp1 directly shapes peripheral ER tubules in human and mouse cells.

137 These changes provoke a state of persistent ER stress that has been demonstrated to govern multiple

138 ncoded Ca(2+) indicator in the photoreceptor ER.

139 inverse associations for estrogen positive (ER(+ve)) breast cancer and for colon cancer.

140 ntly develops in estrogen receptor positive (ER+) breast cancer, but the underlying molecular mechani

141 to treatment of estrogen receptor positive (ER+) breast cancer.

142 f recurrence in estrogen receptor- positive (ER+) breast cancer tissue.

143 As encoding membrane proteins, which promote ER homeostasis by activating the PERK-dependent unfolded

144 nsporter 1 and PRC1 synergistically promoted ER stress and suppressed tumor growth in vivo.

145 sory exposure (OSE) and a lower eating rate (ER).

146 anism of estrogens at the estrogen receptor (ER) complex by different types of estrogens-planar [17be

147 most prescribed selective estrogen receptor (ER) modulator in patients with ER-positive breast cancer

148 but for invasive cancer, estrogen receptor (ER) positive cancer and with broader inclusion of racial

149 Estrogen receptor (ER), progesterone receptor (PR), and human epidermal gro

150 s sirtuins coactivate the oestrogen receptor/ER and the worm steroid receptor DAF-12.

151 The Expert Panel continues to recommend ER testing of invasive breast cancers by validated immun

152 4, using CRISPR/Cas9, led to greatly reduced ER binding at the majority of loci normally bound by ER.

153 Emei disruption reduces ER Ca(2+) level and subsequently leads to JNK activation

154 er disulfide bond formation during reductive ER stress but did not bind to this protein during nonred

155 ER, we examined the effects of the reductive ER stressor DTT.

156 icosanoid and cytokine storm, down-regulated ER stress genes, and promoted macrophage phagocytosis of

157 ne protein complex assembly in the remaining ER.

158 e safely targeted with domperidone to rescue ER-retained ATP7B mutants and, hence, to counter the ons

159 gh frequency in advanced endocrine-resistant ER(+) breast cancer.

160 s also accompanied by endoplasmic reticulum (ER) accumulation and, accordingly, it was blocked by an

161 rotein folding in the endoplasmic reticulum (ER) activates the unfolded protein response (UPR)-a sign

162 Endoplasmic reticulum (ER) acts as the largest intracellular Ca(2+) store that

163 peptide peptidase and endoplasmic reticulum (ER) aminopeptidase 1 (ERAP1) is required for processing

164 al role in regulating endoplasmic reticulum (ER) and global cellular physiology in response to pathol

165 SV40 traffics to the endoplasmic reticulum (ER) and penetrates a virus-induced structure in the ER m

166 MHC) molecules in the endoplasmic reticulum (ER) and reroutes them to lysosomes.

167 brane proteins in the endoplasmic reticulum (ER) are assembled into multiprotein complexes, but littl

168 receptor (S1R) is an endoplasmic reticulum (ER) chaperone that not only regulates mitochondrial resp

169 ption of mitochondria-endoplasmic reticulum (ER) contact sites (MERCs) phenocopies OxPHOS inhibition.

170 S on mitochondria and endoplasmic reticulum (ER) has been well documented, its consequence on the Gol

171 The endoplasmic reticulum (ER) has recently emerged as a promising target for antic

172 The endoplasmic reticulum (ER) immunoglobulin binding proteins (BiPs) are molecular

173 a subapical region of endoplasmic reticulum (ER) in cholangiocytes, but both immunogold electron micr

174 eveals instability of endoplasmic reticulum (ER) in mouse AD models and genome-edited human AD iPS ce

175 The endoplasmic reticulum (ER) is a fundamental organelle in cellular metabolism an

176 D) formation from the endoplasmic reticulum (ER) is accompanied by the targeting and accumulation of

177 ein biogenesis in the endoplasmic reticulum (ER) is complex and failure-prone.

178 The endoplasmic reticulum (ER) membrane complex (EMC) cooperates with the Sec61 tra

179 The endoplasmic reticulum (ER) membrane protein complex (EMC) was identified over a

180 (E3s) embedded in the endoplasmic reticulum (ER) membrane regulate essential cellular activities incl

181 st penetrate the host endoplasmic reticulum (ER) membrane to enter the cytosol in order to promote in

182 TA) proteins into the endoplasmic reticulum (ER) membrane with an insertase (yeast Get1/Get2 or mamma

183 er when comparing the endoplasmic reticulum (ER) membrane, plasma membrane, and nanodomains induced b

184 gand stimulation, the endoplasmic reticulum (ER) protein STING translocates to endosomes for inductio

185 nse (UPR) to mitigate endoplasmic reticulum (ER) stress caused by cellular oncogene activation and a

186 duction by mitigating endoplasmic reticulum (ER) stress in the developing appressorium.

