ライフサイエンスコーパス: Golgi complex

1 th retrograde and anterograde traffic at the Golgi complex.

2 lar transfer of ceramides from the ER to the Golgi complex.

3 erate a functionally and structurally intact Golgi complex.

4 itch once, mutant rapsyn was retained in the Golgi complex.

5 aintaining the structure and function of the Golgi complex.

6 lycoprotein (P-gp) sequestered CA within the Golgi complex.

7 e cell body, where it is concentrated at the Golgi complex.

8 , mediates the structure and function of the Golgi complex.

9 ma membrane by impeding movement through the Golgi complex.

10 dent fusion stage of COPII vesicles with the Golgi complex.

11 esicular trafficking, and homeostasis of the Golgi complex.

12 g to lysosomes, causing its retention in the Golgi complex.

13 but not EG3, induced the disassembly of the Golgi complex.

14 onomers and subsequently oligomerizes in the Golgi complex.

15 fluences the structure and efficiency of the Golgi complex.

16 domain is important for MPR recycling to the Golgi complex.

17 COPI trafficking and the maintenance of the Golgi complex.

18 resulting chimeric protein localized to the Golgi complex.

19 rane association of the Conserved Oligomeric Golgi complex.

20 g LPS-stimulated cytokine secretion from the Golgi complex.

21 ction as well as cytokine secretion from the Golgi complex.

22 of these proteins in the plasma membrane and Golgi complex.

23 ic between the endoplasmic reticulum and the Golgi complex.

24 aps by focusing of endocytic vesicles at the Golgi complex.

25 function, and suggest interactions with the Golgi complex.

26 oteins from the endoplasmic reticulum to the Golgi complex.

27 fic of the full-length S protein through the Golgi complex.

28 e protein trafficking and homeostasis of the Golgi complex.

29 es, localizes to the cytoplasmic face of the Golgi complex.

30 ermediate compartment between the ER and the Golgi complex.

31 ophagosomal structure, mitochondria, and the Golgi complex.

32 secretory pathway markers accumulated in the Golgi complex.

33 asmic face of coated vesicles located at the Golgi complex.

34 tween the endoplasmic reticulum (ER) and the Golgi complex.

35 cess including the endoplasmic reticulum and Golgi complex.

36 os1p blocks transport between the ER and the Golgi complex.

37 ntal regulation of PI4P synthesis within the Golgi complex.

38 essential for COPII vesicle tethering at the Golgi complex.

39 n-160, or by drug-induced disassembly of the Golgi complex.

40 grated from the endoplasmic reticulum to the Golgi complex.

41 ffects were preceded by fragmentation of the Golgi complex.

42 ear compartment previously identified as the Golgi complex.

43 ly required for anterograde transport to the Golgi complex.

44 not retained within the ER, but reached the Golgi complex.

45 to the site of proteolytic activation in the Golgi complex.

46 in their processing is the transport to the Golgi complex.

47 trated and asymmetrically distributed in the Golgi complex.

48 ort vesicles and subsequent targeting to the Golgi complex.

49 rt between the endoplasmic reticulum and the Golgi complex.

50 all known adaptors and coat proteins to the Golgi complex.

51 membrane and one that is transported to the Golgi complex.

52 correlate with dramatic fragmentation of the Golgi complex.

53 ry pathway and perturbs glycosylation in the Golgi complex.

54 e nuclear envelope, endosomes, lysosomes, or Golgi complex.

55 tion of OspA with lysosomes but not with the Golgi complex.

56 clear region identified predominantly as the Golgi complex.

57 re key regulators of membrane traffic at the Golgi complex.

58 king and resulted in p14 accumulation in the Golgi complex.

59 e structural maintenance and function of the Golgi complex.

60 /A' prevents the localization of COH1 to the Golgi complex.

61 on of the catalytically active enzyme in the Golgi complex.

62 otes the efficiency of transport through the Golgi complex.

63 -coupled receptor (GPCR), from the ER to the Golgi complex.

64 s from the endoplasmic reticulum (ER) to the Golgi complex.

65 trafficking and mitotic partitioning of the Golgi complex.

66 ntry in demonstrating the involvement of the Golgi complex.

