ライフサイエンスコーパス: reticulum

1 r protein homeostasis beyond the endoplasmic reticulum.

2 (PC) and causes expansion of the endoplasmic reticulum.

3 aratus and from the Golgi to the endoplasmic reticulum.

4 proprotein that dimerizes in the endoplasmic reticulum.

5 olded proteins accumulate in the endoplasmic reticulum.

6 glycosylation of proteins in the endoplasmic reticulum.

7 luxes in both the cytoplasm and sarcoplasmic reticulum.

8 toyltransferase localized to the endoplasmic reticulum.

9 cent proteins synthesized in the endoplasmic reticulum.

10 ones that normally reside in the endoplasmic reticulum.

11 ant FUS accumulates at the rough endoplasmic reticulum.

12 aring clogged translocons on the endoplasmic reticulum.

13 nus of precursor proteins in the endoplasmic reticulum.

14 a and their interaction with the endoplasmic reticulum.

15 ons from the cytoplasm into the sarcoplasmic reticulum.

16 us and between the Golgi and the endoplasmic reticulum.

17 cover that BAP1 localizes at the endoplasmic reticulum.

18 d in the cytoplasmic side of the endoplasmic reticulum.

19 llagen biosynthesis in the rough endoplasmic reticulum.

20 both the Golgi apparatus and the endoplasmic reticulum.

21 ant ANO5 protein localize to the endoplasmic reticulum.

22 ction-diffusion process from the endoplasmic reticulum.

23 only partially surrounded by the endoplasmic reticulum, a key mediator of mitochondrial Ca(2+) uptake

24 receptors (IP3Rs) located on the endoplasmic reticulum allow the 'quasisynaptical' feeding of calcium

25 cyclic Ca(2+) release from the sarcoplasmic reticulum, although Ca(2+) influx via plasma membrane ch

26 panosomes, (ii) localizes to the endoplasmic reticulum and (iii) represents the unique route for PS f

27 te, disorganised sarcomeres and sarcoplasmic reticulum and a blunted response to isoprenaline.

28 nking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of Ca entry to si

29 for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-indu

30 ranes, specifically those of the endoplasmic reticulum and mitochondria, are crucial factors in APOL1

31 hemical composition of the human endoplasmic reticulum and served as an ER biomimetic.

32 dendrimers, however, localize to endoplasmic reticulum and the Golgi apparatus, presumably through th

33 opy localized TbRFT1 to both the endoplasmic reticulum and the Golgi, consistent with the proposal th

34 mplex and the Get complex in the endoplasmic reticulum and the SecYEG complex and YidC in bacteria an

35 catalyzes membrane fusion of the endoplasmic reticulum and thus establishes a network of branched mem

36 ral abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) attenuated mit

37 use it mostly failed to exit the endoplasmic reticulum and was degraded.

38 (STIM1), a Ca(2+) sensor in the endoplasmic reticulum, and the Ca(2+) ion channel Orai in the plasma

39 Herpud1, a component of the endoplasmic reticulum-associated degradation (ERAD) complex, partici

40 ed ubiquitination and subsequent endoplasmic reticulum-associated degradation of the rate-limiting en

41 n after starvation, nucleates in endoplasmic reticulum-associated foci that colocalize with omegasome

42 the proteasome-a pathway termed endoplasmic reticulum-associated protein degradation (ERAD).

43 Although endoplasmic reticulum association was occasionally noted, associatio

44 nt protein was detectable in the endoplasmic reticulum but that it also could be recognized in chloro

45 ng, Ca transient amplitude, and sarcoplasmic reticulum Ca content in colon ascendens stent peritoniti

46 arcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, Ca transient amplitude and contrac

47 cellular mechanisms involved in sarcoplasmic reticulum Ca loss that mediate altered Ca handling and c

48 (2+) channel (LCC) and the sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) as the principal regula

49 Sarcoplasmic/endoplasmic reticulum Ca(2+) adenosine triphosphatase (SERCA)2a, a c

50 ation was due to increased sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA)-mediated reuptake rather

51 eceptor (DHPR), and sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA).

