ライフサイエンスコーパス: Golgi

1 Golgi cells are the principal inhibitory neurons at the

2 Golgi reassembly stacking protein of 65 kDa (GRASP65) an

3 Golgi stacks in border cells and peripheral cells, precu

4 Golgi staining, ultra-structural and electrophysiologica

5 Colocalization of RabA2 with ArfA1 and a Golgi marker indicates that RabA2 localizes in Golgi sta

6 UL20 binds to GODZ (also known as DHHC3), a Golgi apparatus-specific Asp-His-His-Cys (DHHC) zinc fin

7 dependent on MLO protein localization into a Golgi-associated compartment before PT arrival, indicati

8 rophy gene Retinal Degeneration 3 (RD3) is a Golgi-associated protein required for efficient traffick

9 tially controls the structural features of a Golgi cisterna by regulating its association to curvatur

10 appears generally true that aggregation of a Golgi protein leads to its lysosomal degradation.

11 mor cells gain metastatic capacity through a Golgi phosphoprotein 3-dependent (GOLPH3-dependent) Golg

12 ins (7-46 years of age) were stained using a Golgi-Kopsch impregnation.

13 lia beyond the transition zone, had abnormal Golgi architecture and altered levels of cilia assembly

14 pendent sorting mechanisms target aggregated Golgi membrane proteins for lysosomal degradation.

15 nalysis revealed that Cdc42 is active at all Golgi cisternae and that this activity is controlled by

16 of C-terminal cysteine residues that allows Golgi localization.

17 ll transcriptomes of newborn DGCs, and among Golgi-related genes, found the presence of STK25 and STR

18 g protein located at both the centrosome and Golgi apparatus.

19 ulation, was shown to control centrosome and Golgi reorientation toward the leading edge, a hallmark

20 lowed by subsequent lipidation in the ER and Golgi compartment.

21 in cells and localizing mainly in the ER and Golgi.

22 layer, which mainly consists of granule and Golgi cells, is the first stage of the cerebellar cortex

23 bly stacking protein of 65 kDa (GRASP65) and Golgi reassembly stacking protein of 55 kDa (GRASP55) we

24 sible link between drug-induced toxicity and Golgi morphology alterations.

25 TANGO1 (transport and Golgi organization 1) interacts with CTAGE5 and COPII co

26 kDa (GRASP55) were originally identified as Golgi stacking proteins; however, subsequent GRASP knock

27 To date, image-based Golgi screens have based on a single parameter or superv

28 ansport to the Golgi, where it is cleaved by Golgi-resident proteases, releasing the N-terminal produ

29 ER in NIH3T3 and HEP3B (liver cancer) cells; Golgi were isolated for analysis.

30 ly to GODZ (also known as DHHC3), a cellular Golgi apparatus-specific Asp-His-His-Cys (DHHC) zinc fin

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

32 A condensed cis-Golgi was the first abnormality observed upon Munc18-1 o

33 nt cellular phenotypes, especially early cis-Golgi abnormalities, distinct from abnormalities observe

34 prevented cell death and restored normal cis-Golgi morphology, but not synaptic transmission or synta

35 sing three-dimensional live imaging that cis-Golgi and trans-Golgi remain stable in their composition

36 cleate) from both the centrosome and the cis-Golgi cisternae.

37 e neurogenic zone were eliminated, a compact Golgi apparatus was positioned exclusively at the base o

38 ath via down-regulation of GPP130, a cycling Golgi membrane protein that serves as an endosome-to-Gol

39 hosphoprotein 3-dependent (GOLPH3-dependent) Golgi membrane dispersal process that drives the budding

40 Depletion of PAQR11 dispersed Golgi organelles and impaired anterograde vesicle transp

41 calization, silencing retromer or disrupting Golgi/TGN organization all impair efficient TSH-dependen

42 P and cathepsin B was observed in a distinct Golgi apparatus-like pattern, which required a 1-h OA tr

43 itates clustered GDMT nucleation at distinct Golgi sites.

44 nction in retrograde transport between early Golgi compartments.

45 understanding of the regulation of the early Golgi Arf-GEFs Gea1 and Gea2.

46 re regulatory mechanisms unique to the early Golgi Arf-GEFs.

47 sistent with their localization to the early Golgi.

