ライフサイエンスコーパス: reticulum

1 on Ca(2+) store depletion of the endoplasmic reticulum.

2 trols in calcium content of the sarcoplasmic reticulum.

3 with WT, due to retention in the endoplasmic reticulum.

4 oteins that are assembled at the endoplasmic reticulum.

5 rotein (SCAP) and sterols in the endoplasmic reticulum.

6 chloroplasts, lysosomes, and the endoplasmic reticulum.

7 th post-glycan processing in the endoplasmic reticulum.

8 ical Ca(2+) concentration in the endoplasmic reticulum.

9 are partially colocalized in the endoplasmic reticulum.

10 hrough these interactions in the endoplasmic reticulum.

11 NP + EP treatment upregulated 66 endoplasmic reticulum and 193 mitochondrial proteins, enhancing seve

12 PQC degradation pathways in the endoplasmic reticulum and cytosol have led to the prevailing idea th

13 in EC cytoplasm (associated with endoplasmic reticulum and Golgi proteins).

14 including endosomes, lysosomes, endoplasmic reticulum and Golgi.

15 chaperone protein located in the endoplasmic reticulum and plasma membranes and has been shown to pla

16 mes, the appearance of elongated endoplasmic reticulum and strikingly increased number of mitochondri

17 vage, peptide transport into the endoplasmic reticulum and T-cell receptor repertoire, also contribut

18 the SCAP-SREBP complex from the endoplasmic reticulum and the activation of SREBPs(1,2).

19 16:0 desaturases targeted to the endoplasmic reticulum and the chloroplast to lower 16:0 in leaf lipi

20 those regulating turnover of the endoplasmic reticulum and the clearance of protein aggregates.

21 d the close contacts between the endoplasmic reticulum and the plasma membrane, structures that have

22 olume, and interactions with the endoplasmic reticulum) and MSNs (i.e., dendritic complexity, spine d

23 approach to trap Wntless in the endoplasmic reticulum, and hence prevent all Wnt secretion, specific

24 chondrial communication with the endoplasmic reticulum, and how retrograde signaling upregulates the

25 arance of a model organelle, the endoplasmic reticulum, and of a model protein, polymerogenic ATZ.

26 cellular stress response of the endoplasmic reticulum, and removal of misfolded proteins from the tr

27 ween the Golgi apparatus and the endoplasmic reticulum, as well as intra-Golgi transport.

28 und to be partly retained in the endoplasmic reticulum-associated cell compartments.

29 Here we report endoplasmic reticulum-associated degradation (ERAD) as a protein qua

30 that protein quality control via endoplasmic reticulum-associated degradation (ERAD) governs the func

31 teins are selectively sorted for endoplasmic reticulum-associated degradation (ERAD) in response to t

32 llular homeostasis by regulating endoplasmic reticulum-associated degradation (ERAD), mitochondrial-a

33 In endoplasmic reticulum-associated protein degradation (ERAD), membran

34 lysis revealed downregulation of endoplasmic reticulum-associated protein degradation pathway compone

35 Thus, the UPR, an endoplasmic-reticulum-associated response, quite unexpectedly contri

36 perin (virus-inhibitory protein, endoplasmic reticulum-associated, interferon-inducible) to enhance v

37 the cytochromes P450 (P450s) are endoplasmic reticulum-bound enzymes that rely on the same protein, N

38 localized to the cytosol and the endoplasmic reticulum but also to the nuclei.

39 ed the frequency of spontaneous sarcoplasmic reticulum Ca release, while QX-flecainide and N-methyl f

40 ave shown that dysregulation of sarcoplasmic reticulum Ca(2+) ATPase (SERCA) pump is one of the key d

41 amplitude, 50% decay rate, and sarcoplasmic reticulum Ca(2+) content were not different between WT (

42 Ca(2+), RyR2 inactivation, and sarcoplasmic reticulum Ca(2+) release (ie, Ca(2+) alternans).

43 nt RyR2 inactivation diminishes sarcoplasmic reticulum Ca(2+) release, which, in turn, reduces diasto

44 t physical interactions with the endoplasmic reticulum Ca(2+) sensor stromal interaction molecule 1 (

45 mal Ca(2+) uptake and filling of endoplasmic reticulum Ca(2+) stores, thereby regulating exocytosis i

46 The sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) is a P-type ATPase that

47 sensitivity to the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pump inhibitors, and only the re

48 SERCAs (sarco-endoplasmic reticulum Ca(2+)-ATPases) pump Ca(2+) into internal stor

49 Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity was reduced and w

50 ans mainly due to the increased sarcoplasmic reticulum Ca2+-ATPase (SERCA) Ca2+ reuptake, modulated b

51 transport activity of the sarco(endo)plasmic reticulum calcium ATPase (SERCA) in cardiac myocytes is

52 the ER calcium pump sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA).