52 L-type Ca(2+) channel and sarco/endoplasmic reticulum Ca(2+) ATPase as the principal regulators of s

53 RVH rats, partly due to blunted endoplasmic reticulum Ca(2+) buffering capacity.

54 essential for the maintenance of endoplasmic reticulum Ca(2+) concentration in resting cells, and for

55 marked changes in cytosolic and sarcoplasmic reticulum Ca(2+) levels, likely owing to altered cellula

56 ion molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca(2+) sensor.

57 post HF revealed both increased sarcoplasmic reticulum Ca(2+) spark frequency and disrupted JMC integ

58 t parasites identifies the sarco/endoplasmic reticulum Ca(2+) transporting PfATP6 as a putative deter

59 Sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), a member of the P-type

60 er rate than the purified sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA1a).

61 nt inhibitor of the sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase calcium pump in mammals and is o

62 SERCA1, the sarco(endo)plasmic reticulum Ca(2+)-ATPase of skeletal muscle, is essential

63 The sarcoplasmic reticulum Ca(2+)-ATPase SERCA promotes muscle relaxation

64 nd timing include cytosolic and sarcoplasmic reticulum Ca2+ concentrations, inwardly rectifying potas

65 N), inhibiting the cardiac sarco/endoplasmic reticulum calcium ATPase 2a (SERCA2a) in the regulation

66 ment with inhibitors of the sarcoendoplasmic reticulum calcium ATPase and ryanodine receptor.

67 ed expression of Serca2, reduced endoplasmic reticulum calcium levels, and induction of the UPR.

68 ide acetate directly suppresses sarcoplasmic reticulum calcium release-the cellular mechanism respons

69 Inhibition of the sarcoendoplasmic reticulum calcium trasport ATPase (SERCA) pump activity

70 cyte L-type calcium channel/sarcoendoplasmic reticulum calcium-ATPase activity and cardiac tissue fib

71 CD19 membrane export in the post-endoplasmic reticulum compartment as molecular basis for blinatumoma

72 mpromised, the morphology of the endoplasmic reticulum deteriorates, and these defects can result in

73 functionally interacts with the endoplasmic reticulum droplet assembly factors seipin and Fit2 to ma

74 licit a complex signaling sequence involving reticulum endoplasmic destalilization which leads to Ca(

75 protein folding capacity in the endoplasmic reticulum (ER) according to need.

76 fficient folding capacity of the endoplasmic reticulum (ER) activates the unfolded protein response (

77 n disturb protein folding in the endoplasmic reticulum (ER) and activate the Unfolded Protein Respons

78 ding problems are trapped in the endoplasmic reticulum (ER) and are eventually degraded in the cytopl

79 Although alterations in both endoplasmic reticulum (ER) and cytosolic free calcium levels are kno

80 nied by reduced juxtaposition of endoplasmic reticulum (ER) and mitochondria as well as endosomes.

81 Lipid exchange between the endoplasmic reticulum (ER) and peroxisomes is necessary for the synt

82 the only Hsp70 chaperone in the endoplasmic reticulum (ER) and similar to other Hsp70s, its activity

83 lizes and accumulates within the endoplasmic reticulum (ER) and the transport of Gn from the Golgi co

84 biosynthetic substrates to fuel endoplasmic reticulum (ER) biogenesis, and additional carbon sources

85 sicaceae-specific traits, namely endoplasmic reticulum (ER) body formation and induction of indole gl

86 apsigargin (Tg) blocks the sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA), disrupts Ca(2+) ho

87 avorable redox conditions in the endoplasmic reticulum (ER) can decrease the capacity for protein sec

88 The endoplasmic reticulum (ER) consists of the nuclear envelope and a re

89 Peroxisomes (POs) and the endoplasmic reticulum (ER) cooperate in cellular lipid metabolism an

90 microscopic observation revealed endoplasmic reticulum (ER) dilatation, suggestive of ER stress, and