67 binding proteins (SREBPs) from the ER to the Golgi complex.

68 ellular stores of AICL colocalizing with the Golgi complex.

69 d to the vacuole without passing through the Golgi complex.

70 on was delayed and they accumulated near the Golgi complex.

71 alian homologue is actually localized to the Golgi complex.

72 iridae, which obtain their envelope from the Golgi complex.

73 for the association of betaIII spectrin the Golgi complex.

74 ue, PP6, regulate traffic from the ER to the Golgi complex.

75 phobic proteins resident in membranes of the Golgi complex.

76 hile enhancing PI(4,5)P2 accumulation at the Golgi complex.

77 l regulators of vesicle trafficking from the Golgi complex.

78 ations would assemble an integral, polarized Golgi complex.

79 in the absence of AChR was localized in the Golgi complex.

80 dria, cisternae of endoplasmic reticulum and Golgi complexes.

81 e in proliferation of rough ER membranes and Golgi complexes.

82 to normoxia, but rather, colocalized to the Golgi complex, a finding not previously reported for any

83 How they move through the Golgi complex, a major secretory station composed of sta

84 ramide from the endoplasmic reticulum to the Golgi complex, a process critical in synthesis and maint

85 ected neuronal and non-neuronal cells to the Golgi complex, a subset of synaptic vesicles, to a subse

86 uctural analysis of the type II cells showed Golgi complex abnormalities and aberrant lamellar bodies

87 the centrosome did not alter already-formed Golgi complexes, acentrosomal cells fail to reassemble a

88 is required for efficient reassembly of the Golgi complex after brefeldin A removal.

89 g a causal link between the integrity of the Golgi complex and axonal outgrowth.

90 is likely to be involved from an endoplasmic-Golgi complex and basolateral location in goblet cells.

91 in as a binding partner for myosin VI at the Golgi complex and confirmed this interaction in a range

92 cation between the endoplasmic reticulum and Golgi complex and controls cellular PI4P lipid levels.

93 associated with endomembranes, including the Golgi complex and cytoplasmic vesicles, but its role rem

94 ere found to be oriented in the lumen of the Golgi complex and cytosol, respectively.

95 locates from the plasma membrane (PM) to the Golgi complex and early/recycling endosomes in response

96 c Ras induces c-Src activation mainly on the Golgi complex and endoplasmic reticulum.

97 ate (PI(4)P), which has been detected at the Golgi complex and endosomal compartments and recruits cl

98 e from the endoplasmic reticulum through the Golgi complex and endosomes to melanosomes, and that onl

99 ization involving centrosomes, microtubules, Golgi complex and ER exit sites takes place early during

100 Redistributions of Golgi complex and ER exit sites were incomplete but rema

101 ession of haCER2 caused fragmentation of the Golgi complex and growth arrest in HeLa cells due to sph

102 lasma membrane or cytoplasmic aspects of the Golgi complex and have assessed eNOS activation.

103 hat myosin VI and Rab8 colocalize around the Golgi complex and in vesicles at the plasma membrane and

104 Both proteins colocalize at the Golgi complex and in vesicles at the plasma membrane.

105 (CVB3) proteins (2B, 2BC, and 3A) target the Golgi complex and inhibit protein transit.

106 haCER2 is localized to the Golgi complex and is highly expressed in the placenta.

107 In fat body cells, Ema localizes to the Golgi complex and is recruited to the membrane of autoph

108 alizes to the endoplasmic reticulum (ER) and Golgi complex and is required for a retrograde transport

109 also required for proper positioning of the Golgi complex and mitochondria as well as for hair cell

110 s localized to different extents at both the Golgi complex and plasma membrane, but also in their dea

111 show that optineurin links myosin VI to the Golgi complex and plays a central role in Golgi ribbon f

112 COPI coat forms transport vesicles from the Golgi complex and plays a poorly defined role in endocyt

113 quired for the accumulation of GPRC5B in the Golgi complex and restriction of GPRC5B transport along

114 in A (BFA)-induced tubule formation from the Golgi complex and retrograde trafficking to the ER.

115 ins fail to undergo normal maturation in the Golgi complex and show markedly reduced cell-surface exp

116 ort that THSer(P)-31 co-distributes with the Golgi complex and synaptic-like vesicles in rat and huma

117 its retrograde transport to the juxtanuclear Golgi complex and that STB increases MT assembly.

