ライフサイエンスコーパス: ER

1 ER and ERL1 also prevented premature initiation of the f

2 ER contacts with mitochondria were abundant in all compa

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

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

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

6 ER, stage or menopausal status did not modify the effect

7 ER-targeting increased protein accumulation, and extract

8 AWBCs are calculated for 110 ER and 212 AR bioactive chemicals using high throughput

9 s carried out in an independent cohort of 43 ER+ HER2- and ER- HER2- primary breast tumors, confirmin

10 We conducted a GWAS using 21,468 ER-negative cases and 100,594 controls combined with 18,

11 ER downregulators (SERDs) are able to ablate ER and thus, theoretically, to prevent survival of both

12 Yet, how the UPR achieves ER homeostatic readjustment is poorly investigated, as i

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

14 inuous PM-to-ER cholesterol transport allows ER to constantly monitor PM cholesterol levels, and resp

15 An ER-beta-selective ligand increased markers of tricarboxy

16 ndispensable for function; most likely as an ER retention motif that enables anchoring to the ER-deri

17 nsist of a GPCR and G protein tethered by an ER/K linker flanked by FRET probes.

18 V arises from *CHO formation produced via an ER process of H* with nonadsorbed CO (a unique result).

19 ffect on ERbeta/ligand-mediated activity and ER target genes when co-expressed with mERbeta1.

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

21 18)F-FDHT and (18)F-FES PET and tumor AR and ER expression measured immunohistochemically in patients

22 EB-dependent effects in both the cytosol and ER.

23 caused by double mutation in ERECTA (ER) and ER-LIKE1 (ERL1) receptor-kinase genes to elucidate their

24 the relation of T2D to incidence of ER- and ER+ breast cancer in data from the Black Women's Health

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

26 cer patients, especially those with HER2 and ER negative tumors, who will receive one of the widely-a

27 in an independent cohort of 43 ER+ HER2- and ER- HER2- primary breast tumors, confirming many of the

28 Further, vMIA hydrophobic interactions and ER-mitochondria contacts facilitate proper organization

29 se treated with saponin (plasma membrane and ER membrane permeabilized), BeauIII inhibited SOAT1 (IC5

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

31 d MetaDCN to two breast cancer applications: ER+/ER- comparison using five training and three testing

32 A), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two non-arginyl dipeptides: Asp-Asp (DD) and Gl

33 The mitochondria-associated ER membrane (MAM) plays a critical role in cellular ener

34 tant for localization of STIM1 and E-Syts at ER-PM junctions, were reduced in RASSF4-knockdown cells.

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

36 lum (ER) extends throughout axons and axonal ER dysfunction is implicated in numerous neurological di

37 +) indicators optimized for examining axonal ER Ca(2+).

38 This is because ER-Golgi-cycling FKBP proteins contain a C-terminal KDEL

39 filing revealed a strong association between ER and CA-IKKbeta-driven gene expression and clinically

40 2C9 interact differently with the biomimetic ER and may, in addition to protein conformational change

41 of MNCs of RVH rats, and (2) that a blunted ER Ca(2+) buffering capacity contributes to the altered

42 gen to enhance transcriptional activation by ER-alpha of endogenous estrogen-responsive genes.

43 Gene expression controlled by ER-alpha is modulated by Ca(2+) via calmodulin (CaM).

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

45 >50% of PR binding sites were co-occupied by ER, with a propensity for both receptors to coordinately

46 onents can be utilized to counteract chronic ER proteinopathies.

47 tate glands indicate the presence of chronic ER stress.

48 In a warmer climate, ER increases year-round in the absence of moisture stres

49 icular, when co-expressed with inducible Cre-ER(T2), our system enables parallel, independent manipul

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

51 Using ALOD4, we: (1) deplete ER cholesterol without altering PM or overall cellular c

52 he abilities of Tg and Tg analogs to deplete ER Ca(2+) stores and their detrimental effects on cell v

53 lting in a buildup of virions within dilated ER vesicles.IMPORTANCE In humans, symptoms of RVFV infec

54 Thus, L. pneumophila can shut down ER-mitochondria communication through cleavage of syntax

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

56 oring ability that is required for efficient ER membrane fusion mediated by RHD3.

