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1 ion of the p23 cargo-protein-binding site on coatomer.
2 gain novel insights into the architecture of coatomer.
3 glycoside antibiotics that are known to bind coatomer.
4 at components including AP-2, AP180 and COPI coatomer.
5 dues of the KKXX motif that is known to bind coatomer.
6 of KIF5B and beta'-COP, a component of COP1 coatomer.
7 nt with ARF forming direct interactions with coatomer.
8 the AD7 antibody interacts with undenatured coatomer.
9 he Golgi membrane in molar excess over bound coatomer.
10 blocked the interaction of antibiotics with coatomer.
11 teracting with the di-lysine binding site of coatomer.
12 ch blocked the coating of Golgi membranes by coatomer.
13 T1, a gene that encodes the alpha subunit of coatomer.
14 ontribute to stabilizing membrane-associated coatomer.
15 rf1 bound to the gammazeta-COP subcomplex of coatomer.
16 ctor for wild-type epsilon-COP, a subunit of coatomers.
17 nolayer and thus seem unsuitable targets for coatomers.
18 r membrane and the subsequent recruitment of coatomer, a coat protein complex consisting of seven sta
19 two cytosolic components, ARF G protein and coatomer, a heptameric complex that can polymerize into
22 from that predicted from the current model, coatomer affected the K(m) and not the k(cat) values.
23 fs on transmembrane proteins are captured by coatomer alpha-COP and beta'-COP subunits and packaged i
27 mbda and soluble components, including COPI (coatomer and ADP-ribosylation factor), results in the re
28 e propose and corroborate a simple model for coatomer and Arf1 activity based on results analysing th
29 We propose that this continuous activity of coatomer and Arf1 generates kinetically stable membrane
30 Rapid membrane binding and dissociation of coatomer and Arf1 occur stochastically, even without ves
31 ution and lifetime of fluorescently labelled coatomer and Arf1 on Golgi membranes of living cells.
33 ange dependent on engagement of ArfGAP1 with coatomer and Arf1, and affected by secretory cargo load.
36 required for epsilon-COP incorporation into coatomer and maintainance of normal epsilon-COP levels.
37 eraction with the coatomer protein complex I coatomer and resulted in accumulation of GFP-tpn-aa in t
38 st three-dimensional picture of the complete coatomer and reveal substantial conformational flexibili
39 ics interact with di-lysine binding sites on coatomer and that coatomer contains at least two of thes
41 istinct vesicle coat complexes, termed COPI (coatomer) and COPII, whose assembly is regulated by the
43 rgoes are the size of COPI vesicles, contain coatomer, and functionally require ARF1 and coatomer for
44 tion between the Golgi-vesicle coat protein, coatomer, and the regulatory GTP-binding protein Cdc42.
45 on of epsilon-COP, the assembly of COPs into coatomers, and the participation of coatomers in intrace
47 chemically defined liposomes incubated with coatomer, Arf1p, and guanosine 5'-[gamma-thio]triphospha
50 the distribution of the beta-COP subunit of coatomer because COPI partially localizes to pre-Golgi i
51 th IAP (inhibitor of apoptosis) or COP (COPI coatomer, beta subunit) dsRNA silenced their target gene
52 We suggest that Ist2 dimerization triggers coatomer binding and clustering of this protein into dom
53 om cytosolic pools, acts directly to promote coatomer binding and is in a 3:1 stoichiometry with coat
56 contrast to the behavior of the COPII coat, coatomer binds to liposomes containing a variety of char
60 o donor membranes, leading to recruitment of coatomer, bud formation, and eventual vesicle release.
61 em, vaccinia formation bypasses this role of coatomer, but instead, depends on coatomer interacting w
62 oatomer to p24 tails suggests models for how coatomer can potentially package retrograde-directed and
64 ding to COPI vesicles whereas preventing the coatomer-Cdc42 interaction stimulates dynein binding.