53 f Ser(16) acutely stimulate the sarcoplasmic reticulum calcium pump (SERCA) by relieving its inhibiti

54 of our study indicate a role for endoplasmic reticulum calcium signaling via calreticulin in the diff

55 turn phosphorylates sarcoplasmic/endoplasmic reticulum calcium-ATPase 2a (SERCA2a) and accelerates ca

56 diastolic Ca(2+) leak from the sarcoplasmic reticulum can be normalized by the cardiac ryanodine rec

57 leads to sequestration of HFE in endoplasmic reticulum, causing poorer surface expression of HFE and

58 e substantially localised to the endoplasmic reticulum, cellular sites of cytokinin perception and im

59 ollowing Ca(2+) release from the endoplasmic reticulum, certain pathologic mutations render the chann

60 argeted to the cytosol, nucleus, endoplasmic reticulum, chloroplasts, mitochondria and peroxisomes.

61 ed axons was also accompanied by endoplasmic reticulum (ER) accumulation and, accordingly, it was blo

62 uption of protein folding in the endoplasmic reticulum (ER) activates the unfolded protein response (

63 Endoplasmic reticulum (ER) acts as the largest intracellular Ca(2+)

64 of signal peptide peptidase and endoplasmic reticulum (ER) aminopeptidase 1 (ERAP1) is required for

65 Schwann cells, processed in the endoplasmic reticulum (ER) and delivered to myelin via the secretory

66 contact sites (MCSs) between the endoplasmic reticulum (ER) and endosomes have emerged as important p

67 embranes at the interface of the endoplasmic reticulum (ER) and ERGIC/Golgi (Raote et al., 2018).

68 ays a central role in regulating endoplasmic reticulum (ER) and global cellular physiology in respons

69 ocalized to the plasma membrane, endoplasmic reticulum (ER) and Golgi.

70 onse (UPR) senses defects in the endoplasmic reticulum (ER) and orchestrates a complex program of ada

71 ethered interactions between the endoplasmic reticulum (ER) and other membrane-bound organelles allow

72 olyomavirus SV40 traffics to the endoplasmic reticulum (ER) and penetrates a virus-induced structure

73 steps occur in the lumen of the endoplasmic reticulum (ER) and require dolichylphosphate-activated m

74 y complex (MHC) molecules in the endoplasmic reticulum (ER) and reroutes them to lysosomes.

75 ired for proSP-B export from the endoplasmic reticulum (ER) and sorting to LBs, the conversion of pro

76 olved in trafficking between the endoplasmic reticulum (ER) and the Golgi.

77 nd ZIKV rely on expansion of the endoplasmic reticulum (ER) and the induction of autophagy to establi

78 alize to the luminal face of the endoplasmic reticulum (ER) and to the cell surface, but not to mitoc

79 STING resides on the endoplasmic reticulum (ER) and traffics following stimulation to the

80 l enzymes are synthesized in the endoplasmic reticulum (ER) and transferred to the Golgi complex by i

81 hesized membrane proteins in the endoplasmic reticulum (ER) are assembled into multiprotein complexes

82 Misfolded proteins in the endoplasmic reticulum (ER) are degraded by ER-associated degradation

83 tatin 1 (ES1) is an inhibitor of endoplasmic reticulum (ER) associated protein degradation, Sec61-dep

84 ane (INM) is continuous with the endoplasmic reticulum (ER) but harbors a distinctive proteome essent

85 RP channels, but the function of endoplasmic reticulum (ER) Ca(2+) stores in this important model for

86 However, depletion of endoplasmic reticulum (ER) Ca(2+) stores reduced capsaicin-induced C

87 ulation induces depletion of the endoplasmic reticulum (ER) Ca(2+) stores, which is sensed by stromal