57 These results indicate that efficient ER export is not sufficient to enable normal cell-surfac

58 We developed novel genetically encoded ER-targeted low-affinity Ca(2+) indicators optimized for

59 to detect EDC-mediated changes in endogenous ER target gene expression.

60 from the PM to the nucleus via the endosome-ER network.

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

62 s: TMEM16A provides a mechanism for enhanced ER Ca(2+) store release, possibly engaging Store Operate

63 tophagy-initiation complex, the PIS-enriched ER subdomain, and ATG9A vesicles together initiate autop

64 taDCN to two breast cancer applications: ER+/ER- comparison using five training and three testing stu

65 latures caused by double mutation in ERECTA (ER) and ER-LIKE1 (ERL1) receptor-kinase genes to elucida

66 in a sensitivity and specificity of 100% for ER.

67 ancreatic cancer cells and was essential for ER homoeostasis.

68 ttenuation of IRE1 activity is important for ER remodelling dynamics and cell survival in the face of

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

70 The overall odds ratio (OR) for ER visits for GI illness was 1.09 [95% confidence interv

71 bitor, is currently in phase III studies for ER-positive breast cancer and KRAS mutant lung cancer.

72 We hypothesize that changes to the fungal ER represent a conserved process in specialized eukaryot

73 ction was abolished in the mutated 231 G521R ER cells despite appropriate receptor protein expression

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

75 generated erlotinib-resistant HCC827 (HCC827/ER) cells than in HCC827 cells.

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

77 were shared among three subtypes, ER+ HER2-, ER- HER2-, and HER2+, many events on the exon level were

78 ed VirE2 protein can use the endogenous host ER/actin network for movement inside host cells.

79 How ER shaping is linked to neuronal defects is poorly under

80 ogeneity by localizing immunohistochemically ER-positive metastases that lack receptor-binding functi

81 ative) is a reliable prognostic biomarker in ER positive breast cancer patients, and predictive of pr

82 blish the oncogenic contributions of EVI1 in ER- and HER2-negative subsets of breast cancer.

83 n 2 (Mfn2), a membrane protein implicated in ER-mitochondria tethering, also shows reduced expression

84 ntial recruitment and biochemical process in ER-mediated transcription.

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

86 ith 10 of 11 variants previously reported in ER-negative disease or BRCA1 mutation carrier GWAS and o

87 orm salt bridges with key lysine residues in ER-alpha (Lys-299, Lys-302, and Lys-303), which is likel

88 from Leishmania to understand their role in ER exit of Ldgp63.

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

90 P treatment of breast cancer cells increased ER binding to the NEMO promoter, thereby increasing NEMO

91 he unfolded protein response (UPR) increases ER-protein-folding capacity to restore protein-folding h

92 of both endocrine-dependent and -independent ER+ tumors.

93 enerally leading to an endocrine-independent ER+ phenotype.

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

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

96 exposed to cytokines or thapsigargin-induced ER stress.

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

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

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

100 MED1 mutation in its ER-interacting LxxLL motifs was sufficient to delay tumo

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

102 el, but this effect was not seen in PKR-like ER kinase knockout (PERK-KO) or phosphodeficient eukaryo

103 The di-lysine ER retention motif of AnkB-Paris is indispensable for fu

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

105 RTN3-mediated ER-phagy requires conventional autophagy components, but

106 (PR), which can directly and globally modify ER action to attenuate tumor growth.

107 ogen target gene expression in WT and mutant ER-containing cells and were more effective in D538G tha

108 In estrogen receptor-negative (ER(-)) and triple-negative breast cancer (TNBC), nitric

109 ous concentrations of estradiol (nonspecific ER agonist) or genistein (ERbeta-selective agonist).

110 used to determine the mechanism of action of ER-beta and its ligands.

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

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

113 tors revealed that Ire1-mediated cleavage of ER-associated mRNAs results in ribosome stalling and mRN

114 Moreover, coactivation of ER and IKKbeta promoted cell migration and invasion in v

115 on at these sites and inhibit degradation of ER-alpha.

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

117 However, the morphology and distribution of ER-PM junctions are not well characterized.

118 ubsequently from PM to regulatory domains of ER to suppress activation of SREBPs, halting cholesterol

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

120 PDZD8 was necessary for the formation of ER-mitochondria contacts in mammalian cells.

121 ulators with both native and mutant forms of ER.

