ライフサイエンスコーパス: COPI

1 COPI coated vesicles carry material between Golgi compar

2 COPI coated vesicles mediate trafficking within the Golg

3 COPI components influenced at least two stages of the na

4 COPI in these mutants is released from Golgi membranes b

5 COPI is a coatomer protein complex responsible for intra

6 COPI is a key mediator of protein trafficking within the

7 COPI is recruited to the membrane primarily through bind

8 COPI is required for ER-Golgi transport and early endoso

9 COPI mediates retrograde trafficking from the Golgi to t

10 COPI proteins oligomerize to form coated vesicles that t

11 COPI subunits immunoprecipitated with KA2 subunits from

12 COPI vesicles are generated through activation of the re

13 COPI vesicles likely become tethered while they bud, the

14 COPI vesicles mediate Golgi-to-ER recycling, but COPI ve

15 COPI-coated vesicles form at the Golgi apparatus from tw

16 COPI-coated vesicles mediate trafficking within the Golg

17 des a subunit of coatomer protein complex 1 (COPI) involved in intracellular traffic and autophagy.

18 nt roles for subunits of the coat protein 1 (COPI)-vesicle coatomer, which regulates retrograde traff

19 ve used both site-directed mutagenesis and a COPI complex precipitation assay to demonstrate that int

20 Our results therefore identify GORAB as a COPI scaffolding factor, and support the view that defec

21 ly, followed approximately 10 min later by a COPI component (epsilon-COP) and a trans-Golgi network (

22 Finally, a COPI binding domain swap was used to demonstrate that su

23 ulum and mitochondrial inheritance and for a COPI coatomer subunit in the targeting of a type V myosi

24 we find that mTRAPPII binds to gamma1COP, a COPI coat adaptor subunit.

25 the glycoprotein ERAD signal is generated, a COPI-binding motif was appended to the N terminus of the

26 , implying that Trs120p may participate in a COPI-dependent trafficking step on the early endosomal p

27 suggest that cisternal maturation involves a COPI-dependent pathway that recycles early Golgi protein

28 Assembly of a COPI coated vesicle is initiated by the small GTPase Arf

29 rcy1Delta and drs2Delta single mutants, or a COPI mutant deficient in ubiquitin binding, display a de

30 l requires either COPI coatomer complex or a COPI subcomplex for translocation from the endosomal lum

31 Adv-COPI protected distal and proximal tubules against hypox

32 Adv-COPI significantly improved renal function by restoring

33 Adv-COPI treatment selectively augmented COX-1 and PGIS prot

34 After Adv-COPI transfection, we evaluated the renal COX-1 and PGIS

35 t PGI2 production by intrarenal arterial Adv-COPI administration with renal venous clamping in female

36 Increased PGI2 by Adv-COPI protects the kidney against I/R-induced oxidative s

37 se (COX)-1/prostacyclin synthase (PGIS) (Adv-COPI) gene transfer in rat kidneys with ischemia-reperfu

38 ng clathrin-mediated entry is caveolin-1 and COPI dependent.

39 f TSET, a 'missing link' between the APs and COPI.

40 oid legs radiating from a common center, and COPI shares with COPII highly similar vertex interaction

41 related to those of clathrin heavy chain and COPI subunits.

42 ticulum (ER) export of proteins in COPII and COPI vesicles, respectively.

43 of coat protein complex II and I (COPII and COPI).

44 CUPS biogenesis is independent of COPII- and COPI-mediated membrane transport.

45 endent trafficking through the endocytic and COPI systems.

46 V5-tagged TMEM199 localized with ERGIC and COPI markers in HeLa cells, and electron microscopy of a

47 tors markedly reduced association of KA2 and COPI.

48 of Golgi membranes with mitotic kinases and COPI coat proteins efficiently disassembles the membrane

49 mediated by the interaction of RXR motif and COPI.

50 tivation of Golgi-localized Arf proteins and COPI vesicle formation, proANP secretion by Pam (Myh6-cK

51 e relationship between Snx4, Drs2, Rcy1, and COPI in recycling Snc1 or FM4-64 is unclear.