88 The type 2a sarco/endoplasmic reticulum (ER) Ca(2+)-ATPase (SERCA2a) plays a key role

89 influx at the plasma membrane by endoplasmic reticulum (ER) calcium stores, a process common to inver

90 tion of unfolded proteins in the endoplasmic reticulum (ER) causes ER stress and activates a signalin

91 Sigma-1 receptor (S1R) is an endoplasmic reticulum (ER) chaperone that not only regulates mitocho

92 ed in accumulation of EPO in the endoplasmic reticulum (ER) compartment and that SURF4 and EPO physic

93 t the disruption of mitochondria-endoplasmic reticulum (ER) contact sites (MERCs) phenocopies OxPHOS

94 n, which constricts membranes at endoplasmic reticulum (ER) contact sites.

95 on with HSP70, thus accelerating endoplasmic reticulum (ER) degradation of the mutant protein and con

96 ansmembrane protein localised at endoplasmic reticulum (ER) exit sites, where it binds bulky cargo wi

97 ffect of ROS on mitochondria and endoplasmic reticulum (ER) has been well documented, its consequence

98 The endoplasmic reticulum (ER) has recently emerged as a promising targe

99 t augmented capacity to maintain endoplasmic reticulum (ER) homeostasis under adverse conditions, yet

100 The endoplasmic reticulum (ER) immunoglobulin binding proteins (BiPs) ar

101 and retain MR1 molecules in the endoplasmic reticulum (ER) in an immature form.

102 ntrated in a subapical region of endoplasmic reticulum (ER) in cholangiocytes, but both immunogold el

103 o imaging reveals instability of endoplasmic reticulum (ER) in mouse AD models and genome-edited huma

104 report that DRP1 translocates to endoplasmic reticulum (ER) in response to beta-adrenergic stimulatio

105 The endoplasmic reticulum (ER) is a fundamental organelle in cellular me

106 droplet (LD) formation from the endoplasmic reticulum (ER) is accompanied by the targeting and accum

107 mbrane protein biogenesis in the endoplasmic reticulum (ER) is complex and failure-prone.

108 ded or misfolded proteins at the endoplasmic reticulum (ER) is emerging as a possible driver of human

109 The endoplasmic reticulum (ER) is the entry point to the secretory pathw

110 The endoplasmic reticulum (ER) is the main site of protein synthesis in

111 insic activation of the PKR-like endoplasmic reticulum (ER) kinase (PERK) in the immunoinhibitory act

112 Endoplasmic reticulum (ER) macroautophagy (hereafter called ER-phagy

113 annel expressed primarily on the endoplasmic reticulum (ER) membrane and primary cilia of all cell an

114 The endoplasmic reticulum (ER) membrane complex (EMC) cooperates with th

115 ingly, NRF1 is synthesized as an endoplasmic reticulum (ER) membrane protein and when cellular protea

116 The endoplasmic reticulum (ER) membrane protein complex (EMC) was identi

117 in ligases (E3s) embedded in the endoplasmic reticulum (ER) membrane regulate essential cellular acti

118 0 (SV40) must penetrate the host endoplasmic reticulum (ER) membrane to enter the cytosol in order to

119 -anchored (TA) proteins into the endoplasmic reticulum (ER) membrane with an insertase (yeast Get1/Ge

120 packing order when comparing the endoplasmic reticulum (ER) membrane, plasma membrane, and nanodomain

121 y heavily on the availability of endoplasmic reticulum (ER) membranes throughout their life cycle, an

122 lizes to the plasma membrane and endoplasmic reticulum (ER) of cells, whereas TRPV3 resides primarily

123 Upon ligand stimulation, the endoplasmic reticulum (ER) protein STING translocates to endosomes f

124 proteomics, we elucidate how the endoplasmic reticulum (ER) proteostasis network differentially engag

125 n mutant calreticulin (CALR) and endoplasmic reticulum (ER) resident protein 57 (ERp57) as it pertain

126 -acyltransferase 1 (SOAT1) is an endoplasmic reticulum (ER) resident, multi-transmembrane enzyme that