48 nt pharmacological compounds known to elicit Golgi fragmentation: brefeldin A, golgicide A, and monen

49 We focused on validating endosome/Golgi-localized hits specific for STx2 and found that de

50 ugh the classical endoplasmic reticulum (ER)/Golgi-dependent pathway, but a few are released by uncon

51 ER-Golgi contacts fail to form during ER stress in cells la

52 ers that ultimately fuse with an adjacent ER-Golgi intermediate compartment (ERGIC).

53 This is because ER-Golgi-cycling FKBP proteins contain a C-terminal KDEL-li

54 We observe increased ER-Golgi trafficking, an altered secretome and sensitivity

55 R stress, it relocalizes to and increases ER-Golgi contacts.

56 findings demonstrate that cells regulate ER-Golgi contacts in response to stress and reveal that non

57 transcriptional regulator of upregulated ER-Golgi trafficking genes ARF4, COPB1, and USO1, and silen

58 ition to disrupting protein secretion and ER/Golgi morphology, causes ER stress and defects in cell s

59 By contrast, ER/Golgi defects in Tango1-depleted cells persist in the ab

60 but a few are released by unconventional ER/Golgi-independent means.

61 ecruits ERGIC-53 (endoplasmic reticulum [ER]-Golgi intermediate compartment 53)-containing membranes

62 We suggest that the existing Golgi is a key source of components required to form the

63 show that transfer of GntB from the existing Golgi to the new Golgi can be recapitulated in semiperme

64 The flat Golgi cisterna is a highly conserved feature of eukaryot

65 down either of these two proteins, we found Golgi mislocalization and extensive aberrant dendrite fo

66 om all three individuals showed a fragmented Golgi that could be rescued by expression of wild-type T

67 to wild-type mice, Nhe8(-/-) mice generated Golgi-derived vesicles positive for acrosomal markers an

68 In the "heterogeneous Golgi" model, MT nucleation is dramatically up-regulated

69 y regulator of multiple pathways that impact Golgi morphology.

70 Similarly, changes in Golgi morphology did not affect Cdc42 activity at the Go

71 ractable epilepsy, caused similar defects in Golgi localization and dendrite formation in adult-born

72 lgi marker indicates that RabA2 localizes in Golgi stacks and the trans-Golgi network.

73 of alternative clearance pathways including Golgi membrane-associated and nucleophagy-based LaminB1

74 and transport continue-even when individual Golgi cisternae are separated and "land-locked" between

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

76 yltransferase, an established cargo of intra-Golgi retrograde transport.

77 liogmeric Golgi (COG) complex and with intra-Golgi SNARE proteins.

78 tion, inhibiting PKA II/interfering with its Golgi/TGN localization, silencing retromer or disrupting

79 ClaH localized to distinct domains on late Golgi, and these clathrin "hubs" dispersed in synchrony

80 "hubs" dispersed in synchrony after the late Golgi marker PH(OSBP) .

81 domain that are required for Rab29-mediated Golgi recruitment and kinase activation.

82 ource of components required to form the new Golgi and that this process is regulated by small GTPase

83 r of GntB from the existing Golgi to the new Golgi can be recapitulated in semipermeabilized cells an

84 as performed for compounds that alter normal Golgi structure.

85 that it could be a key modulator of a novel Golgi export checkpoint that coordinates GPCR delivery t

86 To discover novel Golgi-fragmenting agents, transcriptomic profiles of cel

87 To systematically identify novel Golgi stress mediators, we performed a transcriptomic an

88 As determined by Sholl analysis of Golgi-stained brain sections, dendritic arbors of male h

89 KD is known to be involved in the control of Golgi membrane vesicular and lipid transport, we hypothe

90 G) tethering complex, a major coordinator of Golgi vesicular trafficking, thus remodeling Golgi membr

91 Since Cajal's first drawings of Golgi stained neurons, generations of researchers have b

92 fication and characterization of a family of Golgi-localized UDP-Araf transporters in Arabidopsis The

93 the structural organization and function of Golgi cisternae.

94 It is formed by a fusion of Golgi-derived vesicles.

95 indings suggest that the erratic movement of Golgi is a stable cellular phenomenon that might optimiz

96 gradient, which guides the focal movement of Golgi-derived vesicles to the site of uptake.