118 FT20 is highly dynamic and moves between the Golgi complex and the cilium as well as along ciliary mi

119 Since IFT20 dynamically moves between the Golgi complex and the connecting cilium, the current wor

120 -mediated retrograde trafficking between the Golgi complex and the endoplasmic reticulum (ER).

121 bled MHC-II complexes are transported to the Golgi complex and then to late endosomes/lysosomes, wher

122 is important for localization of UL37 in the Golgi complex and thus possibly for cytoplasmic envelopm

123 processing by transporting TLR3 through the Golgi complex and to the endosomes.

124 yers, abnormal positioning of the centrosome-Golgi complex, and aberrant length/orientation of the le

125 Both of these proteins are localized to the Golgi complex, and both regulate phosphatidylinositol 4-

126 fic complex sorting is first detected in the Golgi complex, and compromised by removing the K(b) cyto

127 pha7 protein folding, maturation through the Golgi complex, and expression at the cell surface.

128 vels, enlargement and disorganization of the Golgi complex, and formation of aberrant vesicular struc

129 with cilia, flagella, the centrosome and the Golgi complex, and in Hydin and OCRL whose deficiencies

130 ral defects in the microtubule cytoskeleton, Golgi complex, and mitochondria.

131 odimer from the endoplasmic reticulum to the Golgi complex, and most prevented the formation of stabl

132 recruitment of PI4P-binding proteins to the Golgi complex, and PI4KII alpha, a major producer of Gol

133 wn the exit of basolateral proteins from the Golgi complex, and promoted their mis-sorting into apica

134 (3) expansion through membrane delivery from Golgi complexes; and (4) ER-mediated lipid transfer.

135 e events of N-glycosylation within the plant Golgi complex are a major limitation to the use of plant

136 We also show that centrioles and the Golgi complex are always located immediately beneath the

137 adation was not accelerated, implicating the Golgi complex as the site for glycoprotein ERAD substrat

138 oteins in the endoplasmic reticulum (ER) and Golgi complex as well as influencing the timing and reco

139 to the cell surface: a direct route from the Golgi complex, as in the kidney-derived MDCK cell line,

140 On DMS expansion, Golgi complexes assembled around the pre-DMS, and fusion

141 of the golgin-160 head and identified GCP60 (Golgi complex-associated protein of 60 kDa).

142 We report herein the identification of the Golgi complex-associated protein p115 as an intracellula

143 75 segregate into distinct subdomains of the Golgi complex at 19 degrees C.

144 ng a role in coordinating segregation of the Golgi complex at cell division.

145 opposed by calmodulin, which traffics to the Golgi complex, binds FBXL2 (residues 80 to 90) via its C

146 clear compartment was localized close to the Golgi complex but displayed no overlap with Golgi marker

147 that trypanosomes are able to duplicate the Golgi complex but failed to complete segregation during

148 strate that the endoplasmic reticulum and/or Golgi complex, but not endosomal compartments, play an i

149 pyramidal neurons, with the exception of the Golgi complex, but was dense in the proximal dendrites a

150 pe GFP-HRas and GFP-NRas are recycled to the Golgi complex by a nonvesicular mechanism.

151 The recruitment of p120RasGAP to the Golgi complex by oncogenic Ras facilitated its interacti

152 trafficking of HRas and NRas to and from the Golgi complex by shifting the protein between vesicular

153 membrane, then delivered to the lumen of the Golgi complex by vesicular transport.

154 early segregation to distinct domains of the Golgi complex by virtue of the proteins' luminal and tra

155 Because the Golgi complex can house nucleation sites, we explored wh

156 y results from impaired COH1 function at the Golgi complex, causing decreased neuritogenesis.

157 us degrees, and directly associated with the Golgi complex, causing trafficking proteins to accumulat

158 igands were predominantly transported to the Golgi complex, colocalizing with the Golgi markers bovin

159 Results show that while the position of the Golgi complex depends on the cell geometry, the subcellu

160 e, we show that association of COH1 with the Golgi complex depends on the small GTPase RAB6.

