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1 1b but not other CD1 isoforms bound the AP-3 adaptor protein complex.
2 plex with AP-2, the plasma membrane clathrin adaptor protein complex.
3 for communicating conformational changes to adaptor protein complexes.
4 through E3-mediated ubiquitination of Smad4/adaptor protein complexes.
5 unctional homologies with the beta-chains of adaptor protein complexes.
11 ay rapid movement, colocalize with clathrin, adaptor protein complex 1 (AP-1), and TGN46, but not the
12 toward the subendothelial matrix, using the adaptor protein complex 1 (AP-1), where it may provide t
15 ea, whereas the localization of the clathrin adaptor protein complex 1 in the trans-Golgi network rem
16 identified an essential requirement for both adaptor protein complexes 1 and 3 in this process by emp
23 internalization is mediated by the clathrin adaptor protein complex 2 (AP-2) and epsin-1, rather tha
24 LR9 requires UNC93B1-mediated recruitment of adaptor protein complex 2 (AP-2) for delivery to endolys
25 m HIV-1 and to the medium chain (mu2) of the adaptor protein complex 2 (AP-2) in vitro and in vivo.
26 oding Picalm, clathrin, or components of the adaptor protein complex 2 (AP2) have been previously des
28 ha), a kinase devoid of a clathrin-dependent adaptor protein complex 2 binding site, caused a delay i
29 via clathrin-coated pits, where clathrin and adaptor protein complex 2 nucleate and polymerize upon e
30 the plasma membrane preceding recruitment of adaptor protein complex 2, clathrin, and dynamin-related
32 lar loop of PAR4 and found that the clathrin adaptor protein complex-2 (AP-2) is important for intern
34 unactivated PAR1 is mediated by the clathrin adaptor protein complex-2 (AP-2), where the mu2-adaptin
35 stitutive internalization is mediated by the adaptor protein complex-2 (AP-2), whereas AP-2 and epsin
36 unactivated PAR1 is mediated by the clathrin adaptor protein complex-2 (AP-2), which binds to a dista
41 complex 1 (BLOC-1), which interacts with the adaptor protein complex 3 (AP-3), mediating a common end
42 zygous mutation of the gene encoding the dog adaptor protein complex 3 (AP3) beta-subunit, directing
43 E-) found in its cytoplasmic tail to recruit adaptor protein complex 3 for export from the trans-Golg
47 es mutated in the Hermansky-Pudlak syndrome, adaptor protein complex-3 and biogenesis of lysosome-rel
49 one mutation in each of three genes encoding adaptor protein complex 4 (AP4) subunits: a nonsense mut
50 teract both with the mu2 subunit of the AP-2 adaptor protein complex and with ALG-2-interacting prote
51 res both a functional AP-3 (heterotetrameric adaptor protein complex) and HOPS (homotypic fusion and
54 ions between the mu2 subunit of the clathrin adaptor protein complex AP-2 and tyrosine-based internal
60 oblasts from mocha mice that lack functional adaptor protein complex (AP)-3, small interfering RNA-me
62 own to be important for the interaction with adaptor protein complexes (AP) that mediate the endosoma
63 tive association with the endocytic clathrin adaptor protein complex, AP-2, strongly suggest that Eps
78 ng clathrin and the beta-subunit of the AP-2 adaptor protein complex, at discrete locations that are
79 R-mediated signals modulate a multimolecular adaptor protein complex containing Grb2, Shc, SHIP, CrkL
80 adaptin protein that constitutes part of the adaptor protein complex found at the cytoplasmic face of
81 re of three leukemia transformation-relevant adaptor protein complexes (Grb2/Gab2/Shc1 complex, CrkI
82 IDTS and did not impede interaction with the adaptor protein complex IcmS/IcmW, which is thought to f
83 A new study reveals a key role for the AP4 adaptor protein complex in the Golgi-to-endosome traffic
84 we explore the role of AP-2, a key endocytic adaptor protein complex, in the development of rat hippo
85 Pase domain, was shown to bind both clathrin adaptor protein complexes, indicating a role in membrane
86 ntegration at the postreceptor level through adaptor protein complexes, influencing cellular dependen
87 he major coat constituents, clathrin and the adaptor protein complexes, interact with each other, wit
88 report that both the AP-3 (heterotetrameric adaptor protein complex) interaction domain and clathrin
89 t endocytic processing through disruption of adaptor protein complexes is likely to result from the A
90 stematically examined the effect of ablating adaptor protein complexes on the localization of this pr
91 pp120 co-localized with alpha-adaptin in the adaptor protein complex that anchors endocytosed protein
92 ef to adaptor protein-2 (AP-2), which is the adaptor protein complex that is required for the interna
93 sorting domains with downstream assembly of adaptor protein complexes that constitute the endosomal
94 , results in the recruitment and assembly of adaptor protein complexes that function to transduce sig
95 otif that is similar to motifs recognized by adaptor protein complexes that sort transmembrane protei
96 g., coat protein complex I, II, and clathrin/adaptor protein complex), the exomer does not form buds
97 tifs that are known to interact with various adaptor protein complexes; the other is the sequence ESS
99 encodes sigma3A, a small subunit of the AP-3 adaptor protein complex, was demonstrated to bind IRS-1
100 migration through regulation of Crk and CAS adaptor protein complexes, which are necessary for cell
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