ライフサイエンスコーパス: ER membrane

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

2 ion-competent virion capable of crossing the ER membrane.

3 of calnexin to the retention of PTP1B at the ER membrane.

4 igher eukaryotes causes LDs to remain in the ER membrane.

5 is sequestered in increasing amounts at the ER membrane.

6 ontaining ectodomains if not anchored at the ER membrane.

7 nect these lumenal events with events on the ER membrane.

8 nds and cleaves the majority of mRNAs at the ER membrane.

9 ciated role for this ubiquitin ligase at the ER membrane.

10 V) and SYTA directly interacted caged within ER membrane.

11 mpetent state until it is ready to cross the ER membrane.

12 on is coordinated on the lumenal side of the ER membrane.

13 om SV40 to enable the virus to penetrate the ER membrane.

14 atidylinositol-3-phosphate appearance at the ER membrane.

15 phospholipids that are also abundant in the ER membrane.

16 3 (SH3) domain and DHHC6 is localized to the ER membrane.

17 sociated with the endoplasmic reticulum (ER)/ER membrane.

18 a fragment that is no longer tethered to the ER membrane.

19 are essential for recruitment of Bag6 to the ER membrane.

20 formation involves the interaction with the ER membrane.

21 rion is derived from the luminal side of the ER membrane.

22 r modifications, appeared to trap Rem in the ER membrane.

23 position of the plasma membrane (PM) and the ER membrane.

24 oth the luminal and cytoplasmic sides of the ER membrane.

25 5 was previously shown to associate with the ER membrane.

26 lternately directed to opposite sides of the ER membrane.

27 compromising the permeability barrier of the ER membrane.

28 ote the release of active p110 Nrf1 from the ER membrane.

29 vesicles, while Anks1a remains behind on the ER membrane.

30 teins are translated when they encounter the ER membrane.

31 eract and form low-mobility oligomers in the ER membrane.

32 conserved protein-conducting channel in the ER-membrane.

33 to translocon-engaged 60S subunits on native ER membranes.

34 1 and subsequently impaired its activity at ER membranes.

35 likely involve binding to mitochondrial and ER membranes.

36 coordinated action of RHD3 in the fusion of ER membranes.

37 e lipid droplets closely associated with the ER membranes.

38 Sar1p recruits the Sec23p-Sec24p complex to ER membranes.

39 of Bag6 is required for interaction with the ER membranes.

40 OPII) proteins for their biogenesis from the ER membranes.

41 indicate that TMUB1 bridges SPFH2 to gp78 in ER membranes.

42 uctase to the Insig-1 or Insig-2 proteins of ER membranes.

43 We show that native IP3Rs cluster within ER membranes.

44 ding domain of NS1, which can associate with ER membranes.

45 associated Get1/2 complex for insertion into ER membranes.

46 e (TM) segment in the endoplasmic reticulum (ER) membrane.

47 zyme localized to the endoplasmic reticulum (ER) membrane.

48 of TA proteins to the endoplasmic reticulum (ER) membrane.

49 ctor localized in the endoplasmic reticulum (ER) membrane.

50 ifferent sides of the endoplasmic reticulum (ER) membrane.

51 m the ribosome to the endoplasmic reticulum (ER) membrane.

52 sphatidic acid at the endoplasmic reticulum (ER) membrane.

53 tophagosomes from the endoplasmic reticulum (ER) membrane.

54 ed (TA) proteins into endoplasmic reticulum (ER) membranes.

55 ration from the presumably uniformly fluidic ER membrane, a previously unknown phenomenon.

56 This phenotype originates in mitosis, when ER membranes accumulate on metaphase chromosomes.

57 We identified 24 ER membrane-anchored ubiquitin ligases and found Nixin/Z

58 tein quality control machinery to breach the ER membrane and access the cytosol, a decisive infection

59 e the ER, tagged lipids intercalate with the ER membrane and are subsequently incorporated into ER-as

60 facilitated its deleterious interaction with ER membrane and associated proteins that are essential f

61 fore p97 ATPase-mediated extraction from the ER membrane and can be targeted to nonlysine, as well as

62 The catalytic CTA1 subunit then crosses the ER membrane and enters the cytosol, where it interacts w

63 T-1S113R is unable to form homodimers in the ER membrane and is devoid of acetyl-CoA transport activi

64 hagy serves as a pathway for the turnover of ER membrane and its contents in response to ER stress in