66 port to the endoplasmic reticulum, contain a coatomer coat and that coatomer is required for their fo
69 ng kinetics, is more potent at uncoating the coatomer-coated membrane than EGTA, suggesting that a ca
72 known to promote, by itself, scission of the coatomer-coated vesicles that mediate intra-Golgi transp
80 ein RPL35A, putative RNA helicase DDX24, and coatomer complex I (COPI) subunit ARCN1 most significant
81 ts, we performed RNAi screens and identified coatomer complex I (COPI) vesicle formation as a liabili
82 nction variants in COPB2, a component of the coatomer complex I (COPI), in individuals presenting wit
85 opus extracts, we report a role for the COPI coatomer complex in nuclear envelope breakdown, implicat
87 ry of LF to the cytosol requires either COPI coatomer complex or a COPI subcomplex for translocation
89 d by the small GTPase Arf1 that recruits the coatomer complex to the membrane, triggering polymerizat
92 if at the C-terminus of Sac1 is required for coatomer complex-I (COP-I)-binding and continuous retrie
99 ilar to a region in the beta-subunit of COPI coatomer complexes, which suggests the existence of a sh
100 Arf1-independent process suggests that COPI coatomer components may perform roles unrelated to vesic
103 All of the antibiotics that interacted with coatomer contain at least two close amino groups, sugges
104 di-lysine binding sites on coatomer and that coatomer contains at least two of these di-lysine bindin
105 ivate phospholipase D1 (PLD1), (iii) recruit coatomer (COP-I) to Golgi-enriched membranes, and (iv) e
106 hosphoinositide binding selectivity of Golgi coatomer COPI polypeptides was examined using photoaffin
107 y transient interaction between DRD3 and the coatomer COPI, a complex involved in membrane transport,
110 of the adaptor protein 1 (AP-1) complex and coatomer (COPI) onto these membranes and activates phosp
111 hought to play a critical role in recruiting coatomer (COPI) to Golgi membranes to drive transport ve
114 er, a cytosolic protein fraction depleted of coatomer could not support vesicle formation but it did
117 ent proteins, indicating specific defects in coatomer-dependent ER protein retrieval by KDEL receptor
120 (VLP) and VLP fusogenicity are determined by coatomer-dependent S delivery from the cis-Golgi and res
123 C-terminal acidic residue is critical for S-coatomer dissociation and therefore incorporation into v
125 er with the previously established ancestral coatomer element (ACE1), these two elements constitute t
127 conserved tripartite element, the ancestral coatomer element ACE1, that reoccurs in several nucleopo
128 ment of coat protein I (COPI), but not COPII coatomers, facilitating retrograde transport and explain
130 signals on cargo proteins are recognized by coatomer for selective uptake into COPI (coatomer)-coate
132 hibitor of Arf1 activation required for COPI coatomer formation, revealed that this late COPI-depende
134 We report herein that neomycin precipitates coatomer from cell extracts and from purified coatomer p
138 ensable for yeast cell viability and overall coatomer function, but is required for KKXX-dependent tr
143 nal selection is under kinetic control, with coatomer governing a GTPase discard pathway that exclude
144 tomer into large aggregates and implies that coatomer has two or more binding sites for neomycin.
146 er, once associated with membranes, Arf1 and coatomer have different residence times: coatomer remain
150 ARF is at most a minor component relative to coatomer in coated vesicles from all cell lines tested,
152 hypothesis that these RGS proteins sequester coatomer in the cytoplasm and inhibit its recruitment on
155 mechanism previously documented for Arf GAP1/coatomer in which Arf1 is inactivated in a tripartite co
159 t which replication stage(s) was affected by coatomer inactivation, we used visual and biochemical as
163 ng mode has implications for the dynamics of coatomer interaction with the Golgi and for the selectio
164 This suggested that neomycin cross-linked coatomer into large aggregates and implies that coatomer
166 Our results offer an explanation of why COPI coatomer is frequently identified in screens for cellula
168 RNA interference experiments confirm that coatomer is required for cER induction in vivo, as are m
171 e complex of Coat Protein I (COPI), known as coatomer, is sufficient to induce coated vesicular-like
177 ed to be inefficient in the arf mutants, and coatomer mutants with no detectable anterograde transpor
179 ther aminoglycoside antibiotics precipitated coatomer, or if they did not precipitate, they interfere
182 d to initiate the formation of clathrin- and coatomer protein (COP) I-coated vesicles on these membra
183 her H89 might act at the level of either the coatomer protein (COP)I or the COPII coat protein comple
184 evidence has suggested that subunits of the coatomer protein (COPI) complexes are functionally assoc
185 GBF1 is mainly involved in the formation of coatomer protein complex (COPI) vesicles, maintenance an
187 recombinant SBP-AR and the ligand-sensitive coatomer protein complex I (COPI) retrograde trafficking
188 used by autosomal recessive mutations in the coatomer protein complex I (COPI) subunit zeta 1 (COPZ1)
189 the addition of cytosolic proteins including coatomer protein complex I (COPI) to the reaction mixtur
191 This mutation abolished interaction with the coatomer protein complex I coatomer and resulted in accu
194 the C1 cassette or by the presence of a PDZ/coatomer protein complex II-binding domain in the C2' ca
196 Mutations in the N-terminal WD40 domain of coatomer protein complex subunit alpha (COPA) cause a ty
197 disorder caused by missense mutations in the coatomer protein complex subunit alpha (COPA) gene.