52 In Arabidopsis, COPI and COPII vesicle coat proteins as well as vesicle

53 A subset of the Arf1-COPI vesicular transport proteins also regulated droplet

54 Our findings uncover a function for Arf1/COPI proteins at LDs and suggest a model in which Arf1/C

55 Cells lacking Arf1/COPI function have increased amounts of phospholipids on

56 Recent evidence shows that Arf1/COPI can bud nano-LDs ( approximately 60 nm diameter) fr

57 We show that Arf1/COPI proteins localize to cellular LDs, are sufficient t

58 The Arf1/COPI protein machinery, known for its role in vesicle tr

59 ins at LDs and suggest a model in which Arf1/COPI machinery acts to control ER-LD connections for loc

60 allows peripheral membrane proteins such as COPI to be sequestered rapidly by adding rapamycin.

61 se that neurons utilize the Golgi-associated COPI vesicle to deliver cargoes necessary for motor neur

62 interactions of DOR with COPI, via atypical COPI motifs on the C-terminal tail, retain DOR in the Go

63 Association between COPI proteins and KA2 subunits was significantly reduced

64 omponents are structurally conserved between COPI and clathrin/adaptor proteins.

65 esting a possible direct interaction between COPI and lipid droplets.

66 efinitively explore the relationship between COPI and CFTR in epithelial cells, we depleted beta-COP

67 ransport is achieved, and that bidirectional COPI transport is modulated by environmental cues throug

68 nals, and indeed the dimerized peptide binds COPI in vitro.

69 Blocking COPI recruitment to membranes by expressing an inactive

70 transmembrane helix 1 are essential for both COPI complex binding and the delivery of the catalytic d

71 by the addition of partially purified bovine COPI to the translocation assay mixture.

72 vesicles mediate Golgi-to-ER recycling, but COPI vesicle arrival sites at the ER have been poorly de

73 ifferent from transport vesicle formation by COPI, likely responsible for the diverse lipid droplet p

74 light on the structure of vesicles formed by COPI protein complexes.

75 as Arf1 dependent, as expected for canonical COPI vesicle formation, the early stage was found to be

76 ediate in design between COPII and clathrin: COPI shares with clathrin an arrangement of three curved

77 ponents, including the Class I vesicle coat (COPI), the spliceosome, the proteasome, the nuclear pore

78 e dynamic processes such as coatomer-coated (COPI) vesicle-mediated trafficking.

79 nt interaction between DRD3 and the coatomer COPI, a complex involved in membrane transport, and shif

80 the classical Golgi coat proteins coatomer (COPI) and clathrin.

81 n the formation of coatomer protein complex (COPI) vesicles, maintenance and function of the Golgi ap

82 into the ER, and the coat protein complexes (COPI and COPII), which mediate vesicular transport of pr

83 as trafficking that circumvents conventional COPI-, COPII-, and microtubule-dependent vesicular trans

84 ae with IAP (inhibitor of apoptosis) or COP (COPI coatomer, beta subunit) dsRNA silenced their target

85 ine the RNA-binding profile of Golgi-derived COPI in neuronal cells, we performed formaldehyde-linked

86 helps mediate the tethering of Golgi-derived COPI vesicles at the ER membrane.

87 plex-dependent fusion of retrograde-directed COPI vesicles.

88 retrograde protein trafficking, we disrupted COPI functions in the Yellow Fever mosquito Aedes aegypt

89 Here we found that disrupting COPI function by RNAi inhibited an early stage of vesicu

90 , co-occurring KRAS and LKB1 mutation-driven COPI addiction, and selective sensitivity to a synthetic

91 In contrast, the early COPI-dependent stage was Arf1 independent, with neither

92 elivery of LF to the cytosol requires either COPI coatomer complex or a COPI subcomplex for transloca

93 The heterotetrameric AP and F-COPI complexes help to define the cellular map of modern

94 at the mu-homology domain is dispensable for COPI function in the early secretory pathway, whereas th

95 ation of cargo binding have implications for COPI coat assembly.

96 the receptor and activates the receptor for COPI binding in the cytoplasm.

97 ucleotide exchange factor GBF1, relevant for COPI/Arf1-mediated cellular vesicular transport, partici

98 an inhibitor of Arf1 activation required for COPI coatomer formation, revealed that this late COPI-de

99 ARF1 is a small GTPase that is required for COPI vesicle formation from the Golgi membranes.

100 These include a noncanonical role for COPI, a previously uncharacterized protein complex affec

101 ivity of Arf, they govern vesicle formation, COPI trafficking and the maintenance of the Golgi comple

102 Whereas coatomer forms COPI vesicles in the host early secretory system, vaccin

103 ed 3D structure of a synthetically generated COPI vesicle coat obtained using cryoelectron tomography

104 ides its well-established role in generating COPI vesicles, we find that ARF1 is also involved in the

105 cific interactions stabilize COPI coats, how COPI vesicles recognize their target membranes, and how

106 daptor complexes and coat protein complex I (COPI) and COPII self-assemble to deform the membrane and

107 factor (Arf) and the coat protein complex I (COPI) are involved in vesicle transport.