97 find that IFT20 regulates the nucleation of Golgi-derived microtubules by affecting the GM130-AKAP45

98 We analyzed the presence of Golgi-associated genes using single-cell transcriptomes

99 highly devolved mechanism for recruitment of Golgi-derived secretory vesicles during phagosome biogen

100 s BRD8 and DNA-PK as important regulators of Golgi breakdown mediated by HDAC inhibition.

101 PAQR11 was associated with key regulators of Golgi compaction and vesicle transport in pull-down assa

102 on is known to cause extensive remodeling of Golgi and endoplasmic reticulum membranes, and a number

103 provides a previously unprecedented role of Golgi-derived secretory vesicles in phagocytic uptake, t

104 The study of Golgi stress-induced signaling pathways relies on the se

105 This leads to long distance synchrony of Golgi cells along the transverse axis, powerfully regula

106 by interacting with the conserved oligomeric Golgi (COG) tethering complex, a major coordinator of Go

107 an association with the Conserved Oliogmeric Golgi (COG) complex and with intra-Golgi SNARE proteins.

108 tes ionotropic and metabotropic receptors on Golgi cells through spillover-mediated transmission.

109 Proteins in one Golgi domain exit into predominantly vesicular carriers

110 ticulum, not co-localizing with endosomal or Golgi markers.

111 eport recruitment of mannosidase-II-positive Golgi-derived vesicles during uptake of diverse targets,

112 Post-Golgi secretory vesicles (SVs) containing the RAB11 orth

113 aries among endomembranes with pre- and post-Golgi compartments being poor and rich in sphingolipids,

114 e protein also resides in the Golgi and post-Golgi vesicles.

115 Defects in defined post-Golgi trafficking processes proved causal for this pheno

116 meter or supervised analysis with predefined Golgi structural classes.

117 we demonstrate that PI(4)P, the predominant Golgi phosphatidylinositol (PI) species, directly intera

118 ng the GM130-AKAP450 complex, which promotes Golgi ribbon formation in achieving polarized secretion

119 down assays and was required to reconstitute Golgi compaction in PAQR11-deficient tumor cells.

120 eling Golgi membrane traffic and redirecting Golgi-derived vesicles to the BCV.

121 protists and evolved separately from related Golgi-resident GT32 glycosyltransferases.

122 Golgi vesicular trafficking, thus remodeling Golgi membrane traffic and redirecting Golgi-derived ves

123 ane-bound organelles (endoplasmic reticulum, Golgi, lysosome, peroxisome, mitochondria and lipid drop

124 t localizes within the endoplasmic reticulum-Golgi intermediate compartment.

125 without affecting the endoplasmic reticulum/Golgi pathway.

126 ow suggests the existence of multiple stable Golgi organizational states and provides a proof of conc

127 ivating transcription factor ZEB1 stimulated Golgi compaction and relieved microRNA-mediated repressi

128 was too rapid after syntaxin-1 loss to study Golgi abnormalities.

129 al HDACi/(+)-JQ1 treatment spurs synergistic Golgi dispersal in several cancer cell lines, pinpointin

130 Moreover, we demonstrate that Golgi transport in hypocotyl cells can be accurately pre

131 Last, we show that Golgi fragmentation induced by ilimaquinone and nocodazo

132 Moreover, we show that Golgi-recruited GRK2ct-KERE inhibits model basolaterally

133 e in K-Ras-expressing cells, suggesting that Golgi-localized K-Ras is not as signaling-competent as i

134 The Golgi apparatus is increasingly recognized as a major hu

135 The Golgi is composed of a stack of cis, medial, trans ciste

136 The Golgi/secretory pathway Ca(2+)/Mn(2+)-transport ATPase (

137 Microtubules and the Golgi apparatus of entotic cells provided membrane expan

138 r, localize to endoplasmic reticulum and the Golgi apparatus, presumably through the recycling endoso

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

140 known to localize to the centrosome and the Golgi, but the molecular details of its function at the

141 T1 to both the endoplasmic reticulum and the Golgi, consistent with the proposal that TbRFT1 plays a

142 strains deficient in fusion activity at the Golgi (sed5-1 and sly1-ts).

143 phology did not affect Cdc42 activity at the Golgi but were associated with a substantial reduction i

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

145 ntrosomal microtubule (MT) nucleation at the Golgi generates MT network asymmetry in motile vertebrat

146 lating Rab activation and trafficking at the Golgi in addition to its established role in autophagy.