198 ynthetic T1 peptides the specific binding of coatomer protein complex subunit beta to this region of
199 ction-based genomic screening identified the coatomer protein complex zeta1 (COPZ1) gene as essential
200 of COPZ1, but not of COPZ2 encoding isoform coatomer protein complex zeta2, caused Golgi apparatus c
203 140-kDa protein was the alpha-COP subunit of coatomer protein COPI, usually associated with trans-Gol
206 adaptor protein 1 (AP1) complex subunits and coatomer protein I (COPI) proteins, no longer promoted m
210 in the hKOPR C-tail decreased interaction of coatomer protein I (COPI) with the hKOPR and abolished 1
211 tif was responsible for the interaction with coatomer protein I (COPI), which was inversely correlate
212 the cell surface expression by mediating the coatomer protein I complex-dependent retrograde transpor
213 (ER) and must be transported to the Golgi in coatomer protein II (COPII) vesicles where two sequentia
214 protein, which is an essential component of coatomer protein II (COPII)-mediated cargo transport fro
215 d that decreased expression of the gammaCOPI coatomer protein led to 89% mortality in blood-fed mosqu
218 embles classic coat protein complex I (COPI) coatomer protein-binding KKXX signals, and indeed the di
221 crosomes and partitions with subunits of the coatomer proteins that coat ER-to-Golgi transport vesicl
223 ng suggests that all four subunits are proto-coatomer proteins, with important implications for BLOC-
225 primary target for the effects of calcium on coatomer recruitment is a step that occurs after ADP-rib
227 and coatomer have different residence times: coatomer remains on membranes after Arf1-GTP has been hy
231 ilon-COP and beta-, gamma-, delta-, zeta-COP coatomer subcomplexes and identify links between them th
232 (ALI), autoimmune lung disease (for example, coatomer subunit alpha [COPA] syndrome), and primary gra
233 eterious variants in the COPA gene (encoding coatomer subunit alpha) affecting the same functional do
236 ilar to that of brefeldin A, except that the coatomer subunit beta-COP remained on Golgi-derived memb
237 siRNA knockdown, and two factors, AHNAK and coatomer subunit COPB1, are also essential for productiv
239 and mitochondrial inheritance and for a COPI coatomer subunit in the targeting of a type V myosin to
240 steady state levels in ldlF cells of another coatomer subunit, beta-COP, and the peripheral Golgi pro
242 tosus, and type 1 interferonopathies such as coatomer subunit-alpha syndrome (COPA) and DNASE1L3 defi
243 using dsRNA directed against five other COPI coatomer subunits (alpha, beta, beta', delta, and zeta).
245 35 and other IFT-A subunits to a and B' COPI coatomer subunits and demonstrate an accumulation of 'co
248 we demonstrate novel direct interactions of coatomer subunits with regulatory proteins: beta'- and g
252 tative cargo receptors were shown to bind to coatomer, the coat protein of COPI-coated transport vesi
253 a combination of purified kinases, ARF1 and coatomer, the Golgi membranes were completely fragmented
255 on has been implicated in the recruitment of coatomer to Golgi membranes and release of nascent secre
260 branes with mitotic cytosol or with purified coatomer together with wild type ARF1 or its constitutiv
261 om the ER, whereas Golgi matrix proteins and coatomer undergo constant, rapid exchange between membra
262 tion factor (ARF) is absolutely required for coatomer vesicle formation on Golgi membranes but not fo
264 the antibody to beta-COP confirmed that the coatomer was the sole protein binding to the ASGR mRNA 5
265 alpha-, beta'-, and epsilon-COP subunits of coatomer, whereas other p24 domains bound the beta-, gam
266 ubunits of the coat protein 1 (COPI)-vesicle coatomer, which regulates retrograde trafficking of carg
267 e that this process does not require ARF and coatomers, which are necessary for the formation of Golg