108 les appeared to be vesicular coat complex I (COPI) coated.

109 ce resembles classic coat protein complex I (COPI) coatomer protein-binding KKXX signals, and indeed

110 The coat protein complex I (COPI) has been implicated in the anterograde and retrogr

111 dibasic motif bound the coatomer complex I (COPI) in an in vitro binding assay, suggesting that ER r

112 Unexpectedly, coat protein complex I (COPI) is required for lipid droplet targeting of some pr

113 ligand-sensitive coatomer protein complex I (COPI) retrograde trafficking complex in vitro Extensive

114 RNA helicase DDX24, and coatomer complex I (COPI) subunit ARCN1 most significantly inhibited growth

115 the gamma subunit of coat protein complex I (COPI) that is responsible for Golgi-to-ER retrograde car

116 oteins including coatomer protein complex I (COPI) to the reaction mixture.

117 we identify the coatomer protein complex I (COPI) vesicle coat as a critical mechanism for retention

118 llular transport via coat protein complex I (COPI), we show that COPA variants impair binding to prot

119 hat knockdown of the coat protein complex I (COPI)-Arf79F (also known as Arf1) complex selectively ki

120 Coat protein complex I (COPI)-coated vesicles, one of three major types of vesic

121 e relevance to AD of coat protein complex I (COPI)-dependent trafficking, an early step in Golgi-to-e

122 We have shown that coat protein complex I (COPI)-dependent trafficking, an early step in Golgi-to-e

123 Traffic of Kv4.2 was coat protein complex I (COPI)-dependent, but KChIP1-containing vesicles were not

124 for vesicle formation by the coat protein I (COPI) complex - a finding that reveals an unanticipated

125 on vesicle formation by the Coat Protein I (COPI) complex have contributed to a basic understanding

126 Here we show that the coat protein I (COPI) complex sorts anterograde cargoes into these tubul

127 ere required to bind the coatomer protein I (COPI) complex, a vesicle coat complex that mediates prim

128 ing vesicle formation by the Coat Protein I (COPI) complex, we elucidate that NADH generated by ALDH7

129 at least two subunits of the coat protein I (COPI) complex.

130 MTC, which is essential for coat protein I (COPI) mediated transport from the Golgi to the endoplasm

131 P1) complex subunits and coatomer protein I (COPI) proteins, no longer promoted migration upon blocka

132 efect in the localization of coat protein I (COPI) subunits, implying that Trs120p may participate in

133 In contrast, cytosolic coat protein I (COPI) vesicle coat mutations in sey1Delta cells caused n

134 to the alpha-subunit of the coat protein I (COPI) vesicle coat protein.

135 and COPb proteins of the coatomer protein I (COPI) vesicle complex were reported to interact with spe

136 recent data showing that coatomer protein I (COPI) vesicle transport is involved in cellular processe

137 Coat protein I (COPI) vesicles arise from Golgi cisternae and mediate th

138 decreased interaction of coatomer protein I (COPI) with the hKOPR and abolished 14-3-3zeta-mediated r

139 The core complex of Coat Protein I (COPI), known as coatomer, is sufficient to induce coated

140 I is the beta subunit of the coat protein I (COPI), which is involved in Golgi to endoplasmic reticul

141 for the interaction with coatomer protein I (COPI), which was inversely correlated with the 14-3-3 bi

142 and the Golgi apparatus via Coat Protein I (COPI)- and COPII-coated vesicles.

143 of coatomer and formation of coat protein I (COPI)-coated vesicles is crucial to homeostasis in the e

144 Coat protein I (COPI)-coated vesicles mediate retrograde transport from

145 omposition of Golgi-derived coat protomer I (COPI)-coated vesicles after activating or inhibiting sig

146 d vesicles, while the COat Protein I and II (COPI and COPII) routes stand for the bidirectional traff

147 sistent with the established role of Arf1 in COPI vesicle formation.

148 ation of 12 SNPs and 24 mutations located in COPI genes linked to an increased AD risk.