91 The turnover of endoplasmic reticulum (ER) ensures the correct biological activity o

92 Although the endoplasmic reticulum (ER) extends throughout axons and axonal ER dy

93 Disturbances in endoplasmic reticulum (ER) homeostasis create a condition termed ER

94 Native cargo proteins exit the endoplasmic reticulum (ER) in COPII-coated vesicles, whereas residen

95 that ensures homeostasis of the endoplasmic reticulum (ER) in eukaryotes.

96 ssembling onto subdomains of the endoplasmic reticulum (ER) in two layers to generate cargo-laden tra

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

98 The endoplasmic reticulum (ER) is a network of tubules and sheets stretc

99 The endoplasmic reticulum (ER) is a single organelle in eukaryotic cells

100 Here we report that the endoplasmic reticulum (ER) is asymmetrically partitioned during mito

101 n of the folding capacity of the endoplasmic reticulum (ER) is becoming a common pathological alterat

102 Glycosylation in the endoplasmic reticulum (ER) is closely associated with protein foldin

103 d disulfide formation within the endoplasmic reticulum (ER) is poorly understood.

104 Cholesterol biosynthesis in the endoplasmic reticulum (ER) is tightly controlled by multiple mechani

105 d when cholesterol levels in the endoplasmic reticulum (ER) membrane are high, but the signal for deg

106 rted across or inserted into the endoplasmic reticulum (ER) membrane by the ER protein translocon.

107 the compartmentalization of the endoplasmic reticulum (ER) membrane confine protein deposit formatio

108 polyomavirus SV40 penetrates the endoplasmic reticulum (ER) membrane to reach the cytosol, a crucial

109 kinases are mislocalized in the endoplasmic reticulum (ER) of AML and play an important role in the

110 ntacts between endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the

111 nded synaptotagmins (E-Syts) are endoplasmic reticulum (ER) proteins that bind the plasma membrane (P

112 membrane P/Q Ca(2+) channels and endoplasmic reticulum (ER) ryanodine receptors and another between r

113 e depletion of (Ca(2+)) from the endoplasmic reticulum (ER) store, organizes as puncta that trigger s

114 It induced endoplasmic reticulum (ER) stress and activated the protective inosi

115 pre-rRNA level led to attenuated endoplasmic reticulum (ER) stress and cell death.

116 ocused on a relationship between endoplasmic reticulum (ER) stress and cGVHD, and aimed to create eff

117 Endoplasmic reticulum (ER) stress arises from accumulation of misfol

118 folded protein response (UPR) to endoplasmic reticulum (ER) stress by Mvarphis in a longitudinal stud

119 RATIONALE: Endoplasmic reticulum (ER) stress causes the accumulation of misfold

120 We found that the PERK axis of endoplasmic reticulum (ER) stress elicited prominent nuclear translo

121 Endoplasmic reticulum (ER) stress elicits EC dysregulation in metabo

122 ose tolerance to overt diabetes; endoplasmic reticulum (ER) stress expedites beta cell failure in thi

123 timulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal panc

124 reticulon (RTN) 1A in mediating endoplasmic reticulum (ER) stress in kidney tubular cells and the ex

125 reased ECM accumulation leads to endoplasmic reticulum (ER) stress in the TM.

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

127 Endoplasmic reticulum (ER) stress is a local factor that affects var

128 mmed cell death (PCD) induced by endoplasmic reticulum (ER) stress is implicated in various plant phy

129 he regulatory control of cardiac endoplasmic reticulum (ER) stress is incompletely characterized.

130 Endoplasmic reticulum (ER) stress occurs in the early stages of SCI

131 ac hypertrophy and heart failure.Endoplasmic reticulum (ER) stress promotes cardiac dysfunction.

132 evidence that ECD regulates the endoplasmic reticulum (ER) stress response.

