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1 proteins colocalized with clathrin and alpha-adaptin.
2 N-terminal trunk domains of gamma- and beta1-adaptin.
3 tions of a transmembrane receptor with beta2-adaptin.
4 mplex formation with Rab11, Reps1, and alpha-adaptin.
5 by expression of a dominant negative micro1-adaptin.
6 or, SH3 domains, phosphoinositides, and beta-adaptin.
7 stin-2 interaction with clathrin and beta(2)-adaptin.
8 ed with Golgi-specific 58K protein and gamma-adaptin.
9 logy to the C-terminal "ear" domain of gamma-adaptin.
10 its binding to the appendage domain of alpha-adaptin.
11 bunits of this complex, which we call beta3A-adaptin.
12 nce of cell fate determinants Numb and alpha-Adaptin.
13 ing site for the Nef diacidic motif on alpha-adaptin.
14 milar endocytic roles, e.g., beta1 and beta2-adaptin.
15 of polarized MDCK cells independent of mu1B adaptin.
16 tion of extrasynaptic receptors with the AP2 adaptin.
17 x, as determined by coprecipitation of alpha-adaptin.
18 in xARH abolished binding to alpha- and beta-adaptins.
19 eterotetrameric assemblies of subunits named adaptins.
20 mutation of AP-1, but not AP-2, AP-3, or GGA adaptins.
21 structure, and pseudogenes for the different adaptins.
22 ins, which contain domains homologous to the adaptins.
23 ion with homology to the ear domain of gamma-adaptins.
24 similar to beta-NAP and to beta1- and beta2-adaptins.
29 es lysosomes and related organelles, whereas adaptin-3 is responsible for trafficking among these org
30 ted in these cells and in cells depleted for adaptin-3 or endoplasmic reticulum membrane complex subu
31 ndependent strains with depleted V-ATPase or adaptin-3 subunits were isometamidium resistant, and che
32 en identified 14 V-ATPase subunits and all 4 adaptin-3 subunits, implicating acidic compartment defec
35 roscopy demonstrated colocalization of alpha-adaptin, a component of clathrin-coated pits, with wild-
37 I3K-C2alpha closely paralleled that of gamma-adaptin, a component of the AP-1 adaptor that is present
38 specifically coimmunoprecipitated with alpha-adaptin, a component of the AP-2 complex that interacts
39 first identified a human cDNA encoding delta-adaptin, a structural homolog of the alpha- and gamma-ad
40 apses and decreased binding of NR2B to beta2-adaptin, a subunit of AP-2, thus blocking the activity-d
41 wn to be colocalized with clathrin and alpha-adaptin, a subunit of the AP2 adaptor protein which link
42 ction between Dishevelled2 (Dvl2) and micro2-adaptin, a subunit of the clathrin adaptor AP-2; this in
43 relates with increased interaction with beta-adaptin, a subunit of the clathrin adaptor protein compl
44 tyrosine motif that serves as the signal for adaptin alpha and a dileucine motif that serves as the s
46 ey contain distinct binding motifs for alpha-adaptin (alpha-Ada) and proteins with Eps15 homology (EH
48 n of endocytic proteins CIMPR, clathrin, and adaptin-alpha, and LGMD2B muscle exhibited decreased exp
49 rminal region of arrestin-2 mediated beta(2)-adaptin and clathrin interaction with Phe-391 and Arg-39
51 NA encoding the Drosophila ortholog of delta-adaptin and found that transcripts specified by this cDN
54 Berdnik et al. show that Numb recruits alpha-Adaptin and that this physical interaction plays a role
55 both the beta-arrestin1 interaction with mu-adaptin and the ability to enhance beta2-adrenergic rece
56 ctural and evolutionary relationships of the adaptins and the genetic analyses of their function.
59 uced colocalization of E-selectin with alpha-adaptin, and inhibited E-selectin-mediated neutrophil ro
60 um dependent, inhibited by SNAP-25 and alpha-adaptin, and results in the inhibition of receptor-media
61 ptor internalization and bind clathrin, beta-adaptin, and Src to comparable levels as wild type arres
63 bodies directed against opsin, arrestin, and adaptin, and they have a large distribution of sizes, av
64 erference-mediated knockdown of either alpha adaptin (AP-2 clathrin adaptor) or clathrin heavy chain,
66 the functional analysis of redundant AP-1 mu-adaptins AP1M1 (also known as muB1) and AP1M2 (also know
67 preserved, and the recruitment of the beta2-adaptin, AP2 adaptor complex to clathrin as well as tran
68 e identify dynamin and the EAP-binding alpha-adaptin appendage domain of the AP2 adaptor as switches
69 ic motif on Nef and the basic patch on alpha-adaptin are both required for the cooperative assembly o
72 ata indicate that beta-arrestin2 utilizes mu-adaptin as an endocytic partner, and that the inability
73 Arg-395 having an essential role in beta(2)-adaptin binding and LIELD (residues 376-380) having an e
74 tants defective in both clathrin and beta(2)-adaptin binding functioned as effective dominant negativ
78 s 4 armadillo repeats, and to the N-terminal adaptin-binding domain in mu2 from positions 1 to 145.
