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2 h in stretched axons was also accompanied by endoplasmic reticulum (ER) accumulation and, accordingly
5 bined action of signal peptide peptidase and endoplasmic reticulum (ER) aminopeptidase 1 (ERAP1) is r
6 myelinating Schwann cells, processed in the endoplasmic reticulum (ER) and delivered to myelin via t
7 y, membrane contact sites (MCSs) between the endoplasmic reticulum (ER) and endosomes have emerged as
8 organises membranes at the interface of the endoplasmic reticulum (ER) and ERGIC/Golgi (Raote et al.
9 nse (UPR) plays a central role in regulating endoplasmic reticulum (ER) and global cellular physiolog
11 protein response (UPR) senses defects in the endoplasmic reticulum (ER) and orchestrates a complex pr
14 final seven steps occur in the lumen of the endoplasmic reticulum (ER) and require dolichylphosphate
15 compatibility complex (MHC) molecules in the endoplasmic reticulum (ER) and reroutes them to lysosome
16 4SS effectors localize to and/or disrupt the endoplasmic reticulum (ER) and secretory transport, but
17 ies are required for proSP-B export from the endoplasmic reticulum (ER) and sorting to LBs, the conve
19 Both DENV and ZIKV rely on expansion of the endoplasmic reticulum (ER) and the induction of autophag
20 form vC) localize to the luminal face of the endoplasmic reticulum (ER) and to the cell surface, but
23 f newly synthesized membrane proteins in the endoplasmic reticulum (ER) are assembled into multiprote
27 uclear membrane (INM) is continuous with the endoplasmic reticulum (ER) but harbors a distinctive pro
28 RNA translation to CK2alpha translation with endoplasmic reticulum (ER) Ca(2+) release versus cytopla
29 -permeable TRP channels, but the function of endoplasmic reticulum (ER) Ca(2+) stores in this importa
31 eceptor stimulation induces depletion of the endoplasmic reticulum (ER) Ca(2+) stores, which is sense
33 of calcium influx at the plasma membrane by endoplasmic reticulum (ER) calcium stores, a process com
34 Accumulation of unfolded proteins in the endoplasmic reticulum (ER) causes ER stress and activate
36 SURF4 resulted in accumulation of EPO in the endoplasmic reticulum (ER) compartment and that SURF4 an
37 we show that the disruption of mitochondria-endoplasmic reticulum (ER) contact sites (MERCs) phenoco
39 7B interaction with HSP70, thus accelerating endoplasmic reticulum (ER) degradation of the mutant pro
41 NGO1 is a transmembrane protein localised at endoplasmic reticulum (ER) exit sites, where it binds bu
42 While the effect of ROS on mitochondria and endoplasmic reticulum (ER) has been well documented, its
44 often exhibit augmented capacity to maintain endoplasmic reticulum (ER) homeostasis under adverse con
47 lly is concentrated in a subapical region of endoplasmic reticulum (ER) in cholangiocytes, but both i
49 Here, we report that DRP1 translocates to endoplasmic reticulum (ER) in response to beta-adrenergi
53 ion of unfolded or misfolded proteins at the endoplasmic reticulum (ER) is emerging as a possible dri
57 of the intrinsic activation of the PKR-like endoplasmic reticulum (ER) kinase (PERK) in the immunoin
58 fically phosphorylated protein kinase R-like endoplasmic reticulum (ER) kinase (PERK-P) signaling-a p
61 P) cation channel expressed primarily on the endoplasmic reticulum (ER) membrane and primary cilia of
63 Interestingly, NRF1 is synthesized as an endoplasmic reticulum (ER) membrane protein and when cel
64 se proteins into the membrane depends on the endoplasmic reticulum (ER) membrane protein complex (EMC
67 mian virus 40 (SV40) must penetrate the host endoplasmic reticulum (ER) membrane to enter the cytosol
68 inserts tail-anchored (TA) proteins into the endoplasmic reticulum (ER) membrane with an insertase (y
69 eased lipid packing order when comparing the endoplasmic reticulum (ER) membrane, plasma membrane, an
70 (ZIKV), rely heavily on the availability of endoplasmic reticulum (ER) membranes throughout their li