65 Protein translocation across the ER membrane and N-glycosylation are highly coordinated p

66 iscovery that MP(TVCV), beyond localizing to ER membrane and plasmodesmata, targeted to the nucleus i

67 his, a mutant SV40 that cannot penetrate the ER membrane and promote infection fails to induce C18 fo

68 ) quality control machinery to penetrate the ER membrane and reach the cytosol, a critical infection

69 Mechanistically, Tmem178 localizes to the ER membrane and regulates RANKL-induced Ca(2+) fluxes, t

70 y of utilizing the hydrophobic nature of the ER membrane and selective ER components to gain access t

71 SIK2 co-localizes with p97/VCP in the ER membrane and stimulates its ATPase activity through d

72 lization and distribution of CerS within the ER membrane and that phosphorylation of these sites is f

73 find that the MYRF proteins localize to the ER membrane and that they are cleaved into active N-term

74 smaller vesicles, leading to accumulation of ER membranes and more stable ER exit sites.

75 roper localization of the Opi1p repressor to ER membranes and subsequent INO1 derepression.

76 -ANT1) resides in the endoplasmic reticulum (ER) membrane and acts as an ATP/ADP antiporter.

77 Ds originate from the endoplasmic reticulum (ER) membrane and are mainly composed of a triglyceride (

78 lcium channels in the endoplasmic reticulum (ER) membrane and govern the release of ER calcium stores

79 n S) localizes to the endoplasmic reticulum (ER) membrane and is involved in the process of ER-associ

80 s into the eukaryotic endoplasmic reticulum (ER) membrane and the prokaryotic plasma membrane.

81 wilt, Gc localizes at endoplasmic reticulum (ER) membranes and becomes ER export competent only upon

82 ey are polyubiquitinated, extracted from the ER membrane, and degraded by the proteasome.

83 mbrane-spanning helices, is localized to the ER membrane, and possesses ubiquitin ligase activity.

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

85 ority of NCC polypeptide was integrated into ER membranes, and its turnover rate was sensitive to pro

86 SOD1, its association with mitochondrial and ER membranes, and the levels of sedimentable insoluble S

87 ed protein across the endoplasmic reticulum (ER) membrane, and ubiquitin-mediated targeting to the pr

88 The expanded ER membranes are formed due to deletion of a lipin homol

89 s up to 10-fold higher than wild type, while ER membranes are largely unaffected.

90 esterol levels in the endoplasmic reticulum (ER) membrane are high, but the signal for degradation wa

91 unctioned in vivo to insert TA proteins into ER membranes as demonstrated by the fact that the YFP-ta

92 containing actin-binding domains, is a novel ER membrane-associated actin-binding protein.

93 The conserved ER membrane-associated BAX inhibitor 1 (BI1) modulates E

94 C degradation was primarily dependent on the ER membrane-associated E3 ubiquitin ligase Hrd1.

95 Arabidopsis bZIP28, an ER membrane-associated transcription factor, is activate

96 d role for Get4/5 in recycling Get3 from the ER membrane at the end of the targeting reaction.

97 ns are integrated cotranslationally into the ER membrane at the translocon, where nonpolar nascent pr

98 ulate between mitochondria and INF2-enriched ER membranes at constriction sites.

99 rier in the form of a distinct domain of the ER-membrane at the bud neck, in a septin-, Bud1 GTPase-

100 trafficking to internal membranes modulates ER membrane behavior.

101 cating that a diffusion barrier forms in the ER membrane between these two domains.

102 Endoplasmic reticulum (ER) membrane-bound E3 ubiquitin ligases promote ER-assoc

103 40) hijacks the three endoplasmic reticulum (ER) membrane-bound J proteins B12, B14, and C18 to escap

104 R is not by acquisition of a larger patch of ER membrane, but instead by addition of ERGIC membranes

105 Consistently, ER membranes, but not Golgi or mitochondrial membranes,

106 They localize in the ER membranes, but their cellular function remains unclea

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

108 le-based motor kinesin-1 is recruited to the ER membrane by binding to the transmembrane J-protein B1

109 As a consequence, VKORC1 exits the ER membrane by cellular quality control systems and resu

110 rapid capture of newly synthesized LD at the ER membrane by nascent autophagosomal structures.

