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1 apoptotic cells indicates a requirement for annexin I.
2 pendent manner were identified as S100A8 and annexin I.
3 localized to a carboxyl-terminal fragment of annexin I.
4 han that of annexin V but lower than that of annexin I.
5 ns may play critical roles in the folding of annexin I.
6 ential for Ca2+-dependent vesicle binding of annexin I.
7 to a site within the first 12 amino acids of annexin I.
8 nce in lung cancer sera of autoantibodies to annexin I, 14-3-3 theta, and a novel lung cancer antigen
10 e nucleotide-binding protein (beta-subunit), annexin I, a gene encoding a kinesin-like protein, and T
11 ific polyclonal antibodies identified p37 as annexin I, a member of a family of Ca(2+)-dependent phos
13 Using these methods, it was shown that both annexin I and annexin VII bind to bovine apoA-I in a Ca2
17 that a chimera composed of residues 24-35 of annexin I and the core of annexin V has vesicle aggregat
18 mportance of domain II in vesicle binding of annexin I and the involvement of domains III and IV in v
19 and is highly specific to AIIt because other annexins (I and II monomer, III, IV, V, and VI) were una
20 nclude that an immune response manifested by annexins I and II autoantibodies occurs commonly in lung
21 uorescence microscopy revealed that retained annexins I and III are associated with granule membranes
23 s of highly sensitive and precise assays for annexins I and V, utilizing turbidometric analysis of ph
25 t cytoplasmic lipocortin 1 (LC1, also called annexin I)', and the activity profile of this protein su
26 CA1), SCC antigen 2 (SCCA2), S100A8, S100A9, Annexin I, and Annexin II] in the squamous NHTBE cells w
27 100 proteins to short N-terminal peptides of annexin I (AnI) and annexin II (AnII) was investigated u
32 id monolayer was 31 +/- 2 A, indicating that annexin I binds membranes as a protein monomer or monola
35 eral proteins were eluted from a recombinant annexin I column in the presence of 2 mM EGTA, including
36 f the crystal structure of a truncated human annexin I containing all four domains, indicating that t
37 rally aggregated monolayer of membrane-bound annexin I directly interacts with a secondary membrane v
43 ur annexins containing KFERQ-like sequences, annexins I, II, IV, and VI, are enriched in lysosomes wi
44 These two inclusions were not labeled for annexins I, II, IV, and VI; alpha-adaptin; clathrin heav
46 sized that the reduced or lost expression of annexin I/II might promote certain aggressive phenotypes
50 ing apoA-I immobilized on nitrocellulose and annexin I in solution with binding detected using anti-a
51 ic mutations in the amino-terminal region of annexin I indicated that Lys-26 and Lys-29 are essential
52 exins and with N-terminal truncated forms of annexin I indicated that the 10-kDa protein bound specif
54 peptide corresponding to amino acids 2-18 of annexin I inhibited the binding of the 10-kDa protein to
55 y assays were performed to verify the apoA-I-annexin I interaction using apoA-I immobilized on nitroc
56 the conformational change of membrane-bound annexin I involving modular rotation of domains (I/IV) f
57 tial proteomics technology, we identify that annexin I is a caspase-dependent engulfment ligand; it i
59 ion, we generated truncated mutants of human annexin I lacking various parts of the amino terminus.
60 ty measurements showed that the thickness of annexin I layer bound to the phospholipid monolayer was
61 h immunohistochemical analysis suggests that annexin I may be an essential component for maintenance
62 esults suggest that annexin II, and, likely, annexin I, may be endogenous suppressors of prostate can
64 hese results support a hypothetical model of annexin I-mediated membrane aggregation, in which a late
68 significant degree of lateral association of annexin I molecules precedes its membrane aggregation.
71 , whereas pretreating Jurkat cells with anti-annexin I or removing annexin I with EGTA was inhibitory
73 f apoptotic targets was inhibited by mAbs to annexins I or II, or by pretreatment of macrophages with
74 linded validation study to determine whether annexin I, PGP9.5, and 14-3-3 theta antigens previously
76 loss or a dramatic reduction in the level of annexin I protein expression compared with patient-match
79 membrane via the Orai1/TRPC1-mediated Ca(2+)/Annexin I/S100A11 pathway, partially contributing to SOC
81 aluation of membrane aggregation activity of annexin I separately from its membrane binding, revealed
82 uman S100A8/A9 complex and recombinant human annexin I showed carboxylate-dependent binding to immobi
83 Chemical cross-linking of membrane-bound annexin I showed that a significant degree of lateral as
84 cated that both the amino-terminal region of annexin I spanning residues 26-29 and the carboxy-termin
87 Surface plasmon resonance measurements of annexin I, V, and mutants, which allowed evaluation of m
88 nt study, the spatial expression patterns of annexins I-VI were evaluated in the rat dorsal root gang
89 Immunohistochemical analysis showed that annexin I was expressed diffusely in neoplastic cells in
90 that interact with the N-terminal domain of annexin I, we constructed a fusion protein consisting of
91 POH treatment; p21(Cip1/WAF1), bax, bad, and annexin I were induced; cyclin E and cyclin-dependent ki
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