71 ctivity localizes to the plasma membrane and endoplasmic reticulum (ER) of cells, whereas TRPV3 resid
73 ng MS-based proteomics, we elucidate how the endoplasmic reticulum (ER) proteostasis network differen
74 ction between mutant calreticulin (CALR) and endoplasmic reticulum (ER) resident protein 57 (ERp57) a
75 Sterol O-acyltransferase 1 (SOAT1) is an endoplasmic reticulum (ER) resident, multi-transmembrane
77 Overexpression of GRP78 and PDI following endoplasmic reticulum (ER) stress and activation of the
78 s misfolding and polymerization, which cause endoplasmic reticulum (ER) stress and liver disease thro
79 nstrated that AKT1 protein deficiency caused endoplasmic reticulum (ER) stress and potentiated beta c
80 ion of unfolded immunoglobulins, which cause endoplasmic reticulum (ER) stress and sensitivity to pro
81 rgeting ability and its capability to induce endoplasmic reticulum (ER) stress by reactive oxygen spe
82 unfolded protein response (UPR) to mitigate endoplasmic reticulum (ER) stress caused by cellular onc
87 cilitating mucilage production by mitigating endoplasmic reticulum (ER) stress in the developing appr
88 AS, and CA-BRAF down-regulated expression of endoplasmic reticulum (ER) stress proteins, and reduced
90 l activation of innate immune sensing or the endoplasmic reticulum (ER) stress response contributes t
92 ded proteins in cells exposed to As leads to endoplasmic reticulum (ER) stress response, which, if no
97 ges IRE1alpha signaling in the absence of an endoplasmic reticulum (ER) stress signature, leading to
98 increased lipid peroxidation byproducts and endoplasmic reticulum (ER) stress, (2) decreased protect
99 eptibility to retinal degeneration caused by endoplasmic reticulum (ER) stress, and developmental def
100 rly signs of stress in different conditions: endoplasmic reticulum (ER) stress, calcium overload, oxi
101 ated by several stress conditions, including endoplasmic reticulum (ER) stress, executed by protein k
102 lies and inhibits ERK activity, resulting in endoplasmic reticulum (ER) stress, the unfolded protein
104 ice lacking functional cone CNG channel show endoplasmic reticulum (ER) stress-associated cone degene
105 igenetic state (H3K9me3), and the content of endoplasmic reticulum (ER) stress-associated transcripts
112 tes the delivery of MHC-I molecules from the endoplasmic reticulum (ER) to phagosomes, and increases
113 a critical role in endocytic trafficking and endoplasmic reticulum (ER) to plasma membrane (PM) trans
116 Here, we report the discovery of a family of endoplasmic reticulum (ER) transmembrane proteins that a
117 astin GTPase involved in homotypic fusion of endoplasmic reticulum (ER) tubules in the formation of t
119 anslational targeting and insertion into the endoplasmic reticulum (ER) via the Guided-Entry of TA pr
122 central hubs in the chaperone network of the endoplasmic reticulum (ER), acting as gatekeepers to the
124 lly focus on the links between mitochondria, endoplasmic reticulum (ER), and lysosomes in HSC metabol
125 Myelin proteins, which are produced in the endoplasmic reticulum (ER), are essential and necessary
126 s the unfolded protein response (UPR) in the endoplasmic reticulum (ER), are two mechanisms that enab
127 otein response (UPR) sensor IRE1alpha in the endoplasmic reticulum (ER), but not other UPR sensors, s
128 (PD) and use cell endomembranes, mostly the endoplasmic reticulum (ER), for delivery of viral genome
129 k TMD oligomers locate preferentially to the endoplasmic reticulum (ER), heterooligomerization betwee
130 in 4 (FATP4), a transmembrane protein in the endoplasmic reticulum (ER), is a recently identified neg
131 cts and observed outward co-movement of MTs, endoplasmic reticulum (ER), mitochondria, acidic organel
133 pairs and families within the context of the endoplasmic reticulum (ER), the main cellular hub of lip
134 ge of the signal peptide upon entry into the endoplasmic reticulum (ER), the peptide precursors are p
136 d level, the excess cholesterol moves to the endoplasmic reticulum (ER), where it regulates the SREBP