122 BARAPs is essential for the fragmentation of ER tubules and their delivery to lysosomes.

123 the ER surface to coordinate the function of ER-associated and cytosolic chaperone systems in protein

124 assessed the relation of T2D to incidence of ER- and ER+ breast cancer in data from the Black Women's

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

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

127 hich explains why CaM binds two molecules of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimeri

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

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

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

131 en more provocative questions on the role of ER in cancer-bone interaction.

132 We focus in particular on the role of ER-PM contacts in nonvesicular lipid transport between t

133 enhanced sequestration and stabilization of ER- associated miRNPs observed in infected macrophage ce

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

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

136 erestingly, we discovered that tightening of ER-mitochondria contacts by overexpression of VAPB or PT

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

138 n this review, we evaluate the importance of ERs in bone metastasis and discuss new avenues of invest

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

140 Recent findings on ER mutations, especially their enrichment in bone metast

141 rescued by inhibition of rRNA processing or ER stress.

142 tumorigenesis, through activating pancreatic ER kinase/eukaryotic translation initiation factor 2alph

143 irst molecular mechanism for establishing PO-ER associations in mammalian cells and report a new func

144 ls and report a new function for ACBD5 in PO-ER tethering.

145 this attenuation is mediated only through PR-ER interaction remains unknown.

146 ty drives net Ca(2+) uptake into presynaptic ER although this activity does not contribute significan

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

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

149 subject to GSK-3 phosphorylation, promoting ER retention, while mutation of target serines and drug

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

151 Quetiapine-ER was associated with more metabolic adverse events and

152 ients; estimated 63.5%) than with quetiapine-ER (15 [30%] of 50; estimated 31.3%; p=0.0021), but not

153 aCl, whereas no effect was observed with RE, ER, DD, or ED.

154 ast cancers expresses the estrogen receptor (ER(+)) and is treated with anti-estrogen therapies, part

155 ion of the IL-4Ralpha and estrogen receptor (ER) alpha compared with macrophages from male mice follo

156 Studies of the estrogen receptor (ER) coactivator protein Mediator subunit 1 (MED1) have r

157 e, dynamically modulating estrogen receptor (ER) expression, activity, and trafficking.

158 The estrogen receptor (ER) is a target for endocrine therapy in breast cancer p

159 Greater than 50% of estrogen receptor (ER)-positive breast cancers coexpress the progesterone r

160 s (GWAS) of predominantly estrogen receptor (ER)-positive disease.

161 inst tumors driven by the estrogen receptor (ER).

162 orse clinical outcome in estrogen receptor+ (ER+) breast cancers.

163 nes have an affinity for estrogen receptors (ERs) including beneficial affinity for ERbeta.

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

165 vitro, acute high glucose treatment reduces ER-mitochondrial contact in retinal endothelial cells.

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

167 ly, we present evidence that GGpp-regulated, ER-to-Golgi transport enables UBIAD1 to modulate reducta

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

169 dynamics of IRE1 deactivation by regulating ER-mitochondria physical contacts and the autophosphoryl

170 croRNAs play an important role in regulating ER stress.

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

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

173 e unfolded protein response (UPR) to restore ER homeostasis.

174 lding capacity of the endoplasmic reticulum (ER) activates the unfolded protein response (UPR) to res

175 exchange between the endoplasmic reticulum (ER) and peroxisomes is necessary for the synthesis and c

176 sp70 chaperone in the endoplasmic reticulum (ER) and similar to other Hsp70s, its activity relies on

177 The turnover of endoplasmic reticulum (ER) ensures the correct biological activity of its disti

178 Although the endoplasmic reticulum (ER) extends throughout axons and axonal ER dysfunction i

179 Disturbances in endoplasmic reticulum (ER) homeostasis create a condition termed ER stress.

180 rgo proteins exit the endoplasmic reticulum (ER) in COPII-coated vesicles, whereas resident and misfo

181 The endoplasmic reticulum (ER) integral membrane protein VAP is a common component

182 The endoplasmic reticulum (ER) is a network of tubules and sheets stretching throug

183 The endoplasmic reticulum (ER) is a single organelle in eukaryotic cells that exten

184 re we report that the endoplasmic reticulum (ER) is asymmetrically partitioned during mitosis in epit

185 formation within the endoplasmic reticulum (ER) is poorly understood.

