ライフサイエンスコーパス: Golgi complex

1 g from the endoplasmic reticulum (ER) to the Golgi complex.

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

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

4 alian homologue is actually localized to the Golgi complex.

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

6 for the association of betaIII spectrin the Golgi complex.

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

8 phobic proteins resident in membranes of the Golgi complex.

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

10 l regulators of vesicle trafficking from the Golgi complex.

11 ations would assemble an integral, polarized Golgi complex.

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

13 th retrograde and anterograde traffic at the Golgi complex.

14 erate a functionally and structurally intact Golgi complex.

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

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

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

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

19 ma membrane by impeding movement through the Golgi complex.

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

21 esicular trafficking, and homeostasis of the Golgi complex.

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

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

24 onomers and subsequently oligomerizes in the Golgi complex.

25 fluences the structure and efficiency of the Golgi complex.

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

27 resulting chimeric protein localized to the Golgi complex.

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

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

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

31 ic between the endoplasmic reticulum and the Golgi complex.

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

33 function, and suggest interactions with the Golgi complex.

34 oteins from the endoplasmic reticulum to the Golgi complex.

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

36 e protein trafficking and homeostasis of the Golgi complex.

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

38 ermediate compartment between the ER and the Golgi complex.

39 ophagosomal structure, mitochondria, and the Golgi complex.

40 secretory pathway markers accumulated in the Golgi complex.

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

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

43 cess including the endoplasmic reticulum and Golgi complex.

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

45 ntal regulation of PI4P synthesis within the Golgi complex.

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

47 grated from the endoplasmic reticulum to the Golgi complex.

48 ffects were preceded by fragmentation of the Golgi complex.

49 ly required for anterograde transport to the Golgi complex.

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

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

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

53 otes the efficiency of transport through the Golgi complex.

54 trated and asymmetrically distributed in the Golgi complex.

55 nosomes, the endoplasmic reticulum (ER), and Golgi complex.

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

57 aintaining the structure and function of the Golgi complex.

58 COPI trafficking and the maintenance of the Golgi complex.

59 rane association of the Conserved Oligomeric Golgi complex.

60 essential for COPII vesicle tethering at the Golgi complex.

61 ear compartment previously identified as the Golgi complex.

62 correlate with dramatic fragmentation of the Golgi complex.

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

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

65 e structural maintenance and function of the Golgi complex.

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

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

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

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

70 trafficking and mitotic partitioning of the Golgi complex.

71 ntry in demonstrating the involvement of the Golgi complex.

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

73 ellular stores of AICL colocalizing with the Golgi complex.

74 dria, cisternae of endoplasmic reticulum and Golgi complexes.

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

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

77 monomeric motors are unable to disperse the Golgi complex, a high-load cargo.

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

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

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

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

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

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

84 ranules (SGs) leading to vesiculation of the Golgi complex and arrest of ER export.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 sifies SP1017-induced disorganization of the Golgi complex and significantly reduces secretion of par

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

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

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

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

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

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

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

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

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

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

122 nophosphorylated PPIn species within the PM, Golgi complex, and endosomal compartments.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 75 segregate into distinct subdomains of the Golgi complex at 19 degrees C.

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

140 s from the endoplasmic reticulum through the Golgi complex before reaching the plasma membrane along

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

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

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

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

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

146 lasmic reticulum (ER) and transferred to the Golgi complex by interaction with the Batten disease pro

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

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

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

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

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

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

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

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

155 The architecture and organization of the Golgi complex depend on a family of coiled-coil proteins

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

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

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

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

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

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

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

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

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

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

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

167 Genetic or pharmacologic activation of Golgi complex fragmentation blocks PDAC growth and metas

168 AGUK Scaffold Protein 3 (DLG3), resulting in Golgi complex fragmentation, and reduced protein glycosy

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

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

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

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

173 ial of approximately -35 mV, followed by the Golgi complex > lysosomes > mitochondria ~ peroxisomes >

174 During biosynthesis of lactose in the Golgi complex, H(+) is produced as a by-product, and the

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

176 The Golgi complex has been implicated as a possible componen

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

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

179 t from the Endoplasmic Reticulum (ER) to the Golgi complex have been described, but the mechanisms fo

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 d in the trafficking of ATP7A from the trans-Golgi complex in a Cu-dependent manner, suggesting that

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

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

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

186 at TMEM165 supplies Ca(2+) and Mn(2+) to the Golgi complex in exchange for H(+) to sustain the functi

187 Syt-17 is localized to the Golgi complex in hippocampal neurons, where it coordinat

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

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

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

191 4-kinases (PI4Ks) have been localized to the Golgi complex in mammalian cells, type III PI4Kbeta (PI4

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

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

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

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

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

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

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

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

200 etastasis by activating ISGs and maintaining Golgi complex integrity.

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

202 The Golgi complex is a central processing compartment in the

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

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

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

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

207 The Golgi complex is essential for many aspects of cellular

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

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

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

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

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

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

214 The Golgi complex is recognized as being a central transport

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

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

217 The Golgi complex is the central sorting compartment of euka

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

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

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

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

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

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

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

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

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

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

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

229 ontrolling secretory pathway trafficking and Golgi complex morphology.

230 portance of cation and pH homeostasis in the Golgi complex of professional secretory cells and the cr

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

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

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

234 Both the endoplasmic reticulum (ER) and Golgi complex participated in delivering (D)CDX-modified

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

236 ichment within the cytosolic leaflets of the Golgi complex, peroxisomes, and outer mitochondrial memb

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 ng from the Golgi side of these Tango1-COPII-Golgi complexes, suggesting that these structures repres

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 Golgi complex typically localizes in front of the nucleu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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