137 e most cellular cholesterol resides, and the endoplasmic reticulum (ER), where the protein machinery
138 nuclear envelope (NE) is continuous with the endoplasmic reticulum (ER), yet the NE carries out many
139 l., 2015) revealed that UBIAD1 also inhibits endoplasmic reticulum (ER)-associated degradation (ERAD)
140 clones carry mutations in genes involved in Endoplasmic Reticulum (ER)-based lipid homeostasis and a
141 ation, and protein processing/sorting in the Endoplasmic Reticulum (ER)-Golgi in a temporal order con
142 lasts showed OsPIP1;3 mislocalization in the endoplasmic reticulum (ER)-like neighborhood, whereas co
143 ate that reconstitution of VRCs on GUVs with endoplasmic reticulum (ER)-like phospholipid composition
145 ive 20 (SCAR20)-associated protein Snx14, an endoplasmic reticulum (ER)-lipid droplet (LD) tethering
146 lasmic Ca(2+) concentration ([Ca(2+)](i)) by endoplasmic reticulum (ER)-localized inositol 1,4,5-tris
147 icity, 2) Hsp70, 3) Hsp90, 4) proteasome, 5) endoplasmic reticulum (ER)-mediated folding inhibition,
148 elated protein (Drp1) severs mitochondria at endoplasmic reticulum (ER)-mitochondria contact sites, w
149 interaction molecules STIM1 and STIM2 within endoplasmic reticulum (ER)-plasma membrane (PM) contact
151 calreticulin (TcCalr) is a multifunctional, endoplasmic reticulum (ER)-resident chaperone that, tran
152 that Rab18, by directly interacting with the endoplasmic reticulum (ER)-resident protein kinectin-1,
154 (Ribo-seq) we find specific dysregulation of endoplasmic reticulum (ER)-targeted mRNA translation in
155 Notably, PSEN1 loss of function impedes Endoplasmic Reticulum (ER)-to-lysosome delivery of ClC-7
171 of ethylene receptors in the membrane of the endoplasmic reticulum (ER); a protein kinase, called con
173 such as the unfolded protein response of the endoplasmic reticulum (UPR(ER)), become defunct with age
174 hanks in part to the expert trimming done by endoplasmic reticulum aminopeptidases (ERAPs), the final
175 P alone, TurNP + EP treatment upregulated 66 endoplasmic reticulum and 193 mitochondrial proteins, en
176 Cl(-)/H(+) exchange and was retained in the endoplasmic reticulum and cis-Golgi, but not in early en
177 s studies of PQC degradation pathways in the endoplasmic reticulum and cytosol have led to the prevai
180 peptides in the oxidizing environment of the endoplasmic reticulum and is mediated by protein disulfi
181 a molecular chaperone protein located in the endoplasmic reticulum and plasma membranes and has been
182 free ribosomes, the appearance of elongated endoplasmic reticulum and strikingly increased number of
183 teasome cleavage, peptide transport into the endoplasmic reticulum and T-cell receptor repertoire, al
184 sociation of the SCAP-SREBP complex from the endoplasmic reticulum and the activation of SREBPs(1,2).
185 transgenic 16:0 desaturases targeted to the endoplasmic reticulum and the chloroplast to lower 16:0
186 chanisms to those regulating turnover of the endoplasmic reticulum and the clearance of protein aggre
187 apparatus and the close contacts between the endoplasmic reticulum and the plasma membrane, structure
191 ted by direct physical interactions with the endoplasmic reticulum Ca(2+) sensor stromal interaction
192 n endolysosomal Ca(2+) uptake and filling of endoplasmic reticulum Ca(2+) stores, thereby regulating
193 channel IP(3)R and the activity of the sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) pump during
194 differential sensitivity to the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pump inhibitors, and
198 The results of our study indicate a role for endoplasmic reticulum calcium signaling via calreticulin
199 n, which in turn phosphorylates sarcoplasmic/endoplasmic reticulum calcium-ATPase 2a (SERCA2a) and ac
201 nsulin secretion, transcription, metabolism, endoplasmic reticulum function, and the stress response.
202 unction and highlight that mitochondrial and endoplasmic reticulum functions are intertwined through
203 g to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes.