133 ess, in part due to induction of endoplasmic reticulum (ER) stress that resulted in apoptosis.

134 In response to endoplasmic reticulum (ER) stress, ATF6 migrates from the ER to Golg

135 with metabolic inflammation and endoplasmic reticulum (ER) stress, both of which promote metabolic d

136 monstrate that metformin induces endoplasmic reticulum (ER) stress, calcium release from the ER and s

137 Paneth cells by bacteria-induced endoplasmic reticulum (ER) stress, required extrinsic signals from i

138 Endoplasmic reticulum (ER) stress, triggered by unfolded protein acc

139 5-azacytidine (5-aza) underwent endoplasmic reticulum (ER) stress.

140 ve to differentiation induced by endoplasmic reticulum (ER) stress.

141 nder growth-factor limitation or endoplasmic reticulum (ER) stress.

142 n, which sensitizes cells to the endoplasmic reticulum (ER) stress.

143 unction, impaired autophagy, and endoplasmic reticulum (ER) stress.

144 species, and in the response to endoplasmic reticulum (ER) stress.

145 e cellular manifestations is the endoplasmic reticulum (ER) stress.

146 d in its accumulation within the endoplasmic reticulum (ER) suggesting impaired ER-to-Golgi trafficki

147 While the endoplasmic reticulum (ER) supports dendritic translation, most dend

148 ry protein mRNAs is to encode an endoplasmic reticulum (ER) targeting sequence.

149 e physical associations with the endoplasmic reticulum (ER) that regulate a number of physiological f

150 from the Golgi apparatus to the endoplasmic reticulum (ER) through an interaction with Zeste-White 1

151 onstrate that upregulation of an endoplasmic reticulum (ER) to Golgi trafficking gene signature in me

152 transport of DP(84Gly) from the endoplasmic reticulum (ER) to the endosomal/lysosomal pathway by tra

153 agen I (PC1) molecules, from the endoplasmic reticulum (ER) to the Golgi.

154 es trafficking of GluA2 from the endoplasmic reticulum (ER) to the synapse by enhancing GluA2 binding

155 ClC-4 is retained in the endoplasmic reticulum (ER) upon overexpression in HEK293T cells.

156 TAG-synthesizing enzymes on the endoplasmic reticulum (ER), and nascent TAGs are sequestered in the

157 ted as a membrane protein in the endoplasmic reticulum (ER), and that it undergoes auto-processing to

158 has so far mostly focused on the endoplasmic reticulum (ER), emerging data suggest that the Golgi its

159 of VLDL particles occurs in the endoplasmic reticulum (ER), followed by subsequent lipidation in the

160 showed signs of retention in the endoplasmic reticulum (ER), however co-expression with Rom1 rescued

161 procollagen I, which enters the endoplasmic reticulum (ER), is trafficked through the secretory path

162 ent metabolic overloading of the endoplasmic reticulum (ER), leading to its functional impairment.

163 granules, and alterations in the endoplasmic reticulum (ER), ranging from vesicular ER to markedly ex

164 ates actin polymerization at the endoplasmic reticulum (ER), resulting in increased ER-mitochondria c

165 olded proteins accumulate in the endoplasmic reticulum (ER), the unfolded protein response (UPR) incr

166 protein-folding capacity of the endoplasmic reticulum (ER), thereby provoking a cellular state of "E

167 raction of RIP2 localizes to the endoplasmic reticulum (ER), where it interacts with ZNRF4 under eith

168 retory pathway begin life in the endoplasmic reticulum (ER), where their folding is surveyed by the 1

169 (WT) proinsulin from exiting the endoplasmic reticulum (ER), which is essential for insulin productio

170 al matrix, nucleus, cytosol, and endoplasmic reticulum (ER), with specificity and sensitivity that ri

171 We showed that TMEM24 is an endoplasmic reticulum (ER)-anchored membrane protein whose reversibl

172 at CLas induces the formation of endoplasmic reticulum (ER)-associated bodies.