147 was not required for Cdc42 regulation at the Golgi, although its depletion decreased Cdc42 activity a

148 Active Cdc42 has also been detected at the Golgi, but its role and regulation at this organelle are

149 nown orchestrator of membrane traffic at the Golgi, regulates podosome formation, maintenance, and fu

150 our surprise, FGD1, another Cdc42 GEF at the Golgi, was not required for Cdc42 regulation at the Golg

151 Here we focus on betagamma signaling at the Golgi, where betagamma activates a signaling cascade, ul

152 ase ARF1 in mediating transport steps at the Golgi.

153 nsequences of GPCR-mediated signaling at the Golgi/trans-Golgi network.

154 g within the Golgi apparatus and between the Golgi and the endoplasmic reticulum.

155 eukaryotes, occurs in the lumen of both the Golgi apparatus and the endoplasmic reticulum.

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

157 er variable delay times, are captured by the Golgi apparatus that is reached either by random diffusi

158 PS51 to VPS54 (VPS51-54), which comprise the Golgi-associated retrograde protein (GARP) complex.

159 However, invasive pathogens can disrupt the Golgi apparatus, interfering with secretion and compromi

160 nd in plants is Araf, UDP-Arap must exit the Golgi to be interconverted into UDP-Araf by UDP-Ara muta

161 export of newly synthesized deltaR from the Golgi and delivery to the cell surface, similar to treat

162 NGF treatment displaced PI3K C2A from the Golgi and optogenetic recruitment of the PI3K C2A kinase

163 is essential in vesicle trafficking from the Golgi apparatus to the endoplasmic reticulum (ER) throug

164 f VEGFR2 due to trafficking defects from the Golgi apparatus to the plasma membrane.

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

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

167 This phenotype was distinct from the Golgi fragmentation observed in apoptosis.

168 king within the Golgi apparatus and from the Golgi to the endoplasmic reticulum.

169 ity of Kit(mut) prevents its export from the Golgi to the PM.

170 large vesicles (LVs) after release from the Golgi.

171 lar decision-makers for trafficking from the Golgi.

172 Mn binds to GPP130 in the Golgi and causes GPP130 to oligomerize/aggregate, and th

173 ulated checkpoint that retains deltaR in the Golgi and decreases surface delivery in rat and mice sen

174 d myoblasts, the protein also resides in the Golgi and post-Golgi vesicles.

175 the primary cell wall, is synthesized in the Golgi apparatus and exported to the cell wall in a highl

176 ve shown that binding of UL20 to GODZ in the Golgi apparatus regulates trafficking of UL20 and its su

177 ifications that are expected to occur in the Golgi apparatus.

178 rect role in GPI anchor glycosylation in the Golgi apparatus.

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

180 GFP-tagged Tomt is enriched in the Golgi of hair cells, suggesting that Tomt might regulate

181 nvolved in our predictions colocalize in the Golgi of two cell lines, further confirming the in silic

182 al proteins, RNA, and apolipoproteins in the Golgi stacks.

183 After processing in the Golgi to cleave the N-terminal prodomain from the C-term

184 minal KDEL-like sequence, bind ST-FRB in the Golgi, and are transported together back to the ER by KD

185 also found that these mutations increase the Golgi localization of CERT inside the cell, consistent w

186 Interestingly, the Golgi apparatus, an essential organelle for neurite grow

187 Thus, the transport of UDP-Araf into the Golgi is a prerequisite.

188 ndritic translation, most dendrites lack the Golgi apparatus (GA), an essential organelle for convent

189 organelles (early endosomes, lysosomes, the Golgi apparatus, the endoplasmic reticulum or the nucleu

190 , as exemplified by the fragmentation of the Golgi apparatus (effector function).

191 ng of proteins are critical functions of the Golgi apparatus and depend on its highly complex and com

192 both cells whereas the disintegration of the Golgi apparatus did not affect the process.

193 n within the highly dynamic membranes of the Golgi apparatus.

194 d abnormal swelling and fragmentation of the Golgi apparatus.

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

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

197 aintaining the structure and function of the Golgi complex.

198 ithout inducing pathology due to loss of the Golgi GDP mannose transporter.

199 oligomers are selectively sorted out of the Golgi is unknown.

200 ast, FM-induced lysosomal trafficking of the Golgi protein galactosyltransferase was sortilin indepen

201 raction, or by simultaneous depletion of the Golgi PtdIns4P.