127 The metazoan endoplasmic reticulum (ER) serves both as a hub for maturation of se

128 ssion of GRP78 and PDI following endoplasmic reticulum (ER) stress and activation of the unfolded pro

129 and polymerization, which cause endoplasmic reticulum (ER) stress and liver disease through a gain-o

130 t AKT1 protein deficiency caused endoplasmic reticulum (ER) stress and potentiated beta cells to unde

131 ded immunoglobulins, which cause endoplasmic reticulum (ER) stress and sensitivity to proteasome inhi

132 otein response (UPR) to mitigate endoplasmic reticulum (ER) stress caused by cellular oncogene activa

133 Endoplasmic reticulum (ER) stress in AEC has been observed in idiopa

134 tein expression showed beta-cell endoplasmic reticulum (ER) stress in both sexes.

135 Persistent endoplasmic reticulum (ER) stress in neurons is associated with acti

136 We assessed the role of endoplasmic reticulum (ER) stress in the cross-talk between stellate

137 ucilage production by mitigating endoplasmic reticulum (ER) stress in the developing appressorium.

138 RAF down-regulated expression of endoplasmic reticulum (ER) stress proteins, and reduced unfolded pro

139 ionally, Rebaudioside A improved endoplasmic reticulum (ER) stress related gene expressions, fasting

140 of innate immune sensing or the endoplasmic reticulum (ER) stress response contributes to the change

141 FVIII expression activates the endoplasmic reticulum (ER) stress response, causes oxidative stress,

142 in cells exposed to As leads to endoplasmic reticulum (ER) stress response, which, if not relieved,

143 ion resolution and triggering an endoplasmic reticulum (ER) stress response.

144 hospholipase C2 functions in the endoplasmic reticulum (ER) stress response.

145 ivation of genes involved in the endoplasmic reticulum (ER) stress response.

146 XBP1, a transcription factor of endoplasmic reticulum (ER) stress response.

147 a signaling in the absence of an endoplasmic reticulum (ER) stress signature, leading to the exclusiv

148 ipid peroxidation byproducts and endoplasmic reticulum (ER) stress, (2) decreased protective ER chape

149 o retinal degeneration caused by endoplasmic reticulum (ER) stress, and developmental defects similar

150 stress in different conditions: endoplasmic reticulum (ER) stress, calcium overload, oxidative stres

151 ral stress conditions, including endoplasmic reticulum (ER) stress, executed by protein kinase R-like

152 ibits ERK activity, resulting in endoplasmic reticulum (ER) stress, the unfolded protein response, an

153 Hepatic endoplasmic reticulum (ER) stress, whether triggered by intrinsic or

154 functional cone CNG channel show endoplasmic reticulum (ER) stress-associated cone degeneration.

155 te (H3K9me3), and the content of endoplasmic reticulum (ER) stress-associated transcripts (IRE-1 and

156 Here, we report that the chronic endoplasmic reticulum (ER) stress-induced ATF4-CHOP-GADD34 pathway i

157 ions, activated Rho GTPases, and endoplasmic reticulum (ER) stress.

158 lation of misfolded proteins and endoplasmic reticulum (ER) stress.

159 ctivation as well as thermal and endoplasmic reticulum (ER) stress.

160 ronmental conditions can trigger endoplasmic reticulum (ER) stress.

161 S2P) sequentially in response to endoplasmic reticulum (ER) stress.

162 very of MHC-I molecules from the endoplasmic reticulum (ER) to phagosomes, and increases the levels o

163 ole in endocytic trafficking and endoplasmic reticulum (ER) to plasma membrane (PM) transport.

164 hibited its trafficking from the endoplasmic reticulum (ER) to the Golgi complex.

165 Proteins that clog the endoplasmic reticulum (ER) translocon prevent the movement of other

166 ort the discovery of a family of endoplasmic reticulum (ER) transmembrane proteins that associate wit

167 involved in homotypic fusion of endoplasmic reticulum (ER) tubules in the formation of the interconn

168 stabilize the high curvature of endoplasmic reticulum (ER) tubules.

169 targeting and insertion into the endoplasmic reticulum (ER) via the Guided-Entry of TA proteins (GET)

170 nts for only 5% of lipids in the endoplasmic reticulum (ER)(1).