111 se, TorsinA and TorsinB, are anchored to the ER membrane by virtue of an N-terminal hydrophobic domai

112 ether, these results indicate that fusion of ER membranes by ATL and interaction of ER with growing M

113 s are produced at the endoplasmic reticulum (ER) membrane by a multicomponent enzyme complex termed c

114 or inserted into the endoplasmic reticulum (ER) membrane by the ER protein translocon.

115 rt by constructing a penetration site on the ER membrane called a 'focus'.

116 14 to reorganize into discrete puncta in the ER membrane called foci, structures postulated to repres

117 the formation of punctate structures in the ER membrane, called foci, that serve as the portal for c

118 ith intramembrane hairpin domains that model ER membranes, cause an axon degenerative disease, heredi

119 e for a component of the recently identified ER membrane complex (EMC).

120 tmentalization of the endoplasmic reticulum (ER) membrane confine protein deposit formation to aging

121 taining family member, Osh3, localizes to PM/ER membrane contact sites dependent upon PM PI4P levels.

122 rect sensing of the lipid composition of the ER membrane contributes to the UPR.

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

124 n formations of hypertrophied tightly packed ER membranes devoted to specific biosynthetic and secret

125 dation ubiquitin ligases (E3s) reside in the ER membrane, Doa10 and Hrd1.

126 ht to channel misfolded proteins through the ER membrane during retrotranslocation.

127 Yeast ERAD employs two integral ER membrane E3 Ub ligases: Hrd1 (also termed "Der3") and

128 etachment of the Hsp40 protein Ydj1 from the ER membrane elicited a similar phenotype, suggesting tha

129 itional, and Teb4, an endoplasmic reticulum (ER) membrane-embedded ubiquitin ligase, was able to regu

130 hat also inhibits ryanodine receptors on the ER membrane, enhances folding, trafficking and lysosomal

131 ompartmentalization of this process to rough ER membrane ensures enrichment of miRNA-targeted message

132 When cholesterol in ER membranes exceeds a threshold, the sterol binds to Sc

133 ut likely is the direct result of changes in ER membrane fluidity and composition.

134 rated phospholipids, which ultimately reduce ER membrane fluidity.

135 isfolded or misassembled proteins across the ER membrane for degradation by cytosolic proteasomes, pl

136 ocation of misfolded polypeptides across the ER membrane for ER-associated degradation (ERAD).

137 rotein complexes, which are recruited to the ER membrane for insertion.

138 rsor protein into the endoplasmic reticulum (ER) membrane for subsequent routing to the cell surface.

139 either peroxisomal or endoplasmic reticulum (ER) membranes for replication.

140 We showed that efficient ER membrane fusion mediated by RHD3 requires a proper di

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

142 IVE3 (RHD3) has been demonstrated to mediate ER membrane fusion, but how exactly RHD3 is involved in

143 of the cytosolic domain to achieve homotypic ER membrane fusion.

144 We found that ER membranes in spf1 cells become similar in their ergos

145 sphatase (ALPP) mRNA can be localized to the ER membrane independently of translation, and this local

146 ere was no effect on protein mobility within ER membranes, indicating that cisternal connectivity was

147 e nucleotides cannot cross mitochondrial and ER membranes, inhibiting mitochondrial function with an

148 the lumen of the ER, likely through plastid:ER membrane interaction domains.

149 ing the diffusion barriers that separate the ER membrane into mother and bud compartments caused prem

150 misfolded proteins are dislocated across the ER membrane into the cytosol is unclear.

151 recognized and retrotranslocated across the ER membrane into the cytosol.

152 h membrane curvature, thus helping shape the ER membrane into tubules.

153 The COPII proteins deform the ER membrane into vesicles at the ER exit sites.

154 jacent membranes must associate to bring the ER membranes into molecular contact.

155 uitinated, reductase becomes dislocated from ER membranes into the cytosol for degradation by 26 S pr

156 tes subsequent dislocation of reductase from ER membranes into the cytosol for proteasomal degradatio

157 n of reductase from lipid droplet-associated ER membranes into the cytosol for proteasome-mediated, E

158 ent spherules that were invaginations of the ER membranes into the lumen.