186 een endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the mechanisms

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

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

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

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

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

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

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

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

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

196 manifestations is the endoplasmic reticulum (ER) stress.

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

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

199 While the endoplasmic reticulum (ER) supports dendritic translation, most dendrites lack

200 at upregulation of an endoplasmic reticulum (ER) to Golgi trafficking gene signature in metastatic ce

201 mbrane protein in the endoplasmic reticulum (ER), and that it undergoes auto-processing to release it

202 rticles occurs in the endoplasmic reticulum (ER), followed by subsequent lipidation in the ER and Gol

203 s of retention in the endoplasmic reticulum (ER), however co-expression with Rom1 rescued this phenot

204 ic overloading of the endoplasmic reticulum (ER), leading to its functional impairment.

205 ins accumulate in the endoplasmic reticulum (ER), the unfolded protein response (UPR) increases ER-pr

206 lding capacity of the endoplasmic reticulum (ER), thereby provoking a cellular state of "ER stress."

207 RIP2 localizes to the endoplasmic reticulum (ER), where it interacts with ZNRF4 under either 55 unsti

208 wed that TMEM24 is an endoplasmic reticulum (ER)-anchored membrane protein whose reversible localizat

209 DNAJB12 (JB12) is an endoplasmic reticulum (ER)-associated Hsp40 family protein that recruits Hsp70

210 anisms, including the endoplasmic reticulum (ER)-induced unfolded protein response (UPR), the ubiquit

211 iated largely through endoplasmic reticulum (ER)-localized vIL-6, which can induce signal transductio

212 e ERMES complex is an endoplasmic reticulum (ER)-mitochondria tether composed of four proteins, three

213 lgi apparatus and the endoplasmic reticulum (ER).

214 proteins (TAs) to the endoplasmic reticulum (ER).

215 login/password access to its expert review (ER) companion system.

216 or product, is produced via the Eley-Rideal (ER) mechanism using H2O + e(-) The rate-determining step

217 bundant beta-glucosidase in A. thaliana root ER bodies, hydrolyzes indole glucosinolates (IGs) in add

218 Selective ER downregulators (SERDs) are able to ablate ER and thus

219 of CaM bind to the same site on two separate ER-alpha molecules (residues 292, 296, 299, 302, and 303

220 motifs that can be O-glycosylated by several ER-localized enzymes, including protein O-glucosyltransf

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

222 y, we reveal that the contact area of single ER-PM junctions is mainly oblong with the dimensions of

223 of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimerization.

224 mon events were shared among three subtypes, ER+ HER2-, ER- HER2-, and HER2+, many events on the exon

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

226 protein response, associated with sustained ER stress.

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

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

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

230 Here, we show that ER Ca(2+)-store depletion rapidly induces STIM1 phosphor

231 Here we show that ER-localized THBS1 is cytoprotective to rat, mouse, and

232 The ER consists of 2 isoforms, ERalpha and ERbeta, which hav

233 The ER protein-conducting channel is permeable to small mole

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

235 AtBAG7 has functional roles in both the ER and the nucleus.

236 dentified branch of the UPR initiated by the ER-localized co-chaperone from Arabidopsis thaliana, AtB

237 We found that glutathione enters the ER by facilitated diffusion through the Sec61 protein-co

238 A facilitate the extraction of SV40 from the ER and transport of the virus into the cytosol.

239 GluA2 exit from the ER further depends on IP3 and Ryanodine receptor-control

240 t, it did not affect protein export from the ER lumen or from endosomes into the cytosol, suggesting

241 nally, mature autophagosomes detach from the ER membrane by an as yet unknown mechanism, undergo intr

242 nding domain (DBD), is auto-cleaved from the ER membrane, and then enters the nucleus to participate

243 c61 mediates the release of beta-DG from the ER membrane, making it accessible for importins and nucl

244 ost pathways by which vMIA traffics from the ER to mitochondria and clusters at the OMM.