171 rted, modified and folded at the endoplasmic reticulum (ER)(2).

172 in the chaperone network of the endoplasmic reticulum (ER), acting as gatekeepers to the early secre

173 istinct from hydrogenosomes, the endoplasmic reticulum (ER), and Golgi complex.

174 the links between mitochondria, endoplasmic reticulum (ER), and lysosomes in HSC metabolism.

175 teins, which are produced in the endoplasmic reticulum (ER), are essential and necessary for maintain

176 ed protein response (UPR) in the endoplasmic reticulum (ER), are two mechanisms that enable plants to

177 se (UPR) sensor IRE1alpha in the endoplasmic reticulum (ER), but not other UPR sensors, such as prote

178 e cell endomembranes, mostly the endoplasmic reticulum (ER), for delivery of viral genomes to PD and

179 ers locate preferentially to the endoplasmic reticulum (ER), heterooligomerization between the TMDs o

180 , a transmembrane protein in the endoplasmic reticulum (ER), is a recently identified negative regula

181 rved outward co-movement of MTs, endoplasmic reticulum (ER), mitochondria, acidic organelles, F-actin

182 In the endoplasmic reticulum (ER), secretory proteins are packaged into COP

183 milies within the context of the endoplasmic reticulum (ER), the main cellular hub of lipid biosynthe

184 gnal peptide upon entry into the endoplasmic reticulum (ER), the peptide precursors are processed in

185 The cholesterol moves to the endoplasmic reticulum (ER), where it inhibits production of LDL rece

186 excess cholesterol moves to the endoplasmic reticulum (ER), where it regulates the SREBP2 pathway an

187 lar cholesterol resides, and the endoplasmic reticulum (ER), where the protein machinery that regulat

188 lope (NE) is continuous with the endoplasmic reticulum (ER), yet the NE carries out many functions di

189 vealed that UBIAD1 also inhibits endoplasmic reticulum (ER)-associated degradation (ERAD) of ubiquiti

190 y mutations in genes involved in Endoplasmic Reticulum (ER)-based lipid homeostasis and autophagy.

191 rotein processing/sorting in the Endoplasmic Reticulum (ER)-Golgi in a temporal order consistent with

192 OsPIP1;3 mislocalization in the endoplasmic reticulum (ER)-like neighborhood, whereas co-expression

193 onstitution of VRCs on GUVs with endoplasmic reticulum (ER)-like phospholipid composition results in

194 SEIPIN proteins are localized to endoplasmic reticulum (ER)-lipid droplet (LD) junctions where they m

195 20)-associated protein Snx14, an endoplasmic reticulum (ER)-lipid droplet (LD) tethering protein, as

196 ) concentration ([Ca(2+)](i)) by endoplasmic reticulum (ER)-localized inositol 1,4,5-trisphosphate re

197 p70, 3) Hsp90, 4) proteasome, 5) endoplasmic reticulum (ER)-mediated folding inhibition, and 6) oxida

198 in (Drp1) severs mitochondria at endoplasmic reticulum (ER)-mitochondria contact sites, where periphe

199 molecules STIM1 and STIM2 within endoplasmic reticulum (ER)-plasma membrane (PM) contact sites.

200 K-L augmented SOCE by increasing endoplasmic reticulum (ER)-plasma membrane (PM) junctions and STIM1

201 n (TcCalr) is a multifunctional, endoplasmic reticulum (ER)-resident chaperone that, translocated to

202 by directly interacting with the endoplasmic reticulum (ER)-resident protein kinectin-1, controls the

203 The endoplasmic reticulum (ER)-resident protein TANGO1 assembles into a

204 e find specific dysregulation of endoplasmic reticulum (ER)-targeted mRNA translation in DIS3L2-defic

205 , PSEN1 loss of function impedes Endoplasmic Reticulum (ER)-to-lysosome delivery of ClC-7.

206 rage organelles assembled at the endoplasmic reticulum (ER).

207 peroxisomes and degraded in the endoplasmic reticulum (ER).

208 ted and localized largely to the endoplasmic reticulum (ER).

209 iled to properly assemble in the endoplasmic reticulum (ER).

210 molecules (STIM) located in the endoplasmic reticulum (ER).