159 s occurs in vesicular endoplasmic reticulum (ER) membrane invaginations, each induced by many copies

160 Together, our data indicate that the ER membrane is compartmentalized in cells as diverse as

161 However, how the ER membrane is involved in autophagy initiation and to w

162 ecise mechanism of how the toxin crosses the ER membrane is unknown.

163 e homotypic fusion of endoplasmic reticulum (ER) membranes is mediated by atlastin (ATL), which consi

164 chanism involving its phosphorylation by the ER membrane kinase PERK.

165 -Syt2 positions the ER and Sac1, an integral ER membrane lipid phosphatase, in discrete ER-PM junctio

166 surrounding ETHYLENE-INSENSITIVE2 (EIN2), an ER membrane-localized Nramp homolog that positively regu

167 , thus suggesting a general role of CDC48 in ER membrane maintenance upon ER stress.

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

169 ssociation with the mitochondrion-associated ER membrane (MAM) and mitochondrial proteins.

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

171 ubcompartment termed mitochondria-associated ER membrane (MAM).

172 referred to as the mitochondrion-associated ER membrane (MAM).

173 ochondria [i.e., the mitochondria-associated ER membrane (MAM)], they dynamically change the cellular

174 ochondrion-associated endoplasmic reticulum (ER) membrane (MAM).

175 tochondria-associated endoplasmic reticulum (ER) membranes (MAM) and that ER-mitochondrial connectivi

176 tochondria-associated endoplasmic reticulum (ER) membranes (MAM), a structurally and functionally dis

177 R are referred to as mitochondria-associated ER membranes (MAMs), and they play an important role in,

178 at sites defined as mitochondria-associated ER membranes (MAMs), which are essential for calcium, li

179 mitochondria, called mitochondria-associated ER membranes (MAMs).

180 culum (ER), known as mitochondria-associated ER membranes (MAMs).

181 tochondria-associated endoplasmic reticulum (ER) membranes (MAMs) are functional domains between both

182 Co-localization with an ER membrane marker showed that mCherry-AtCEP2 was stored

183 Desaturation of the ER membrane may serve as an auxiliary signal of the fed

184 tions of MP(TMV) with endoplasmic reticulum (ER) membrane, microtubules, and plasmodesmata throughout

185 lls, it is logically assumed that defects in ER membrane morphogenesis due to impaired fusion activit

186 tiple components in and on both sides of the ER membrane, most likely via TMS-dependent L17 and/or rR

187 ly protein NBK/Bik on endoplasmic reticulum (ER) membranes, most likely by blocking loading and autop

188 Fourth, upon docking to the ER membrane NAC remains bound to RNCs, allowing NAC to s

189 y associated with the endoplasmic reticulum (ER) membrane network, whereas upon exposure to carbon st

190 ions in the degradation of substrates in the ER membrane, nuclear envelope, cytoplasm, and nucleoplas

191 asmic reticulum (ER; mitochondria-associated ER membranes or 'MAM').

192 or catalyzing the most proximal event before ER membrane penetration of PyVs.

193 These foci, postulated to represent the ER membrane penetration site, harbor ER components, incl

194 Prior to ER membrane penetration, ER lumenal factors impart struc

195 r data illuminate C18's contribution to SV40 ER membrane penetration, strengthening the idea that SV4

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

197 nonequilibrium metabolic activity modulates ER membrane phase has not been investigated.

198 Cholesterol accumulation in ER membranes prevents Scap transport and decreases chole

199 The deposits localized to the ER membrane, primarily to the nuclear envelope (NE).

200 ne to trigger extraction of reductase across ER membranes prior to its cytosolic release.

201 ochondrion-associated endoplasmic reticulum (ER) membrane programs antiviral signaling.

202 Because Selk is also an ER membrane protein and contains an SH3 binding domain,

203 We show that the ER membrane protein Bax inhibitor-1 (BI-1) promotes auto

204 In this study, we clarify the role of an ER membrane protein called C18 in mobilizing the simian

205 cumulates at the MAM by associating with the ER membrane protein calnexin.