81 utations in AAGAB, encoding alpha- and gamma-adaptin-binding protein p34, located at a previously lin
83 rescued by transfection with wild-type delta-adaptin but not by delta-adaptin containing mutations th
84 ion of cell fate determinants Numb and alpha-adaptin by confocal microscopy were used to assess frequ
85 ge of migrating cells and depletion of beta2-adaptin by RNAi increases cell spreading and inhibits di
86 uated using mutant constructs of the beta(2)-adaptin C terminus containing either the clathrin and th
88 abeled for annexins I, II, IV, and VI; alpha-adaptin; clathrin heavy chain; or beta-coatomer protein.
90 In contrast, beta3, beta4, and all other adaptin complex subunits, as well as paralogues of the s
91 IFNAR1 promotes its interaction with the AP2 adaptin complex that is required for the robust internal
93 family mediates suramin uptake, and the AP1 adaptin complex, lysosomal proteases and major lysosomal
94 es and in trans through mutation of the AP-3 adaptin complex; both cis- and trans-mutations result in
95 ocytosis of transferrin receptors, a beta(2)-adaptin construct capable of associating with beta-arres
97 ith wild-type delta-adaptin but not by delta-adaptin containing mutations that abolish VAMP7 binding,
98 ecipitation analyses demonstrate that beta3A-adaptin corresponds to the approximately 140-kDa subunit
102 he first report to our knowledge that an AP2 adaptin dileucine recognition motif is critical for the
104 moted apical accumulation of clathrin, alpha-adaptin, dynamin, and F-actin and increased the amounts
105 the endocytic syntaxins, Rab 5, and the beta-adaptins each reveal a pattern of ancestral, undifferent
106 The carboxyl-terminal ear domains (or gamma-adaptin ear (GAE) domains) of two gamma-adaptin subunit
108 have identified the golgi-associated, gamma adaptin ear containing, ARF binding protein 1 (GGA1) as
109 (alpha2-ARs) by GGA3 (Golgi-localized, gamma-adaptin ear domain homology, ADP ribosylation factor-bin
110 etermined the role of Golgi-localized, gamma-adaptin ear domain homology, ADP ribosylation factor-bin
111 clathrin-associated Golgi-localizing, gamma-adaptin ear domain homology, ARF-binding proteins (GGA).
112 us identify a binding sequence for GAE/gamma-adaptin ear domains and reveal a functional link between
113 of expressed GGA1myc (Golgi-localizing gamma-adaptin ear homology ARF-binding protein) but with no si
114 agenesis of the LR11 Golgi-localizing, gamma-adaptin ear homology domain, ADP-ribosylation factor (GG
116 eins have been named Golgi-localizing, gamma-adaptin ear homology domain, ARF-binding proteins, or GG
119 athrin adaptors, Gga (Golgi-localized, gamma-adaptin ear homology, Arf-binding) proteins and the AP-1
121 or activity requires hRME-6 binding to alpha-adaptin ear, which displaces the ear-associated mu2 kina
122 se subunit II (COX2), Golgi-associated gamma adaptin ear-containing ARF binding protein 1 (GGA1), pol
124 n 1 (AP-1), AP-3, and Golgi-localized, gamma adaptin ear-containing, Arf-binding (GGAs) protein.
125 e we demonstrate that Golgi-localized, gamma adaptin-ear-containing ADP ribosylation factor-binding p
126 ce also recognized by the gamma1- and gamma2-adaptin ears), while GGA-GAT domains bind to the C-termi
127 ticle, we report the results of a survey for adaptins from sequenced genomes including those of man,
128 tion of macrophages or mice, indicating that adaptin function is crucial for pathogenesis in these un
129 unoprecipitation confirmed adaptin alpha and adaptin gamma complexes, but adaptor protein 180 complex
132 ng and characterization of sigma 1- and mu 1-adaptin gene homologues from the eukaryotic protozoan pa
133 equence comparisons also suggest that beta3A-adaptin has a domain organization similar to beta-NAP an
134 r, the beta-arrestin-binding site in beta(2)-adaptin has not been identified, and little is known abo
136 itro with beta-NAP, a neuronal-specific beta-adaptin homolog that was identified as an autoantigen in
139 not truncated, pp120 co-localized with alpha-adaptin in the adaptor protein complex that anchors endo
140 describing the association of ATM with beta-adaptin in vesicles indicate that ATM may play a role in
142 a complex containing Src, dynamin, and alpha-adaptin indicates that Src may play a more general role
143 n 2 minigene constructs containing the beta2-adaptin interacting region inhibits beta2AR endocytosis.