161 dicating that trafficking of UL37eGFP to the Golgi complex did not require capsid structures.

162 protein synthesis or disorganization of the Golgi complex did not result in diminished intragranular

163 eometry, the subcellular localization of the Golgi complex does not define the cell's leading edge.

164 Therefore, UL37 traffics to the Golgi complex during infection.

165 ans from oligomannose to complex type in the Golgi complex enhances the proteolytic activity of the p

166 equires microfilaments, microtubules and the Golgi complex for cell invasion, but not for internalize

167 ramide from the endoplasmic reticulum to the Golgi complex for conversion into sphingomyelin (SM).

168 thereby prevent the SREBPs from reaching the Golgi complex for processing to the mature forms that ac

169 l regulatory element-binding proteins to the Golgi complex for proteolytic activation.

170 MEK1-dependent Golgi complex fragmentation is through activation by RAF

171 rtments and provides a mechanism to grow the Golgi complex from a stable progenitor, in an ordered ma

172 The Golgi complex functions to posttranslationally modify ne

173 r), via generating sphingosine, disrupts the Golgi complex (GC), which is associated with various cel

174 Golgi complexes (Golgi) play important roles in the deve

175 plexes such as exocyst, conserved oligomeric Golgi complex, Golgi-associated retrograde protein compl

176 The Golgi complex has a central role in the intracellular so

177 The Golgi complex has been implicated as a possible componen

178 ycosylation of beta1 integrin (beta1) in the Golgi complex has been related to its function in multip

179 The striking morphology of the Golgi complex has fascinated cell biologists since its d

180 opriately regulated flippase activity in the Golgi complex helps establish a plasma membrane phosphol

181 phology and to recruit GDP-loaded ARF to the Golgi complex in a Ca(2+)-dependent manner.

182 ATP2C1-encoded protein is detected in the Golgi complex in a calcium-dependent manner.

183 subunit of the particle is localized to the Golgi complex in addition to the basal body and cilia wh

184 FP, a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalize

185 We observed reversible fragmentation of the Golgi complex in cultured hippocampal neurons cultured i

186 ing pathway controls the architecture of the Golgi complex in Drosophila photoreceptor (PR) neurons.

187 ntly discovered that MAN1B1 localizes to the Golgi complex in human cells and uncovered its participa

188 localize to discrete subcompartments of the Golgi complex in Madin-Darby canine kidney (MDCK) cells.

189 ty between the membranes of cisternae in the Golgi complex in mammalian cells rarely has been observe

190 4-kinases (PI4Ks) have been localized to the Golgi complex in mammalian cells, type III PI4Kbeta (PI4

191 OS splice variant nNOSbeta, localized at the Golgi complex in mouse skeletal muscle cells.

192 ntrated at synapses and in the region of the Golgi complex in neuronal perikarya.

193 keley bodies, a structure generated from the Golgi complex in sec7 cells, are immunolabeled with Atg8

194 um, whereas MTP-B localizes primarily to the Golgi complex in these cells.

195 cytosol-dependent formation of tubules from Golgi complexes in vitro and increased the levels of lys

196 other hand, HRAS signals emanating from the Golgi complex induce apoptosis and can prevent heregulin

197 and microtubules, and disintegration of the Golgi complex inhibited entosis.

198 Knockdown of PAFAH Ib subunits fragments the Golgi complex, inhibits tubule-mediated reassembly of in

199 novel function for p53 in the maintenance of Golgi complex integrity and for myosin VI in the p53-dep

200 thering Golgi stacks but not of establishing Golgi complex integrity or polarity.

201 VI attenuates activation of p53 and impairs Golgi complex integrity, which makes myosin VI-deficient

202 associated with a visible disassembly of the Golgi complex into discrete aggregates.

203 The Golgi complex is a central processing compartment in the

204 Traffic through the Golgi complex is controlled by small GTPases of the Arf

205 sted that the functional organization of the Golgi complex is dependent on phospholipid remodeling en

206 Assembly of an integral Golgi complex is driven by microtubule (MT)-dependent tr

207 he Cog2p subunit of the conserved oligomeric Golgi complex is either functionally redundant or is not

208 The Golgi complex is essential for many aspects of cellular

209 c from the endoplasmic reticulum (ER) to the Golgi complex is initiated when the activated form of th

210 ontrast, dynein-independent transport to the Golgi complex is insensitive to mutant Cdc42.