206 ol pathways, including the sumoylation of an ER membrane protein central to phospholipid synthesis an

207 We find that a member of the ER membrane protein complex (EMC) called EMC1 promotes S

208 missing multiple components of the conserved ER membrane protein complex (EMC) has decreased phosphat

209 oplasmic reticulum (ER), where the conserved ER membrane protein complex (EMC) was shown to be essent

210 solated a partial loss-of-function allele of ER membrane protein complex-6 (emc-6), a previously unch

211 onal changes enable SV40 to engage BAP31, an ER membrane protein essential for supporting membrane pe

212 present in a stoichiometric complex with the ER membrane protein Hrd3, which is also required for HRD

213 on of the ER depends on the highly conserved ER membrane protein Jagunal (Jagn).

214 t the yeast seipin Fld1, in complex with the ER membrane protein Ldb16, prevents equilibration of ER

215 hatidic acid (PA) and the conserved integral ER membrane protein Scs2p regulate localization of the t

216 The ER membrane protein Scs2p tethers the cER to the PM and

217 hway requires the Sec translocase-associated ER membrane protein Sec62 and can be uncoupled from tran

218 orm of EDEM1 efficiently associated with the ER membrane protein SEL1L and accelerated the turnover o

219 circuit in yeast is controlled by Scs2p, an ER membrane protein that binds the transcriptional repre

220 SEL1L is an ER membrane protein that is highly expressed in the panc

221 nd vIL-6 with the previously uncharacterized ER membrane protein vitamin K epoxide reductase complex

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

223 ansduction and interaction of vIL-6 with the ER membrane protein VKORC1v2.

224 ONAUTE1, the miRNA effector and a peripheral ER membrane protein.

225 pressed transmembrane endoplasmic reticulum (ER) membrane protein that has previously been implicated

226 racts with Erlin2, an endoplasmic reticulum (ER) membrane protein that is located in lipid rafts and

227 dentified as Scs2, an endoplasmic reticulum (ER) membrane protein that regulates phosphatidylinositol

228 ast Sac1, an integral endoplasmic reticulum (ER) membrane protein, controls PI4P levels at the ER, Go

229 is a type I integral endoplasmic reticulum (ER) membrane protein, molecular chaperone, and a compone

230 show that ERG-28, an endoplasmic reticulum (ER) membrane protein, promotes the trafficking of SLO-1

231 codes a member of the endoplasmic reticulum (ER)-membrane protein complex (EMC), an evolutionarily co

232 xcess sterols cause the reductase to bind to ER membrane proteins called Insig-1 and Insig-2, which a

233 e results from its sterol-induced binding to ER membrane proteins called Insig-1 and Insig-2.

234 p-flop in proteoliposomes reconstituted with ER membrane proteins from yeast indicate that GlcCer tra

235 ed a novel, evolutionarily diverse family of ER membrane proteins with StART-like lipid transfer doma

236 Multispanning ER membrane proteins, called ERAD-M substrates, are retr

237 Here, we identify two ER membrane proteins, SPFH2 and TMUB1, as associated pro

238 uted from Triton X-100-solubilized rat liver ER membrane proteins, we demonstrate rapid (t((1/2)) < 2

239 eased expression of mitochondrial-associated ER membrane proteins, which favor cholesterol translocat

240 (RTNs) are a class of endoplasmic reticulum (ER) membrane proteins that are capable of maintaining hi

241 and SOAT2), which are endoplasmic reticulum (ER) membrane proteins, in an enzyme-based assay, and sel

242 oteins that can form complexes with integral ER-membrane proteins, thereby potentially influencing th

243 Ds form lens-like structures that are in the ER membrane, raising the question of how these nascent L

244 omes mature and traffic while coupled to the ER membrane rather than in isolation.

245 he ER chaperone Kar2/BiP fused to GFP and an ER membrane reporter, Hmg1-GFP, behave differently in th

246 iP co-chaperones, ERj3 and ERj6, but not the ER membrane-resident co-chaperones (such as Sec63 protei

247 In S. pombe, the ER membrane-resident kinase/endoribonuclease Ire1 utiliz

248 tors, is conserved and dependent on Ire1, an ER membrane-resident kinase/endoribonuclease.

249 Two ER membrane-resident transmembrane kinases, IRE1 and PER

250 bilizes autophagy, which sequesters stressed ER membranes, resolves ER stress, and curtails phagocyte

251 cks the translocation of tetherin across the ER membrane, resulting in cytosolic accumulation of a no

252 phasis on the role of the recently described ER membrane signaling mechanisms.