173 DNAJB12 (JB12) is an endoplasmic reticulum (ER)-associated Hsp40 family protein that recr

174 es associated with intracellular endoplasmic reticulum (ER)-derived membranes.

175 l changes dramatically decreased endoplasmic reticulum (ER)-exit and plasma membrane localization of

176 static mechanisms, including the endoplasmic reticulum (ER)-induced unfolded protein response (UPR),

177 The endoplasmic reticulum (ER)-localized Hsp70 chaperone BiP contributes

178 ies are mediated largely through endoplasmic reticulum (ER)-localized vIL-6, which can induce signal

179 n yeast, the ERMES complex is an endoplasmic reticulum (ER)-mitochondria tether composed of four prot

180 izes to the same fractions as an endoplasmic reticulum (ER)-specific marker.

181 l-anchored proteins (TAs) to the endoplasmic reticulum (ER).

182 ria are closely apposed with the endoplasmic reticulum (ER).

183 cholesterol transport from PM to endoplasmic reticulum (ER).

184 between viral membranes and the endoplasmic reticulum (ER).

185 with the Golgi apparatus and the endoplasmic reticulum (ER).

186 , exported through the classical endoplasmic reticulum (ER)/Golgi-dependent pathway, but a few are re

187 sembly of the MECA (mitochondria-endoplasmic reticulum [ER]-cortex anchor), which tethers mitochondri

188 inhibitor pifithrin-mu such that endoplasmic reticulum export of and radioligand binding and substrat

189 sed by manoeuvres that decrease sarcoplasmic reticulum function.

190 erent membrane-bound organelles (endoplasmic reticulum, Golgi, lysosome, peroxisome, mitochondria and

191 rotein that localizes within the endoplasmic reticulum-Golgi intermediate compartment.

192 secretion without affecting the endoplasmic reticulum/Golgi pathway.

193 phospholipid synthesis maintains endoplasmic reticulum homeostasis and is critical for triple-negativ

194 GRP78/HSPA5), a key regulator of endoplasmic reticulum homeostasis and PI3K/AKT signaling, is overexp

195 es, (ii) Ca(2+) release from the endoplasmic reticulum, (iii) intercellular coupling, and (iv) both t

196 mediated Ca(2+) release from the endoplasmic reticulum in several rare monogenic syndromes highly com

197 nd the 2D and 3D dynamics of the endoplasmic reticulum, in living cells.

198 ntegral membrane proteins to the endoplasmic reticulum is controlled by the signal recognition partic

199 The endoplasmic reticulum is particularly intriguing, as it comprises mo

200 s as they enter the lumen of the endoplasmic reticulum, is a membrane-bound hetero-pentameric complex

201 al division spots contacting the endoplasmic reticulum, it appears on IMM independently of OMM.

202 uced protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) expression or activity in the hi

203 The endoplasmic reticulum kinase inositol-requiring enzyme 1 (IRE1) and

204 Hilpda localized to the endoplasmic reticulum-LD interface, the site of LD formation.

205 ns with misfolded domains in the endoplasmic reticulum lumen or membrane are discarded through the ER

206 g from the cytosol almost to the endoplasmic reticulum lumen, while a segment of the neighbouring Hrd

207 evisiae Hrd1 in complex with its endoplasmic reticulum luminal binding partner, Hrd3.

208 k1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expression in COS

209 ) domain that is anchored to the endoplasmic reticulum membrane by Sec71.

210 ects on lipid synthesis, nuclear/endoplasmic reticulum membrane morphology, and lipid droplet formati

211 terized secreted protein, EMC10 (endoplasmic reticulum membrane protein complex subunit 10), showing

212 Insig-2 is one of two endoplasmic reticulum membrane proteins that inhibit cholesterol syn

213 structural component of a large endoplasmic reticulum membrane-embedded protein complex that coordin

214 sfolded polypeptides through the endoplasmic reticulum membrane.