211 The mechanism of transport through the Golgi complex is not completely understood, insofar as n

212 s neuronal microtubule polarity but that the Golgi complex is not directly involved in housing nuclea

213 and we have shown that the disruption of the Golgi complex is not necessary for cytotoxicity.

214 mbrane localization at the entry face of the Golgi complex is novel for an actin nucleation-promoting

215 hat in Candida albicans, the majority of the Golgi complex is redistributed to the distal region duri

216 e cell lines, where myosin VI is absent, the Golgi complex is reduced in size by approximately 40% co

217 ortantly, VSV-G transport between the ER and Golgi complex is restored when an in vitro trafficking a

218 The Golgi complex is the central sorting compartment of euka

219 of oligomannose to complex N-glycans in the Golgi complex, is important for secretion.

220 ructural motif in the tail is sufficient for Golgi complex localization of a reporter protein.

221 minal portion of the TMD that eliminated the Golgi complex localization of the chimeric CD4 proteins

222 ed in decreased RVFV replication, reduced Gn Golgi complex localization, and increased Gn ER accumula

223 for functional roles of plasma membrane- and Golgi complex-localized eNOS and supports the concept th

224 orenal syndrome of Lowe protein 1 (OCRL1), a Golgi complex-localized phosphatidylinositol (PI)-5-phos

225 mplex, and PI4KII alpha, a major producer of Golgi complex-localized PI4P, also localize to chlamydia

226 i structure and how the conserved oligomeric Golgi complex maintains Golgi enzymes in different Golgi

227 ed in a compartment that co-localizes with a Golgi complex marker.

228 Trafficking via the Golgi complex may underlie new roles in G protein-couple

229 ngle hydrophobic domain (HD), is targeted to Golgi complex membranes, and has cation channel activity

230 s that PTAR1-deficient cells exhibit altered Golgi complex morphology and glycosylation defects.

231 ontrolling secretory pathway trafficking and Golgi complex morphology.

232 ing processing of membrane and lipids in the Golgi complex of the cell body and one in which endoplas

233 t, translocation occurs predominantly to the Golgi complex or the endoplasmic reticulum.

234 transports Rab6A-vesicles and can influence Golgi complex organization.

235 rientation of the migrating neurons with the Golgi complex oriented toward the cortical upper layers

236 embrane ruffles, and cytosol migrates to the Golgi complex, perinuclear membrane, and nucleus.

237 emble by budding into the lumen of the early Golgi complex prior to exocytosis.

238 ynthesized GPRC5B protein accumulates in the Golgi complex prior to its release into exosomes.

239 ollectively, these data demonstrate that the Golgi complex retention signal of the ORF7b protein resi

240 ease in plasma membranes and increase in the Golgi complex stimulates cPLA2alpha release of arachidon

241 yr(P) ERK) may be involved in regulating the Golgi complex structure during the G2 and M phases of th

242 teins identified are localized within the ER/Golgi complex, suggesting a role for S-nitrosylation in

243 In plasma membrane- and Golgi complex-targeted constructs, Ser1179 is critical f

244 In contrast, cis-Golgi complex-targeted eNOS behaved similarly to wild-ty

245 coronaviruses), where it also functions as a Golgi complex-targeting signal.

246 ed a significantly less fragmentation of the Golgi complex than that in wild-type cells after exposed

247 undescribed intracellular itinerary via the Golgi complex that is associated with the sequential S-p

248 -coil protein on the cytoplasmic face of the Golgi complex that is cleaved by caspases during apoptos

249 ialized population of actin filaments at the Golgi complex that is selectively required for the emerg

250 al signals in the endoplasmic reticulum (ER)/Golgi complex that will determine protein fate.

251 At the Golgi complex, the biosynthetic sorting center of the ce

252 RNA interference, myosin VI is lost from the Golgi complex, the Golgi is fragmented and exocytosis of

253 ing located in the endoplasmic reticulum and Golgi complex, the lipids that accumulate in its absence

254 acilitate the functional organization of the Golgi complex, thereby suggesting a model that links pho

255 ic acid is transported into the lumen of the Golgi complex through the CMP-sialic acid transporter, a

256 orted from the endoplasmic reticulum via the Golgi complex to be delivered at the cell surface to cat

257 hosphorylated ATP7B was transferred from the Golgi complex to cytosolic trafficking vesicles.