245 ibitor of apoptosis (vMIA) traffics from the ER to mitochondria and clusters at the outer mitochondri

246 ytically processed and translocated from the ER to the nucleus, where interaction with the WRKY29 tra

247 63-containing COPII vesicle budding from the ER was inhibited by LdSar1:T34N in an in vitro budding a

248 to release its N-terminal fragment from the ER, which enters the nucleus to work as a transcription

249 side of the ER and extracts the LD from the ER-LD to cytosol.

250 l for targeting and retention of RHD3 in the ER and can also facilitate an oligomerization of RHD3.

251 shows impaired substrate binding both in the ER and extracellular environments and reduced interactio

252 R), followed by subsequent lipidation in the ER and Golgi compartment.

253 Proper gp160 folding in the ER requires core glycosylation, disulfide-bond formation

254 he existence of a distinct pool of PA in the ER that is required for regulation of Opi1p localization

255 he accumulation of misfolded proteins in the ER, activating the transcription factor, ATF6 (activatin

256 ered by unfolded protein accumulation in the ER, contributes to apoptosis and organ injury.

257 in is synthesized on the cytosol side of the ER and extracts the LD from the ER-LD to cytosol.

258 he phase characteristics and fluidity of the ER biomimetic was characterized with fluorescence microg

259 The formation of the ER requires homotypic membrane fusion, which is mediated

260 is localized to a cortical subdomain of the ER that is involved in asymmetric spindle positioning.

261 that is located on the cytosolic side of the ER, while BeauIII is not accessible to the corresponding

262 and was present on the cytosolic side of the ER.

263 ed proteins when protein load overwhelms the ER folding capacity, which activates the unfolded protei

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

265 We now find that the ER chaperone Grp170 participates in the degradation proc

266 Thus, the ER redox poise is tuned by reciprocal control of glutath

267 gi, and are transported together back to the ER by KDEL receptor-mediated retrograde transport.

268 sed by the proteasome and transported to the ER by the transporter associated with antigen processing

269 helix in SM N100 attaches reversibly to the ER membrane depending on cholesterol levels; with excess

270 Hsc70-SGTA-Hsp105 complex is tethered to the ER membrane, where Hsp105 and SGTA facilitate the extrac

271 40 family protein that recruits Hsp70 to the ER surface to coordinate the function of ER-associated a

272 etention motif that enables anchoring to the ER-derived LCV membrane.

273 mals and yeast, several PMPs traffic via the ER in a Pex3- and Pex19-dependent manner.

274 vironments and reduced interactions with the ER HSP70 chaperone BiP.

275 ignaling, and interactions of vIL-6 with the ER membrane protein vitamin K epoxide reductase complex

276 ing ULK and FIP200 first associates with the ER membrane.

277 were abundant in all compartments, with the ER often forming a network that embraced mitochondria.

278 clusion, establishes direct contact with the ER.

279 tion on autophagy are a consequence of their ER-mitochondria tethering function.

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

281 sly showed that actin polymerization through ER-bound inverted formin 2 (INF2) stimulates Drp1 recrui

282 roximal coupling of ubiquitin conjugation to ER degradation (CUE) domain in SMARCAD1 mediate their di

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

284 ane protein whose reversible localization to ER-plasma membrane (PM) contacts is governed by phosphor

285 lags behind the binding of SRC-3 and p300 to ER.

286 ry of polyunsaturated phosphatidylcholine to ER accelerated SREBP-1c processing through a mechanism t

287 sis; and (3) determine that continuous PM-to-ER cholesterol transport allows ER to constantly monitor

288 potent transcription factor adaptive toward ER stress.

289 lonidine participants (22 [61.1%]); tramadol ER retention was intermediate and did not differ signifi

290 y within the clonidine (8 [22.2%]), tramadol ER (7 [19.4%]), or buprenorphine (3 [9.7%]) groups did n

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

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

293 athway to control ubiquitination and tubular ER function independently of the host ubiquitin machiner

294 rt that RNF145, a previously uncharacterized ER membrane ubiquitin ligase, participates in crosstalk

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

296 these findings, we propose a model in which ER Ca(2+) depletion promotes the activation of SREBP2 an

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

298 AS and observed consistent associations with ER-negative disease for 105 susceptibility variants iden

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

300 ERX-11 interacts directly with ER and blocks the interaction between a subset of coregu