202 relieved microRNA-mediated repression of the Golgi scaffolding protein PAQR11.

203 ated outside on the cytosolic surface of the Golgi.

204 become fully auto-phosphorylated only on the Golgi and only if in a complex-glycosylated form.

205 mutation, Kit localizes predominantly on the Golgi apparatus.

206 vation of Src-family tyrosine kinases on the Golgi is essential for oncogenic Kit signaling.

207 mpartment in COPII vesicles to embark on the Golgi secretory route.IMPORTANCE HCV assembly and releas

208 Furthermore, Kit(mut) on the Golgi signals and activates the phosphatidylinositol 3-k

209 t localizes to organelles, in particular the Golgi apparatus, and has a preference for acetylating N

210 These results suggest that the Golgi apparatus serves as a platform for oncogenic Kit s

211 ticulum (ER), emerging data suggest that the Golgi itself serves as an important signaling hub capabl

212 ning human cDNA library, we uncover that the Golgi resident protein acyl-coenzyme A binding domain-co

213 otes the efficiency of transport through the Golgi complex.

214 and LVPs thus formed are carried through the Golgi network by vesicular transport.

215 of mature VLDL particles occurs through the Golgi secretory pathway.

216 of Sec7, which controls transit through the Golgi.

217 TP binding are more readily recruited to the Golgi and activated by Rab29 than wild-type LRRK2.

218 that XBAT35.2 localizes predominantly to the Golgi and is involved in cell death induction and pathog

219 LR and PDGFRbeta are then transported to the Golgi apparatus, where those complexes trigger Galphai3-

220 ramide from the endoplasmic reticulum to the Golgi by the multidomain protein ceramide transfer prote

221 ssemble in the ER and are transported to the Golgi compartment in COPII vesicles to embark on the Gol

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

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

224 tic activity and prevention of export to the Golgi due to prolonged association with the chaperone ca

225 ecycles through the endocytic pathway to the Golgi for reuse in exocytosis.

226 ded inconsistent results with respect to the Golgi structure, indicating a limitation of RNAi-based d

227 ts ER retention and forward transport to the Golgi, where it is cleaved by Golgi-resident proteases,

228 o Ypt1 and its coiled-coil tail binds to the Golgi-associated SNARE, Sed5.

229 nucleotide exchange factor (ARF-GEF), to the Golgi.

230 tes recycling of cargo from endosomes to the Golgi.

231 , from the endoplasmic reticulum (ER) to the Golgi.

232 g receptors via tubular carriers back to the Golgi.

233 on of K-Ras but not H-Ras from the PM to the Golgi.

234 well as retrograde vesicle tethering to the Golgi.

235 egradation, promoting cargo recycling to the Golgi.

236 hes: a morphological investigation using the Golgi technique to provide qualitative and quantitative

237 46 dorsolateral prefrontal cortex using the Golgi-Cox technique in 12 age-matched pathology-free con

238 ed a higher level of colocalization with the Golgi apparatus and the endoplasmic reticulum (ER).

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

240 ion, specifically, those associated with the Golgi-associated retrograde protein (GARP) complex.

241 ated vesicles mediate trafficking within the Golgi apparatus and between the Golgi and the endoplasmi

242 ated vesicles mediate trafficking within the Golgi apparatus and from the Golgi to the endoplasmic re

243 Sorting within the Golgi apparatus and trafficking along microtubules and t

244 cosylation reactions, are located within the Golgi lumen, and UDP-Arap, synthesized within the Golgi,

245 lumen, and UDP-Arap, synthesized within the Golgi, is not their preferred substrate.

246 at discrete and sparse locations within the Golgi.

247 l cells lacked the ability to polarize their Golgi and coordinate motility systems for efficient move

248 res and macromolecular compositions of these Golgi stacks, we examined high-pressure frozen/freeze-su

249 Furthermore, this Golgi-associated mechanism for dendrite establishment mi

250 um (ER) stress, ATF6 migrates from the ER to Golgi to undergo regulated intramembrane proteolysis to

251 gulation of an endoplasmic reticulum (ER) to Golgi trafficking gene signature in metastatic cells enh

252 depletion of UNC50 blocked early endosome-to-Golgi trafficking and induced lysosomal degradation of S

253 host factors required for early endosome-to-Golgi trafficking of STx2, we performed a viability-base

254 mbrane protein that serves as an endosome-to-Golgi trafficking receptor for the toxin.