144 n of Numb, but not mutant Numb lacking alpha-adaptin-interacting domain, leads to accumulation of Not
146 t-negative mutants lacking clathrin- or beta-adaptin interaction sites fails to block GPER internaliz
147 Biochemical analyses demonstrated that delta-adaptin is a component of the adaptor-like complex AP-3
154 of AP complexes arises from the existence of adaptin isoforms encoded by distinct genes or resulting
156 s cell polarity and migration and that beta2-adaptin may control the balance between the formation of
157 tain a similar degree of interaction with mu-adaptin may result from coordination of Tyr-54 by neighb
158 signals have a well-appreciated role in the adaptin-mediated sorting of mammalian cells, this is the
160 ly prevents the interaction of Env with host adaptin molecules that recruit plasma membrane molecules
163 ed by a direct interaction between the beta2-adaptin N-terminal trunk domain and the cytoplasmic tail
166 a telangiectasia mutated (ATM) binds to beta-adaptin, one of the components of the AP-2 adaptor compl
167 e interaction with endocytic (clathrin, beta-adaptin) or signaling (Src) components and is in contras
168 AP-3 complex, the other subunits being delta-adaptin, p47A (now called mu3A) and sigma3 (A or B).
170 ith linear endocytic motifs that recruit the adaptin protein complex 2 (AP2)-clathrin molecules, mono
175 ic motif within IFNAR1 to recruitment of the adaptin protein-2 complex (AP2) and ensuing receptor end
178 photoinactivation blocked Clathrin and alpha-adaptin relocalization to synaptic membranes upon nerve
180 he interaction of beta-arrestin with beta(2)-adaptin represents a selective endocytic trigger for sev
182 The predicted amino acid sequence of beta3A-adaptin reveals that the protein is closely related to t
183 could associate with both dynamin and alpha-adaptin simultaneously, further supporting a role for am
184 wt hearts had fewer cells with uniform alpha-adaptin staining indicative of symmetrically dividing CP
185 2 is mediated by the ear domain of its alpha-adaptin subunit and binding of clathrin by the amino-ter
186 ptor protein complex-2 (AP-2), where the mu2-adaptin subunit binds directly to a tyrosine-based motif
187 amma-adaptin ear (GAE) domains) of two gamma-adaptin subunit isoforms of AP-1 and of the GGAs are str
188 and ARF6 interacted directly with the beta1-adaptin subunit of AP-1 in the presence of GTPgammaS.
189 ow that Rab11-FIP2 associates with the alpha-adaptin subunit of AP-2 complexes, which are known to re
190 trating specific colocalization of the alpha adaptin subunit of AP-2 with the EIAV p9 protein at site
200 bound directly and specifically to the beta-adaptin subunit of the clathrin adaptor complexes AP-1 a
202 antly decreased the phosphorylation of large adaptin subunits and the normally punctate AP-2 distribu
204 a structural homolog of the alpha- and gamma-adaptin subunits of the clathrin coat adaptors AP-1 and
205 re distantly related to the beta1- and beta2-adaptin subunits of the clathrin-associated adaptor comp
207 duced interaction between arrestin and beta2-adaptin, suggesting that the mutation impairs a property
208 te residues (Glu-849 and Glu-902) in beta(2)-adaptin that are important in beta-arrestin binding.
209 d residue in the appendage domain of beta(2)-adaptin that is required for interaction with the adapte
210 mplex contains a specific medium subunit, mu-adaptin, that selects cargo proteins bearing sequence-sp
211 arrestin interaction with clathrin, beta(2)-adaptin (the beta-subunit of the adaptor protein AP2), a
212 on, which requires arrestin binding to beta2-adaptin (the beta2 subunit of the clathrin-associated ad
213 beta-arrestin 2 to clathrin heavy chain/beta-adaptin, thereby accelerating receptor internalization.
215 th in vivo and in vitro the ability of beta2-adaptin to directly couple TGF-beta receptors to AP2 and
217 AP-2 complex, via an interaction with beta2-adaptin, to focal adhesions mediates cell polarity and m
220 domain of synaptotagmin binds mu2- and alpha-adaptin, two of the four subunits of the endocytic adapt
221 Genetic analysis of cdk-5 and the clathrin adaptin unc-11 AP180 suggests that CDK-5 functions prior
222 Genetic analysis of klp-4 and the clathrin adaptin unc-11/AP180 suggests that klp-4 functions befor
225 examined after shearing, clathrin and alpha-adaptin were colocalized with beta PP on the surface tha
226 tform subdomain of the C terminus of beta(2)-adaptin, where accessory/adapter endocytic proteins for
227 es its binding to the alpha c subunit of AP2 adaptin, which is also concentrated in nerve terminals.
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