211 ganelles that originate from the endoplasmic reticulum (ER).

212 ndosomes/lysosomes (LEL) and the endoplasmic reticulum (ER).

213 ssential for its assembly in the endoplasmic reticulum (ER).

214 -dependent Ca2+ release from the endoplasmic reticulum (ER).

215 ded or misfolded proteins in the endoplasmic reticulum (ER).

216 hesis enriched this lipid in the endoplasmic reticulum (ER).

217 membrane enzymes located in the endoplasmic reticulum (ER).

218 UNV, causes GPC retention in the endoplasmic reticulum (ER).

219 receptors in the membrane of the endoplasmic reticulum (ER); a protein kinase, called constitutive tr

220 te that became aggregated in the endoplasmic reticulum following ERAD deficiency.

221 tion, transcription, metabolism, endoplasmic reticulum function, and the stress response.

222 highlight that mitochondrial and endoplasmic reticulum functions are intertwined through galactose me

223 s independently of the classical endoplasmic reticulum-Golgi exocytic route.

224 In lipid bilayers that mimic the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) membran

225 global calcium release from the sarcoplasmic reticulum in LV myocytes, without affecting intrinsic ry

226 ontrols calcium release from the endoplasmic reticulum in macrophages and monocytes.

227 tein generally restricted to the endoplasmic reticulum in normal tissues, but which is expressed on t

228 in, cause ATP7B retention in the endoplasmic reticulum, inhibit Cu-transport, and lower ATP7B protein

229 facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in the distal a

230 changes in the location of the sarcoplasmic reticulum, inter-organelle distances, and differential d

231 The endoplasmic reticulum is a cellular hub of lipid metabolism, coordin

232 to linoleic acid (C18:2) in the endoplasmic reticulum is critical to the accumulation of polyunsatur

233 blation of protein kinase R-like endoplasmic reticulum kinase (PERK) also ameliorated the S63del neur

234 onditions, protein kinase R-like endoplasmic reticulum kinase (PERK) phosphorylates eukaryotic initia

235 xecuted by protein kinase R-like endoplasmic reticulum kinase (PERK).

236 ss using a protein kinase R-like endoplasmic reticulum kinase inhibitor (GSK2606414) or the translati

237 se and the protein kinase R-like endoplasmic reticulum kinase.

238 xon, whilst removing Protrudin's endoplasmic reticulum localization, kinesin-binding or phosphoinosit

239 ird P4H-the poorly characterized endoplasmic reticulum-localized transmembrane prolyl 4-hydroxylase (

240 specific biological alterations (endoplasmic reticulum, lysosomes, and NFkB) caused by these samples.

241 lipid droplet formation, nuclear/endoplasmic reticulum membrane morphology, vacuole fusion, and growt

242 IRE1 spans the endoplasmic reticulum membrane, comprising a sensory lumenal domain,

243 the other COPII proteins to the endoplasmic reticulum membrane.

244 its translocation to the nuclear/endoplasmic reticulum membrane.

245 chinery associates with modified endoplasmic reticulum membranes that are transformed into the viral

246 irculation due to improvement of endoplasmic reticulum-mitochondria calcium homeostasis with hepatic

247 her protein abundance) and novel endoplasmic reticulum morphology.

248 internal release from the smooth endoplasmic reticulum) near the postsynaptic density to promote the

249 lose proximity to the BCR in the endoplasmic reticulum of MCD cell line models and promotes the turno

250 Endoplasmic reticulum omega-oxidation, a minor fatty acid degradatio

251 Ste24 as a key factor in several endoplasmic reticulum processes, including the unfolded protein resp

252 CMT1A conditions overwhelms the endoplasmic reticulum quality control system, leading to formation o

253 Sarcoplasmic reticulum (SR) Ca(2+) content increased during CH then d

254 ne receptor 2 (RYR2), the major sarcoplasmic reticulum (SR) Ca(2+)-release channel in the heart, how

255 s smaller, although spontaneous sarcoplasmic reticulum (SR) Ca(2+)-release events and L-type Ca(2+)-c

256 Because sarcoplasmic reticulum (SR) calcium has been shown to play a critical

257 nt of calcium released from the Sarcoplasmic Reticulum (SR) during systole.