258 roteins containing the DXXLL signal from the Golgi complex to endosomes.

259 ntially in the endoplasmic reticulum and the Golgi complex to form beta1 precursor and mature beta1,

260 ffinities, and the requirement for an intact Golgi complex to induce cell cycle arrest.

261 ally complement one another; 3A disrupts the Golgi complex to inhibit anterograde transport, while 2B

262 ncorporated with different efficiencies into Golgi complex to plasma membrane vesicular carriers, and

263 toreceptors function in association with the Golgi complex to regulate the export of proteins from th

264 , is required for protein transport from the Golgi complex to the cell surface in Drosophila S2 cells

265 dispersal of vesicles cycling cargo from the Golgi complex to the cilium, including the IFT protein I

266 livery of ciliary membrane proteins from the Golgi complex to the cilium.

267 iculum (ER) and the transport of Gn from the Golgi complex to the host cell membrane is reduced.

268 d being the transport of hydrolases from the Golgi complex to the lysosome.

269 ChRs enable the transport of rapsyn from the Golgi complex to the plasma membrane through a molecule-

270 required for anterograde transport from the Golgi complex to the plasma membrane.

271 irus-glycoprotein G; VSV-G) protein from the Golgi complex to the plasma membrane.

272 rafficking through the endoplasmic reticulum-Golgi complex to the plasma membrane.

273 ric ERGIC-53 protein directs export from the Golgi complex to the plasma membrane.

274 sential for efficient export of p14 from the Golgi complex to the plasma membrane.

275 irected export of membrane proteins from the Golgi complex to the plasma membrane.

276 t trafficking routes as they travel from the Golgi complex to their common destination at the cell su

277 nnels (from the endoplasmic reticulum or the Golgi complex) to the surface membrane.

278 oteins from the endoplasmic reticulum to the Golgi complex, to facilitate their replication.

279 G) complex, one of the central components of Golgi complex trafficking.

280 Golgi complex typically localizes in front of the nucleu

281 vesicular transport of proteins between the Golgi complex, vacuole/lysosome, and plasma membrane.

282 dothelial nitricoxide synthase (eNOS) on the Golgi complex versus the plasma membrane has made it dif

283 nce of UL36, accumulation of UL37eGFP at the Golgi complex was not evident.

284 as mislocalized and its association with the Golgi complex was reduced.

285 FP/DeltaVP5, localization of UL37eGFP to the Golgi complex was similar to that for the parental virus

286 patial control of PI4P generation across the Golgi complex, we quantitated the steady state distribut

287 ENaC maturation involves transit through the Golgi complex where Asn-linked glycans are processed to

288 showed that nascent WT ATP7B transits to the Golgi complex where it undergoes serine phosphorylation

289 r from the endoplasmic reticulum (ER) to the Golgi complex, where ceramides are converted to complex

290 ium-dependent activation of FBXL2 within the Golgi complex, where it engages CCTalpha.

291 ectrin, we here show its distribution in the Golgi complex, where it is enriched in the trans-Golgi a

292 human homologue predominantly resides in the Golgi complex, where it is subjected to O-glycosylation.

293 causes TBC1D14 to relocalize from REs to the Golgi complex, whereas TfnR and Tfn localize to forming

294 was present in the endoplasmic reticulum and Golgi complex, whereas the excess neutral lipids in the

295 rmation in the plasma membrane, nucleus, and Golgi complex while diverting DISC formation to the mito

296 The enzyme resides in the Golgi complex with its active site facing the lumen, con

297 m with folate metabolism and integrating the Golgi complex with the vimentin intermediate filament cy

298 sent in the PBM dictates p14 export from the Golgi complex, with a minimum of three basic residues re

299 plasma membrane, endoplasmic reticulum, and Golgi complex, with a small fraction in early and recycl

300 brane proteins unable to recycle back to the Golgi complex, yet these class E vps mutants had what se