149 Finally, the reduction in COPI binding was correlated with an increased associatio

150 COP homo-oligomerization plays a key role in COPI coat stability, with potential implications for the

151 are known to be involved in cargo sorting in COPI transport.

152 uctures of membrane protein coats, including COPI, have been extensively studied with in vitro recons

153 intracellular trafficking systems, including COPI, COPII, and clathrin complexes.

154 ch activates the small GTPase Arf1 to induce COPI transport processes, is required for rotavirus repl

155 ADP-Ribosylated Substrate (BARS) to inhibit COPI vesicle fission.

156 omotes expression of the hKOPR by inhibiting COPI and RVR motif-mediated endoplasmic reticulum locali

157 Similarly, inhibiting COPI dissociation from membranes by expressing a constit

158 ase 1 and alpha-2,6-sialyltransferase 1 into COPI vesicles.

159 t with GOLPH3, was neither incorporated into COPI vesicles nor was dependent on GOLPH3 for proper loc

160 e mutant, converted the Golgi membranes into COPI vesicles.

161 COP and beta'-COP subunits and packaged into COPI-coated vesicles for Golgi-to-ER retrieval.

162 ion as recycling signal to sort a SNARE into COPI vesicles in a non-degradative pathway.

163 l sites (ERAS) can be visualized by labeling COPI vesicle tethers such as Tip20.

164 coatomer formation, revealed that this late COPI-dependent stage was Arf1 dependent, consistent with

165 cipated mechanistic flexibility in mammalian COPI transport.

166 s early Golgi proteins, followed by multiple COPI-independent pathways that recycle late Golgi protei

167 and DAG promote the vesiculation ability of COPI fission factors.

168 We find that a substantial amount of COPI is associated with Golgi membranes in the gea2-ts m

169 The assembly of COPI into a cage-like lattice sculpts membrane vesicles

170 4-3-3zeta knockdown increased association of COPI with the hKOPR.

171 Budding of COPI-coated vesicles from Golgi membranes requires an Ar

172 of stacks likely affects dynamic control of COPI budding and vesicle fusion at the rims.

173 Temperature-sensitive degradation of COPI complex proteins was correlated with an increase in

174 which encodes the coatomer subunit delta of COPI.

175 ccumulates in the ERGIC in cells depleted of COPI.

176 plet phenotypes associated with depletion of COPI subunits.

177 The conformational dynamics of COPI during cargo capture and vesicle formation is incom

178 HAZV exploitation of COPI components in a noncanonical Arf1-independent proce

179 These data support the novel function of COPI in inter-compartmental trafficking of RNA.

180 stive of a previously unreported function of COPI unrelated to vesicle formation.

181 transport by targeting the dual functions of COPI in cargo sorting and carrier formation.

182 Immunodepletion of COPI coatomer complex and associated proteins from cytos

183 Loss of GORAB causes impairment of COPI-mediated retrieval of trans-Golgi enzymes, resultin

184 Our findings demonstrate the importance of COPI-mediated transport in human development, including

185 Acute inhibition of COPI complex recruitment to the Golgi apparatus with pha

186 g brefeldin A (BFA), a chemical inhibitor of COPI function, we demonstrate that short-term (1-h) BFA

187 of proteins that influence the lifecycle of COPI-coated vesicles; this conclusion is supported by th

188 Loss of COPI causes defects in early endosome function, as both

189 Although loss of COPI results in the fragmentation of the Golgi, this doe

190 bition of early endosome function by loss of COPI subunits (beta', beta, or alpha) results in accumul

191 By simultaneous masking of COPI and endocytic signals, we were able to generate a s

192 To explore the mechanism of COPI action in CFTR traffic we tested whether CFTR was C

193 ARF activation to facilitate recruitment of COPI to membranes, whereas GBF1 localized at the TGN med

194 We show the requirement of COPI-coatomer subunits impacted at least two stages of t

195 er, these demonstrate the functional role of COPI association with the SMN protein in neuronal develo

196 Here, we investigated the role of COPI in CFTR trafficking.

197 between Golgi compartments, but the role of COPI in the secretory pathway has been ambiguous.

198 To study the role of COPI transport in ovarian development, we injected gamma

199 grade and retrograde cargoes are the size of COPI vesicles, contain coatomer, and functionally requir

200 usly to be required for the fission stage of COPI vesicle formation.