215 to and translocation across the endoplasmic reticulum membrane.

216 xtensive remodeling of Golgi and endoplasmic reticulum membranes, and a number of the host proteins i

217 localization associated with the endoplasmic reticulum, not co-localizing with endosomal or Golgi mar

218 ERthermAC accumulated in the endoplasmic reticulum of BAs and displayed a marked change in fluore

219 y proteins into the lumen of the endoplasmic reticulum or the periplasm of bacteria is mediated by a

220 sible for cytoprotection against ectoplasmic reticulum/oxidative stress-induced apoptosis both in vit

221 2b gene, a critical regulator of endoplasmic reticulum-phagosome traffic required for cross-presentat

222 oll-like receptors (TLRs) in the endoplasmic reticulum prevents their activation under basal conditio

223 Misfolded endoplasmic reticulum proteins are retro-translocated through the me

224 r membrane network with purified endoplasmic reticulum proteins.

225 ulfide isomerases (PDIs) support endoplasmic reticulum redox protein folding and cell-surface thiol-r

226 , reduction of Ca(2+) uptake to sarcoplasmic reticulum, reduced K(+) currents, and increased propensi

227 would lead to Ca leak from the sarcoplasmic reticulum, reducing sarcoplasmic reticulum Ca content, C

228 as the ortholog of the mammalian endoplasmic reticulum-resident chaperone gp96.

229 ructural elements with MEC-6, an endoplasmic reticulum-resident molecular chaperone in Caenorhabditis

230 aling its identity as TMEM97, an endoplasmic reticulum-resident transmembrane protein that regulates

231 orm highly dynamic contacts with endoplasmic reticulum-resident VAP proteins that regulate late endos

232 dentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs).

233 LN) is an inhibitor of the sarco/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally e

234 or 2 (RyR2) phosphorylation and sarcoplasmic reticulum (SR) Ca(2+) leak.

235 rse tubule system, dividing the sarcoplasmic reticulum (SR) Ca(2+) store into the peripheral subsarco

236 iated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts with the small

237 intimately associated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a median separat

238 Does this rule apply inside the sarcoplasmic reticulum (SR) of a working cell?

239 increased Ca(2+) leak from the sarcoplasmic reticulum (SR) through the RyR1.

240 release channel located in the sarcoplasmic reticulum (SR), or calsequestrin 2 (CASQ2), a SR Ca(2+)

241 or-mediated calcium release from endoplasmic reticulum stores, leading to calcineurin-mediated dephos

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

243 Endoplasmic reticulum stress causes unfolded proteins to populate th

244 Cytokine-induced endoplasmic reticulum stress enhanced exosome secretion by beta-cell

245 ptor, induces AR aggregation and endoplasmic reticulum stress in the prostate glands of ERG transgeni

246 Endoplasmic reticulum stress is an evolutionarily conserved cell str

247 ted by demonstrating increase in endoplasmic reticulum stress of MDA-MB-468 cells with time and with

248 gnaling branch of the integrated endoplasmic reticulum stress response (IERSR) is activated by Leishm

249 otein synthesis, resulting in an endoplasmic reticulum stress response mediated by Perk.

250 of the proapoptotic arms of the endoplasmic reticulum stress response that is probably secondary to

251 pha independent but involved the endoplasmic reticulum stress response.

252 t specific TG6 mutants elicit an endoplasmic reticulum stress response.

253 ing cardiac hypertrophy involves endoplasmic reticulum stress sensor PERK (protein kinase-like kinase

254 therapy and miR-183-5p regulate endoplasmic reticulum stress signaling and block endoplasmic reticul

255 1-mediated regulatory system for endoplasmic reticulum stress signaling associated with increased p-e

256 The major endoplasmic reticulum stress signaling pathway causing cardiac hyper

257 n of misfolded proteins triggers endoplasmic reticulum stress that leads to unfolded protein response

258 elial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance o

259 translational analyses revealed endoplasmic reticulum stress was not the etiology of our findings.