255 Early endosome-to-Golgi transport allows the toxins to evade degradation i

256 mic reticulum (ER) suggesting impaired ER-to-Golgi trafficking of pre-very low-density lipoprotein (V

257 family, have been shown to control the ER-to-Golgi transport and maturation of TACE.

258 present evidence that GGpp-regulated, ER-to-Golgi transport enables UBIAD1 to modulate reductase ERA

259 ctase, permitting its maximal ERAD and ER-to-Golgi transport of UBIAD1.

260 nd swelling of the trans cisternae and trans-Golgi network (TGN) compartments.

261 sional live imaging that cis-Golgi and trans-Golgi remain stable in their composition and size.

262 esicle trafficking and a dysfunctional trans-Golgi network phenotype in patient-derived fibroblasts a

263 vesicle trafficking and dysfunctional trans-Golgi network phenotypes were reversed, suggesting that

264 ype of secretory vesicles derived from trans-Golgi cisternae.

265 f GPCR-mediated signaling at the Golgi/trans-Golgi network.

266 es Arl1 and Arl8, suggesting a role in trans-Golgi membrane trafficking.

267 the calcium-binding centrin Cdc31, in trans-Golgi network (TGN) to endosome traffic and TGN homotypi

268 Margins of trans-Golgi cisternae accumulate the LM8 xylogalacturonan (XGA

269 ted during cyst formation, as are some trans-Golgi network-to-endosome trafficking genes.

270 TBC1D23 localized at the trans-Golgi and was regulated by the small GTPases Arl1 and Ar

271 trograde transport of endosomes to the trans-Golgi apparatus.

272 described the regulation of Sec7, the trans-Golgi Arf-GEF, through autoinhibition, positive feedback

273 t sphingomyelin (SM) metabolism at the trans-Golgi membranes in mammalian cells essentially controls

274 e localization of ARF1 and BIG4 at the trans-Golgi network (TGN) depends on ECHIDNA (ECH), a plant ho

275 -kDa species that colocalizes with the trans-Golgi network (TGN) marker TGN46 in KSHV-infected PEL ce

276 signaling-regulated checkpoint at the trans-Golgi network (TGN) that controls the surface delivery o

277 y required both for transport from the trans-Golgi network (TGN) to the late endosome/prevacuolar com

278 a selected number of cargoes from the trans-Golgi network (TGN) to the plasma membrane in Saccharomy

279 hat Mn-induced exit of GPP130 from the trans-Golgi network (TGN) toward lysosomes is mediated by the

280 at controls sphingolipid levels at the trans-Golgi network (TGN).

281 resulting in vesicle fission from the trans-Golgi network (TGN).

282 The L2/DNA complex traffics to the trans-Golgi network (TGN).

283 show that Rab29 recruits LRRK2 to the trans-Golgi network and greatly stimulates its kinase activity

284 SPCA1 regulates proteases within the trans-Golgi network that require calcium for their activity an

285 gnal-mediated export of ATG9A from the trans-Golgi network to the peripheral cytoplasm, contributing

286 ough endocytic trafficking towards the trans-Golgi network, and, ultimately, the entry into the nucle

287 binding of regulatory proteins in the trans-Golgi network, followed by full activation by PI4P.

288 erol and sphingolipid transport to the trans-Golgi network, PtdIns(4)P consumption interrupts this tr

289 s, NRAMP2 is a resident protein of the trans-Golgi network.

290 ning secretory vesicle material to the trans-Golgi network.

291 -selectin colocalizes with AP-1 at the trans-Golgi network.

292 abA2 localizes in Golgi stacks and the trans-Golgi network.

293 o a disruption in the structure of the trans-Golgi network.

294 cargo retrieval from endosomes to the trans-Golgi network.

295 in the sequence-dependent endosome-to-trans-Golgi network (TGN) transport of the cation-independent

296 ential network mechanisms, including tunable Golgi cell oscillations, on-beam inhibition and NMDA rec

297 vity is controlled by Tuba and ARHGAP10, two Golgi-associated Cdc42 regulators.

298 acid-induced phosphorylation of Akt, whereas Golgi-recruited GRK2ct-KERE inhibits cargo transport fro

299 Whether Golgi dispersal underlies the pro-metastatic vesicular t

300 olic amino terminal (NT) domain of the yeast Golgi V-ATPase a-isoform Stv1.