201 s has been made in defining the structure of COPI coats, in vitro and in vivo, at resolutions as high

202 Goldberg present X-ray crystal structures of COPI suggesting that these coats combine selected featur

203 SEC28 encodes the epsilon-COP subunit of COPI (coat protein complex I) coatomer proteins.

204 hat the alpha-, beta-, and gamma-subunits of COPI co-immunoprecipitated with CFTR.

205 ts and alpha, beta', and epsilon subunits of COPI, and trace the origins of the IFT-A, IFT-B, and the

206 rotein shell that encompasses the surface of COPI vesicles.

207 on in midgut, fat body, and ovary tissues of COPI-deficient mosquitoes.

208 d is essential for the retrograde traffic of COPI-coated vesicles from the Golgi to the ER.

209 produced evidence for two distinct types of COPI vesicles, but the in vivo sites of operation of the

210 al approach, we can distinguish two types of COPI vesicles, COPIa and COPIb.

211 mTRAPPII is enriched on COPI (Coat Protein I)-coated vesicles and buds, but not

212 a suggest that the heterodimer is exposed on COPI vesicles, while the remaining part of the B-subcomp

213 splacement or degradation of either COPII or COPI components disrupts ERAS organization.

214 ined using dsRNA directed against five other COPI coatomer subunits (alpha, beta, beta', delta, and z

215 vestigation revealed reduced levels of other COPI subunit proteins and defects in COPBI-relatedproces

216 i compartments form at ERES and then produce COPI vesicles to generate ERAS.

217 with the COPI-binding protein Scyl1, promote COPI recruitment to these domains.

218 rectly imparts membrane curvature to promote COPI tubule formation.

219 lel recycling pathways mediated by Drs2/Rcy1/COPI, Snx4-Atg20, and retromer that retrieve an exocytic

220 ructural model of the in vitro reconstituted COPI coat (Dodonova et al., 2017.

221 GBF1 recruits COPI to pre-Golgi and Golgi compartments, whereas BIG1 a

222 hat selectively abrogate SMN binding, retain COPI-mediated Golgi-ER trafficking functionality, but we

223 ors, revealing the existence of two separate COPI-dependent pathways.

224 Among these proteins, several COPI coatomer subunits (alpha, beta, gamma, and delta) a

225 cluding what specific interactions stabilize COPI coats, how COPI vesicles recognize their target mem

226 proteins of the golgin family help to tether COPI vesicles to Golgi membranes.

227 ose that mTRAPPII is a Rab1 GEF that tethers COPI-coated vesicles to early Golgi membranes.

228 tants yielded the surprising conclusion that COPI was dispensable both for the secretion of certain p

229 Our results demonstrate that COPI function in sorting of at least three retrograde ca

230 Here, we find that COPI coat components can bud 60-nm triacylglycerol nanod

231 We found that COPI defects disrupt epithelial cell membrane integrity,

232 Our data indicate that COPI vesicle-mediated recycling of PAM from the cis-Golg

233 ion of the vesicular transport model is that COPI vesicles are responsible for trafficking anterograd

234 Our findings further reveal that COPI tubular transport complements cisternal maturation

235 Video fluorescence microscopy revealed that COPI inactivation causes an early Golgi protein to remai

236 Here we show that COPI binds K63-linked polyubiquitin and this interaction

237 Together, these data show that COPI functions are critical to mosquito blood digestion

238 led to biochemical experiments, we show that COPI subunit delta (delta-COP) affects the biology of AP

239 Taken together, our findings suggest that COPI complexes likely function indirectly in influenza v

240 The data suggest that COPI vesicles traffic both small secretory cargo and ste

241 nical Arf1-independent process suggests that COPI coatomer components may perform roles unrelated to

242 The COPI coat forms transport vesicles from the Golgi comple

243 The COPI coatomer complex, which plays a major role in membr

244 The COPI, COPII, and clathrin cargo adaptors are structurall

245 Rcy1), a sorting nexin (Snx4-Atg20), and the COPI coat complex.

246 er protein disulfide isomerase (PDI) and the COPI coat protein beta-COP.

247 Vesiculation is mediated by the COPI budding machinery ARF1 and the coatomer complex.

248 quire biosynthetic membrane transport by the COPI coatomer complex for efficient replication.

249 the receptor-complex to be recognized by the COPI system.

250 he Golgi apparatus is likely mediated by the COPI vesicle coat complex, but the mechanism is poorly u

251 and ubiquitously expressed gene encoding the COPI-associated protein pseudokinase SCYL1, causes an ea

252 alpha-COP binds to SMN, linking the COPI vesicular transport pathway to SMA.