204 haperone protein generally restricted to the endoplasmic reticulum in normal tissues, but which is ex
206 acid (C18:1) to linoleic acid (C18:2) in the endoplasmic reticulum is critical to the accumulation of
208 ER-stress conditions, protein kinase R-like endoplasmic reticulum kinase (PERK) phosphorylates eukar
209 ctivation of the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), a key component of
211 the SG process using a protein kinase R-like endoplasmic reticulum kinase inhibitor (GSK2606414) or t
213 the distal axon, whilst removing Protrudin's endoplasmic reticulum localization, kinesin-binding or p
214 synthesis, lipid droplet formation, nuclear/endoplasmic reticulum membrane morphology, vacuole fusio
218 thesizing machinery associates with modified endoplasmic reticulum membranes that are transformed int
220 HL14 is in close proximity to the BCR in the endoplasmic reticulum of MCD cell line models and promot
223 s implicate Ste24 as a key factor in several endoplasmic reticulum processes, including the unfolded
224 PMP22 under CMT1A conditions overwhelms the endoplasmic reticulum quality control system, leading to
225 1) and TRP vanilloid-3 (TRPV3) in regulating endoplasmic reticulum stress (ERS) and cytotoxicity in h
226 ons promote protein misfolding, resulting in endoplasmic reticulum stress and activation of the unfol
227 response in COVID-19 infection by modulating endoplasmic reticulum stress and stimulating the resolut
232 ion causes tissue damage, which triggers the endoplasmic reticulum stress response and subsequent eic
233 itochondrial respiration, as a result of the endoplasmic reticulum stress response induced by high pr
236 e incidence of inflammation and induction of endoplasmic reticulum stress responses during an extende
237 ndidate genes at the beta-cell level and the endoplasmic reticulum stress signalling that contributes
238 HFpEF-specific downregulated genes engaged endoplasmic reticulum stress, autophagy, and angiogenesi
239 esterol (FC) in macrophages, which can cause endoplasmic reticulum stress, cholesterol crystal format
240 ly response genes, oxidative, heat shock and endoplasmic reticulum stress, DNA damage responses, indu
241 ted on PCs demonstrated that LCDD LC induces endoplasmic reticulum stress, likely accounting for the
242 ipotoxicity with impaired membrane function, endoplasmic reticulum stress, mitochondrial dysfunction,
243 lular stress, including oxidative stress and endoplasmic reticulum stress, secondary to increased dem
247 , ubiquitous Ca(2+)-buffering protein in the endoplasmic reticulum that controls transcriptional acti
248 MHC I) proteins, from their synthesis in the endoplasmic reticulum to folding and trafficking via the
252 es displayed substantial distribution in the endoplasmic reticulum with partial colocalization in mit
253 spiration, volume, and interactions with the endoplasmic reticulum) and MSNs (i.e., dendritic complex
254 els, and/or internal release from the smooth endoplasmic reticulum) near the postsynaptic density to
255 nobody-based approach to trap Wntless in the endoplasmic reticulum, and hence prevent all Wnt secreti
256 volving mitochondrial communication with the endoplasmic reticulum, and how retrograde signaling upre
257 ysosomal clearance of a model organelle, the endoplasmic reticulum, and of a model protein, polymerog
258 response, a cellular stress response of the endoplasmic reticulum, and removal of misfolded proteins
259 of cargo between the Golgi apparatus and the endoplasmic reticulum, as well as intra-Golgi transport.
260 (F/-)) triggers Golgi dispersal, dilation of endoplasmic reticulum, autophagy and exosome biogenesis
261 interaction leads to sequestration of HFE in endoplasmic reticulum, causing poorer surface expression
262 receptors are substantially localised to the endoplasmic reticulum, cellular sites of cytokinin perce
263 ally opens following Ca(2+) release from the endoplasmic reticulum, certain pathologic mutations rend
264 g proteins targeted to the cytosol, nucleus, endoplasmic reticulum, chloroplasts, mitochondria and pe
265 binding domain, cause ATP7B retention in the endoplasmic reticulum, inhibit Cu-transport, and lower A
266 erexpression facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in
267 henols with specific biological alterations (endoplasmic reticulum, lysosomes, and NFkB) caused by th
268 ses the accumulation of PILS proteins at the endoplasmic reticulum, thereby increasing nuclear abunda
269 membranes of other organelles, including the endoplasmic reticulum, via N-terminal glycine myristoyla
271 ation through sequestration of beta2M inside endoplasmic reticulum, which contributes toward inhibiti
274 , we report that protein quality control via endoplasmic reticulum-associated degradation (ERAD) gove
275 ked glycoproteins are selectively sorted for endoplasmic reticulum-associated degradation (ERAD) in r
276 l role in cellular homeostasis by regulating endoplasmic reticulum-associated degradation (ERAD), mit
278 iptomics analysis revealed downregulation of endoplasmic reticulum-associated protein degradation pat
279 s including intranuclear vesicles containing endoplasmic reticulum-associated proteins, web-like adhe
280 AM enzyme viperin (virus-inhibitory protein, endoplasmic reticulum-associated, interferon-inducible)
281 (HO-1) and the cytochromes P450 (P450s) are endoplasmic reticulum-bound enzymes that rely on the sam
284 r P4Hs, a third P4H-the poorly characterized endoplasmic reticulum-localized transmembrane prolyl 4-h
285 ile acid recirculation due to improvement of endoplasmic reticulum-mitochondria calcium homeostasis w
286 ed ADHCAI and suggested a role for FAM83H in endoplasmic reticulum-to-Golgi vesicle trafficking and p
287 Here, we show circadian clock regulation of endoplasmic reticulum-to-plasma membrane procollagen tra