187 baudioside A improved endoplasmic reticulum (ER) stress related gene expressions, fasting glucose lev

188 immune sensing or the endoplasmic reticulum (ER) stress response contributes to the changes in m(6)A

189 ression activates the endoplasmic reticulum (ER) stress response, causes oxidative stress, and induce

190 xposed to As leads to endoplasmic reticulum (ER) stress response, which, if not relieved, results in

191 port that the chronic endoplasmic reticulum (ER) stress-induced ATF4-CHOP-GADD34 pathway is activated

192 onditions can trigger endoplasmic reticulum (ER) stress.

193 tially in response to endoplasmic reticulum (ER) stress.

194 -I molecules from the endoplasmic reticulum (ER) to phagosomes, and increases the levels of peptide-e

195 trafficking from the endoplasmic reticulum (ER) to the Golgi complex.

196 covery of a family of endoplasmic reticulum (ER) transmembrane proteins that associate with and modul

197 n homotypic fusion of endoplasmic reticulum (ER) tubules in the formation of the interconnected ER ne

198 y 5% of lipids in the endoplasmic reticulum (ER)(1).

199 m hydrogenosomes, the endoplasmic reticulum (ER), and Golgi complex.

200 between mitochondria, endoplasmic reticulum (ER), and lysosomes in HSC metabolism.

201 preferentially to the endoplasmic reticulum (ER), heterooligomerization between the TMDs of Mcl-1 and

202 mbrane protein in the endoplasmic reticulum (ER), is a recently identified negative regulator of the

203 d co-movement of MTs, endoplasmic reticulum (ER), mitochondria, acidic organelles, F-actin, keratin,

204 in the context of the endoplasmic reticulum (ER), the main cellular hub of lipid biosynthesis and the

205 e upon entry into the endoplasmic reticulum (ER), the peptide precursors are processed in the cis-Gol

206 erol resides, and the endoplasmic reticulum (ER), where the protein machinery that regulates choleste

207 of VRCs on GUVs with endoplasmic reticulum (ER)-like phospholipid composition results in a complete

208 ted protein Snx14, an endoplasmic reticulum (ER)-lipid droplet (LD) tethering protein, as a factor re

209 is a multifunctional, endoplasmic reticulum (ER)-resident chaperone that, translocated to the externa

210 ific dysregulation of endoplasmic reticulum (ER)-targeted mRNA translation in DIS3L2-deficient cells.

211 sosomes (LEL) and the endoplasmic reticulum (ER).

212 hed this lipid in the endoplasmic reticulum (ER).

213 nzymes located in the endoplasmic reticulum (ER).

214 GPC retention in the endoplasmic reticulum (ER).

215 lles assembled at the endoplasmic reticulum (ER).

216 perly assemble in the endoplasmic reticulum (ER).

217 tress syndrome (ARDS) in the emergency room (ER) is distinguishing between cardiac vs infectious etio

218 2+) imbalance caused by dysfunction of sarco/ER Ca(2+) ATPase, ryanodine receptor, and inositol 1,4,5

219 sis through the ER Ca(2+) uptake pump, sarco/ER Ca(2+) ATPase, ER Ca(2+) release channels, inositol 1

220 -2 (COX-2), soluble epoxide hydrolase (sEH), ER stress-response genes including BiP, CHOP, and PDI in

221 nd Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.

222 tion in mouse cardiac myocytes results in SR/ER membrane destabilization and luminal vacuolization al

223 for cancers with 1% to 10% of cells staining ER positive.

224 IL6/STAT3 activity is refractory to standard ER-targeted therapies.

225 AR metabolites, toxic aldehydes, steatosis, ER stress, apoptosis, and liver injury.

226 ing epithelial dysfunction in PF and suggest ER stress as a potential mechanism linking aging to IPF.

227 g2 cytosolic complex that also mediates SV40 ER-to-cytosol transport.

228 Targeting ER Glu I with UV-4B-derived compounds may alter treatmen

229 Our data suggest that ER's can regulate nitrergic function by improving Nrf2/n

230 The ER enzyme sterol O-acyltransferase 1 (also named acyl-co

231 The ER-mitochondrial Mg(2+) dynamics is selectively stimulat

232 mediated by Na(+)/Ca(2+) exchange across the ER membrane induced by Na(+) influx via the light-sensit

233 remains unknown whether IRE1alpha adapts the ER in TNBC cells and modulates their TME, and whether IR

234 s, and also between these organelles and the ER and mitochondria, controls their metabolic flux and t

235 or UPF1, which is partially localized at the ER in the proximity of the translocon.

236 of STING and innate immune signalling at the ER membrane.

237 Vps13 resides at contact sites between the ER and several organelles, including late endosomes.

238 into the ER lumen and are recognized by the ER-associated degradation (ERAD) pathway for removal.

239 omains (DRMs) within the ER, also called the ER regulatory pool of cholesterol.

240 Arabidopsis lnp1-1 lnp2-1 mutant cells, the ER becomes a dense tubular network.

241 te-binding pocket that alternately faced the ER lumen and cytosol and an endogenous substrate resembl

242 requirement for sustained PI supply from the ER for the maintenance of monophosphorylated PPIn specie

243 novel group of proteins trafficking from the ER to the early Golgi apparatus.