258 00 nm resolution located GPa at sarcoplasmic reticulum (SR) junctional cisternae, and apo-GP at Z dis

259 iadin (T95) is localized in the sarcoplasmic reticulum (SR) subdomain of triads where it forms large

260 ular release of Ca(2+) from the sarcoplasmic reticulum (SR) through RyR2 generates localized elevatio

261 (RyR2s) release Ca(2+) from the sarcoplasmic reticulum (SR) via a positive feedback mechanism in whic

262 lcium in the cell stored in the sarcoplasmic reticulum (SR), and another, with open RyRs and a deplet

263 gical' calcium release from the sarcoplasmic reticulum (SR), the major calcium storage organelle in s

264 from the cytosol into the sarco(endo)plasmic reticulum (SR/ER) lumen, driven by ATP.

265 The sarco-endoplasmic reticulum (SR/ER) plays an important role in the develop

266 from increased Ca(2+) leak from sarcoplasmic reticulum stores via dysregulated ryanodine receptor (Ry

267 COVID-19 infection by modulating endoplasmic reticulum stress and stimulating the resolution of infla

268 inase, whereas mitochondrial and endoplasmic reticulum stress did not.

269 Cells undergoing endoplasmic reticulum stress express spliced X-box binding protein 1

270 Induction of endoplasmic reticulum stress in knockout macrophages increases miR-1

271 -inducible nitric oxide synthase-endoplasmic reticulum stress pathway.

272 issue damage, which triggers the endoplasmic reticulum stress response and subsequent eicosanoid and

273 respiration, as a result of the endoplasmic reticulum stress response induced by high production of

274 olded protein response (UPR), an endoplasmic reticulum stress response pathway, has been implicated i

275 o the latter's ability to induce endoplasmic reticulum stress response.

276 of inflammation and induction of endoplasmic reticulum stress responses during an extended period of

277 s at the beta-cell level and the endoplasmic reticulum stress signalling that contributes to beta-cel

278 ific downregulated genes engaged endoplasmic reticulum stress, autophagy, and angiogenesis.

279 in macrophages, which can cause endoplasmic reticulum stress, cholesterol crystal formation, and inf

280 genes, oxidative, heat shock and endoplasmic reticulum stress, DNA damage responses, induction of xen

281 emonstrated that LCDD LC induces endoplasmic reticulum stress, likely accounting for the high efficie

282 with impaired membrane function, endoplasmic reticulum stress, mitochondrial dysfunction, cell death,

283 , including oxidative stress and endoplasmic reticulum stress, secondary to increased demand for insu

284 rom mutant ELANE, which triggers endoplasmic reticulum stress, UPR, and apoptosis.

285 , such as nutrient deficiency or endoplasmic reticulum stress.

286 ell type 17 (Th17) signaling and endoplasmic reticulum stress.

287 Ca(2+)-buffering protein in the endoplasmic reticulum that controls transcriptional activity of vari

288 ins, from their synthesis in the endoplasmic reticulum to folding and trafficking via the secretory p

289 nal proton transport across the sarcoplasmic reticulum to maintain the charge balance of the transpor

290 rs of vesicular traffic from the endoplasmic reticulum to the Golgi apparatus.

291 folding and trafficking from the endoplasmic reticulum to the LE/Ly compartments.

292 P3R), thereby linking the endo-/sarcoplasmic reticulum to the plasma membrane.

293 d suggested a role for FAM83H in endoplasmic reticulum-to-Golgi vesicle trafficking and protein secre

294 ow circadian clock regulation of endoplasmic reticulum-to-plasma membrane procollagen transport by th

295 unfolded protein response of the endoplasmic reticulum (UPR(ER)), become defunct with age.

296 other organelles, including the endoplasmic reticulum, via N-terminal glycine myristoylation.

297 umber and decreased postsynaptic subsynaptic reticulum volume, with the emergence of filopodial-like

298 rylated PCK1 translocates to the endoplasmic reticulum, where it uses GTP as a phosphate donor to pho

299 h sequestration of beta2M inside endoplasmic reticulum, which contributes toward inhibition of MHC cl

300 substantial distribution in the endoplasmic reticulum with partial colocalization in mitochondria an