260 ired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signalin

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

262 vation, proinflammatory markers, endoplasmic reticulum stress, and insoluble phosphorylated TDP-43.

263 ts on mitochondrial function and endoplasmic reticulum stress, could have contributed to the neutral

264 erved of liver tissue persistent endoplasmic reticulum stress, defects in acute-phase response, and i

265 BIM and BAX, JNK signaling, and endoplasmic reticulum stress, explaining why SRp55 depletion trigger

266 t with facets of T2DM, including endoplasmic reticulum stress, inflammation, and hyperproliferation.

267 rine disrupting chemicals induce endoplasmic reticulum stress, perturb NF-kappaB, and p53 signaling,

268 hibited only subtle increases in endoplasmic reticulum stress, suggesting that an altered unfolded pr

269 icrobial stimulation to suppress endoplasmic reticulum stress, thereby assuring antiinflammatory func

270 culum stress signaling and block endoplasmic reticulum stress-induced apoptosis, cardiac hypertrophy,

271 In addition, acrolein induced endoplasmic reticulum stress-mediated death of epithelial cells, whi

272 n of tight junction proteins and endoplasmic reticulum stress-mediated epithelial cell death, thereby

273 d to aggregate and induce robust endoplasmic reticulum stress.

274 daptation to AKI associated with endoplasmic reticulum stress.

275 ered autophagy, and pathological endoplasmic reticulum stress.

276 olism and adaptive activation of endoplasmic-reticulum-stress-induced survival pathways.

277 d the IRE1-alpha-MKK4 arm of the endoplasmic-reticulum-stress-response pathway.

278 oach was developed to model the sarcoplasmic reticulum structure at the whole-cell scale, by reducing

279 ic (CREBH), is a liver-enriched, endoplasmic reticulum-tethered transcription factor known to regulat

280 acts between FYCO1 lysosomes and endoplasmic reticulum that contain the PtdIns3P effector Protrudin.

281 ing, lipid metabolism and in the endoplasmic reticulum that could impact viral entry and replication.

282 The endoplasmic reticulum, the cytoplasmic organelle that matures a mass

283 atically expanded, including the subsynaptic reticulum, the postsynaptic density, and the glutamate r

284 Like the endoplasmic reticulum, these vesicles are a distributed system for d

285 xtracellular calcium through the endoplasmic reticulum to activate SK channels.

286 ediates Ca(2+) release from the sarcoplasmic reticulum to initiate skeletal muscle contraction and is

287 d with MKC-3946, an inhibitor of endoplasmic reticulum to nucleus signaling 1 (ERN1, also called IRE1

288 iquitin-proteasome system at the endoplasmic reticulum to regulate hERG levels and channel activity.

289 for transport of UNC5A from the endoplasmic reticulum to the cell surface.

290 receptor to translocate from the endoplasmic reticulum to the cytosol and nucleus.

291 r transport of ceramide from the endoplasmic reticulum to the Golgi by the multidomain protein cerami

292 rry211 and GFP11, revealing that endoplasmic reticulum translocon complex Sec61B has reduced abundanc

293 unfolded protein response of the endoplasmic reticulum (UPR(ER)).

294 imary release of Ca(2+) from the endoplasmic reticulum via Ca(2+) release channels placed close to th

295 utants that were retained in the endoplasmic reticulum when heterologously expressed in HEK293 cells.

296 holesterol from endosomes to the endoplasmic reticulum, where it was converted to cholesteryl esters

297 resides in the jSR (junctional sarcoplasmic reticulum), whereas KCNE1 resides on the cell surface.

298 s and reduced complexity of the sub-synaptic reticulum, which could be rescued by pre- but not postsy

299 tNTT5 is probably located in the endoplasmic reticulum, which in diatoms also represents the outermos

300 e to the lumen of the epiplastid endoplasmic reticulum, with its expression regulated by the external