244 The key UPR sensor IRE1alpha resides in the ER and deploys a cytoplasmic kinase-endoribonuclease mod

245 nt secretory protein forms aggregates in the ER lumen and can be rapidly disaggregated by addition of

246 an accumulation of unfolded proteins in the ER lumen, IRE1 activates its cytoplasmic kinase and ribo

247 penetrates a virus-induced structure in the ER membrane called "focus" to reach the cytosol, where i

248 Here, we show that Can GPC aggregates in the ER of infected cells, forming incorrect cross-chain disu

249 tivated by a lipid-sensing peptide(s) in the ER that can cluster PM-derived cholesterol into transien

250 hat increased levels of uncleaved C99 in the ER, an early phenotype of the disease, upregulates the f

251 nity Ca(2+) indicator (ER-GCaMP6-150) in the ER, and measured its fluorescence both in dissociated om

252 In the ER, excess cholesterol acts to reduce cholesterol uptake

253 is focused on: i) Ca(2+) homeostasis in the ER, ii) ER Ca(2+) dyshomeostasis and apoptosis, and iii)

254 ent can be caused by reductive stress in the ER, we examined the effects of the reductive ER stressor

255 release under conditions of higher pH in the ER.

256 ognate TMDs are slowly translocated into the ER lumen and are recognized by the ER-associated degrada

257 lti-pass integral membrane proteins into the ER membrane, and it is also responsible for inserting th

258 hat ARK1 acts together with RHD3 to move the ER on microtubules to generate a fine ER network.

259 The folding capacity of the ER is regulated by the unfolded protein response (UPR) a

260 r, and Ca(2+)-binding proteins inside of the ER lumen.

261 This review starts with a description of the ER, its function, and its role in cancer progression and

262 ecently identified negative regulator of the ER-associated retinal pigment epithelium (RPE)65 isomera

263 w that GALA induces the glycosylation of the ER-resident calnexin (Cnx) in breast and liver cancer.

264 normal ER lipid metabolism and protects the ER from dysfunction.

265 red for LDL-derived cholesterol to reach the ER.

266 hat maintains Ca(2+) homeostasis through the ER Ca(2+) uptake pump, sarco/ER Ca(2+) ATPase, ER Ca(2+)

267 DGK2 and DGK4 were localized to the ER and were involved in PA production for pollen tube gr

268 transport of cholesterol from the PM to the ER is believed to be activated by a lipid-sensing peptid

269 -null cells, cholesterol was diverted to the ER resulting in normalization of de novo cholesterol syn

270 sed in plant tissues and is localized to the ER, Golgi apparatus, prevacuolar compartment, and plasma

271 These EMC subunits also bind to the ER-resident fusion machinery component syntaxin18, which

272 GLUT1 transporter and localize CHC22 to the ER-to-Golgi intermediate compartment (ERGIC).

273 8, which is required for SV40-arrival to the ER.

274 of PS restores cholesterol transport to the ER.

275 terol and its trafficking from the PM to the ER.

276 Neonatal treatment with the ER stress-relieving drug tauroursodeoxycholic acid impro

277 he NE despite its direct continuity with the ER.

278 FVIII forms amyloid-like fibrils within the ER lumen upon increased FVIII synthesis or inhibition of

279 resistant membrane domains (DRMs) within the ER, also called the ER regulatory pool of cholesterol.

280 This ER-NMD pathway requires the interaction of NBAS with the

281 show that SOX11 confers distinct features to ER-negative DCIS.com breast cancer cells, leading to pop

282 In response to ER stress, FORCP depletion results in decreased apoptosi

283 2+)-induced insulin secretion in response to ER stress.

284 e an attenuated unfolded protein response to ER stress.

285 better clinical outcome in tamoxifen treated ER-positive breast cancer patients by repressing estroge

286 ominantly estrogen receptor positive tumors (ER + 85%) and their normal tissue counterparts (n = 61)

287 ith no known structural homologs and unclear ER function.

288 response (UPR) signaling and cell death upon ER stress induction.

289 nd that TRIM25 is significantly induced upon ER stress.

290 and RIC interneurons, induced intestinal UPR(ER) activation and extended longevity, and exposure to s

291 Before the WWTP replacement, in vitro ER (24 ng 17beta-estradiol equivalents/L)-, GR (60 ng de

292 Methods: Patients with ER+/human epidermal growth factor receptor 2 (HER2)-nega

293 gen receptor (ER) modulator in patients with ER-positive breast cancers.

294 cells in metastatic lesions with or without ER mutations.

295 reast cancer cells expressing wild-type (WT) ER or an activating ESR1 mutation, Y537S-ER, were used t

296 uptake was compared between Y537S-ER and WT-ER tumors.

297 similar early metabolic response for both WT-ER and Y537S-ER tumors.

298 metabolic response for both WT-ER and Y537S-ER tumors.

299 (18)F-FES uptake was compared between Y537S-ER and WT-ER tumors.

300 WT) ER or an activating ESR1 mutation, Y537S-ER, were used to generate tumor xenografts in ovariectom