253 , CD4 remains integrally associated with the ER membrane, suggesting that dislocation from the ER int

254 al that GPRC5A at the endoplasmic reticulum (ER) membrane suppresses synthesis of the secreted or mem

255 tion and oligomerization, creating localized ER membrane tensions that result in membrane curvature.

256 and revealed DHHC6/Selk interactions in the ER membrane that depended on SH3/SH3 binding domain inte

257 t these mitotic NPC remnants persisted on an ER membrane that juxtaposes the mitotic spindle.

258 polytopic protein of endoplasmic reticulum (ER) membranes that transports sterol regulatory element-

259 which has been suggested to localize to the ER membrane, the ER-derived quality control compartment

260 howed that following ribosome docking on the ER membrane, the nascent polypeptide was shielded from t

261 STIM1, located in the endoplasmic reticulum (ER) membrane, the calcium channel ORAI1 in the plasma me

262 c lipid transfer protein, flipped across the ER membrane, then delivered to the lumen of the Golgi co

263 e1 also cleaves other mRNAs localized to the ER membrane through regulated Ire1-dependent decay (RIDD

264 and must therefore be dislocated across the ER membrane to be degraded.

265 fungi, acts as a lipid-packing sensor in the ER membrane to control the production of unsaturated fat

266 e activated, IRE1alpha recruits TRAF2 to the ER membrane to initiate inflammatory responses via the N

267 nsor proteins able to translocate within the ER membrane to physically couple with and gate plasma me

268 smic reticulum (ER), where it penetrates the ER membrane to reach the cytosol before mobilizing into

269 l, this virus family must penetrate the host ER membrane to reach the cytosol, a critical entry step.

270 l surface to the ER, where it penetrates the ER membrane to reach the cytosol.

271 n elongation of crescents by the addition of ER membrane to the growing edge.

272 d proteins activate UPR signaling across the ER membrane to the nucleus by promoting oligomerization

273 translocates from its site of latency in the ER membrane to the nucleus, where it activates RNA polym

274 show that XendoU functions on the surface of ER membranes to promote RNA cleavage and ribonucleoprote

275 virus penetrates the endoplasmic reticulum (ER) membrane to reach the cytosol and then traffics to t

276 s SV40 penetrates the endoplasmic reticulum (ER) membrane to reach the cytosol, a crucial infection s

277 ceptor complex at the endoplasmic reticulum (ER) membrane to transcription factors in the nucleus is

278 idae, invaginates the endoplasmic reticulum (ER) membranes to form spherules in infected cells.

279 nome is translated on endoplasmic reticulum (ER) membranes to produce a single polyprotein, which is

280 R lumenal factors that prepare the virus for ER membrane translocation and connect these lumenal even

281 nal factors that coordinately prime SV40 for ER membrane translocation and establishes a functional c

282 s domain appears to exert an unexpected post-ER membrane translocation function during SV40 entry.

283 isulfide bonds, a reaction important for its ER membrane transport and infection.

284 tein complex (EMC) called EMC1 promotes SV40 ER membrane transport and infection.

285 unfolded protein response by activating the ER membrane transporter SLC33A1/AT-1, which ensures cont

286 Accumulation of GGpp in ER membranes triggers release of UBIAD1 from reductase,

287 binding to Insigs in endoplasmic reticulum (ER) membranes triggers ubiquitination of the cholesterol

288 e and stabilize positively curved peripheral ER membrane tubules.

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

290 molecule 1 (STIM1), translocates within the ER membrane upon store depletion to the juxtaplasma memb

291 We also show that the ER membrane VAP proteins, Scs2/Scs22, control PM PI4P le

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

293 R-luminal domain of CPXV012 inserts into the ER membrane, where it interacts with TAP.

294 age site form an extended alpha-helix in the ER membrane, which covers the cleavage site, thus preven

295 y, tombusviruses could also exploit expanded ER membranes, which provide enhanced subcellular environ

296 in biogenesis on the cytoplasmic side of the ER membrane, whose activity is negatively regulated by H

297 hanisms underlying stable interaction of the ER membrane with actin are unknown.

298 ated bridging, which dynamically anchors the ER membrane with actin filaments.

299 unknown proteins facilitate anchoring of the ER membrane with the cytoskeleton.

300 Treatment of ER membranes with myristic acid in the presence of cytos