253 hat the trimer constitutes the vertex of the COPI cage.

254 veraging, we determined the structure of the COPI coat assembled on membranes in vitro at 9 A resolut

255 yeast orthologue of the gamma subunit of the COPI coat complex (Sec21p), a known Arf1p effector.

256 ing to determine the native structure of the COPI coat within vitrified Chlamydomonas reinhardtii cel

257 s with at least zeta-COP and beta-COP of the COPI coatomer complex.

258 Arf1-independent role for components of the COPI coatomer complex.

259 In contrast, knockdown of the COPI complex does not hinder craniofacial morphogenesis.

260 enes that express multiple components of the COPI complex, which regulates transport of Golgi apparat

261 rmia osteodysplastica, as a component of the COPI machinery.

262 Modeling of the COPI subunit betaCOP based on the clathrin adaptor AP2 s

263 it delta-COP function, the moderation of the COPI-dependent trafficking in vivo leads to a significan

264 Secretory protein trafficking relies on the COPI coat, which by assembling into a lattice on Golgi m

265 influenza virus infection cycle rely on the COPI complex.

266 lography to identify a conserved site on the COPI subunit alpha-COP that binds to flexible, acidic se

267 In both organisms, the COPI-type vesicles were further characterized by a combi

268 Golgi-to-ER recycling of WLS requires the COPI regulator ARF as well as ERGIC2, an ER-Golgi interm

269 Our model proposes that the COPI cage is intermediate in design between COPII and cl

270 Our results indicate that the COPI complex plays a critical role in CFTR trafficking t

271 al and molecular experiments showed that the COPI retrograde complex regulates ligand-mediated AR tra

272 target membrane by binding at one end to the COPI coat and at the other to ER-associated SNAREs.

273 ng at the Golgi involves p115 binding to the COPI coat.

274 e show that WDR35 has strong homology to the COPI coatamers involved in vesicular trafficking and tha

275 e lysine-rich transmembrane helix 1 with the COPI binding portion of the p23 adaptor cytoplasmic tail

276 plasmic reticulum (ER) in a complex with the COPI protein subunit beta-COP1.

277 trans-Golgi that, via interactions with the COPI-binding protein Scyl1, promote COPI recruitment to

278 the same entry defects as observed with the COPI-depleted cells but did result in specific decreases

279 Golgi membranes that are liberated of their COPI cover.

280 peptide from the cis-Golgi to the ER through COPI retrograde transport.

281 CCDC115 mainly localized to the ERGIC and to COPI vesicles, but not to the ER.

282 ability of transmembrane helix 1 to bind to COPI complex appears to be the essential feature for cat

283 nonredundant roles, perhaps contributing to COPI recruitment platforms on both the nuclear and cytop

284 ound effects on the recruitment of dynein to COPI vesicles.

285 duction, we found that prolonged exposure to COPI complex disruption through siRNA depletion resulted

286 regions of the protein, we localized GIV to COPI, endoplasmic reticulum (ER)-Golgi transport vesicle

287 y more disordered (~23%) than the other two, COPI (~9%) and COPII (~8%).

288 hinery components are returned to the ER via COPI-coated vesicles, which undergo similar tethering an

289 n in CFTR traffic we tested whether CFTR was COPI cargo.

290 s, explaining how secretion can persist when COPI has been inactivated.

291 Our results offer an explanation of why COPI coatomer is frequently identified in screens for ce

292 l Galpha-interacting protein associated with COPI transport vesicles that may play a role in Galpha-m

293 esults suggest that interactions of DOR with COPI, via atypical COPI motifs on the C-terminal tail, r

294 that shares common structural elements with COPI, COPII, and clathrin coats.

295 ripheral Golgi protein able to interact with COPI coat as well as with a binding motif present in the

296 This effect is mediated by interactions with COPI vesicles, but not by 14-3-3 proteins.

297 ticulum and the Golgi involves vesicles with COPI and COPII coats, whereas clathrin is the predominan

298 ge during assembly of infectious virus, with COPI knockdown reducing titers by approximately 1,000-fo

299 ssembly and egress of infectious virus, with COPI-knockdown reducing titers by approximately 1,000-fo

300 Previous studies of thermosensitive yeast COPI mutants yielded the surprising conclusion that COPI