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1 ll-cell contacts through an interaction with annexin II.
2 A second, 36 kDa, protein was identified as annexin II.
3 ne was found to abolish S-glutathiolation of annexin II.
4 of these were identical to sequences within annexin II.
5 ssue plasminogen activator binding domain of annexin II.
6 nd C335G was equivalent to that of wild type annexin II.
7 B (gpUL55) (gB) can physically interact with annexin II.
8 e conclusion that HCMV gB can bind host cell annexin II.
9 activities are blocked by antibodies against annexin II.
10 th high affinity to a cell surface receptor, annexin II.
11 vator (t-PA) which we recently identified as annexin II.
12 subunit of PI3-kinase and Na,K-beta binds to annexin II.
13 es through the phospholipid-binding protein, annexin II.
14 fic mRNA, and a 7.9-fold increase in surface annexin II.
15 ls as well as altered expression patterns of annexin II.
16 nd this activity was largely attributable to annexin II.
17 membrane domains via their interactions with annexin II.
20 n (14 amino acids), directly associates with annexin II, a lipid raft-associated molecule, which is a
21 er coat of HIV-1, we define a novel role for annexin II, a PS-binding moiety, as a cellular cofactor
22 lcium-regulated phospholipid-binding protein annexin II, an interaction that is inhibited by the prot
24 amily of proteins, is the cellular ligand of annexin II and also interacts with the C-terminal region
27 promoted the association of Hsp90alpha with annexin II and increased the expression of annexin II on
28 cross-linking experiments with biotinylated annexin II and intact PSV10 cells identified a 55-kDa ba
30 dentified the plasminogen binding protein as annexin II and the angiostatin binding protein as the al
31 all-trans-retinoic acid on the expression of annexin II and the generation of cell-surface plasmin.
32 ssue plasminogen activator binding domain of annexin II and to determine the mechanism of its modulat
34 regulated interaction between Hsp90alpha and annexin II, and raise the possibility that increased exp
36 t N-terminal peptides of annexin I (AnI) and annexin II (AnII) was investigated under controlled expe
37 Prior work in our laboratory has identified annexin II (Ann-II) as a co-receptor for Plg and t-PA th
38 noprecipitations using anti-CEACAM1 and anti-annexin II antibodies and second by confocal laser micro
39 -beta(2)GPI than control cells and that anti-annexin II antibodies inhibited the binding of (125)I-be
40 s increase in plasmin was blocked by an anti-annexin II antibody and was induced by transfection of t
48 ssary to trigger the activation and identify annexin II as its probable binding partner-receptor.
51 but not cysteine 143 or 156 is required for annexin II association with caveolin and the rapid trans
61 calcium-binding "endonexin" motif (KGXGT) of annexin II, blocked its interaction with endothelial cel
63 nexin II was inhibited by intact fluid phase annexin II but not by its "core" fragment (residues 25-3
64 f synthesis of the thiol-containing protein, annexin II, but no change in synthesis of the cysteinele
65 6 kDa protein was subsequently identified as annexin II by proteomic approach and confirmed by Wester
66 Moreover, this HIV-1 PS interaction with annexin II can be disrupted by SLPI or other annexin II-
67 ed that the endothelial cell surface protein annexin II can stimulate t-PA-mediated plasminogen activ
68 ophy, including those coding for Sp3, c-Jun, annexin II, cathepsin B, and HB-EGF, thus showing the ge
69 , Ch), G3PDH (Hu, Ch), pyruvate kinase (Ch), Annexin II (Ch), and protein disulfide isomerase (Ch).
72 16 h of biosynthesis, and that cell surface annexin II comprises 4.3 +/- 1.0% of the total cellular
74 um, caveolin IgG precipitated four proteins: annexin II, cyclophilin 40, caveolin, and cyclophilin A.
77 nied by an increased amount of extracellular annexin II detected in the media of PC12, NIH-3T3(IR), a
79 ents, we indeed observed that restoration of annexin II expression inhibited the migration of the tra
80 y insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied b
85 of RAW264.7 macrophages with monoclonal anti-annexin II IgG inhibited (35%) their binding of 125I-Lys
86 Preincubation of THP-1 monocytes with anti-annexin II IgG inhibited (60%) their plasminogen-depende
88 jor physiological plasmin inhibitor, or anti-annexin II IgG, blocked EMT by approximately 80%, and 50
93 copy showing co-localization of CEACAM1 with annexin II in mammary epithelial cells grown in Matrigel
95 crophages and indicate an important role for annexin II in their invasive and degradative phenotype.
96 escribed receptor for fibrinolytic proteins, annexin II, in cells from patients with APL or other leu
97 of the crystal adhesion molecules, CD44 and annexin II, in tubular epithelial cells in vitro and in
98 en 2 (SCCA2), S100A8, S100A9, Annexin I, and Annexin II] in the squamous NHTBE cells was further conf
105 ith a highly significant correlation between annexin II levels and factors associated with impeded fi
108 ces the selective loss of p11 (also known as annexin II light chain, S100A10), a multifunctional prot
118 Abnormally high levels of expression of annexin II on APL cells increase the production of plasm
119 pendently blocked the stimulatory effects of annexin II on human osteoclast formation, demonstrating
125 s identified the plasminogen binding protein annexin II on the surface of macrophages and determined
127 re cholesterol, and increased binding of the annexin II-p11 complex to membranes, consistent with oth
128 binding protein that forms a heterotetramer (annexin II-p11 heterotetramer; A2t) with p11 (S100A10).
129 approaches demonstrated that three proteins, annexin II/p36, stratifin/14-3-3 sigma, and heat shock p
130 n lattices in vitro was also reduced, and an annexin II peptide mimicking sequences necessary for t-P
131 tosis (caveolin-1, dynamin-2, Arp2, NSF, and annexin II), phagocytosis (RhoA, dynamin-2, Rac1, and Ar
134 igens involved in signal transduction [e.g., annexin II, protein kinase C alpha, the G alpha subunits
136 t in 5' untranslated region (5'UTR) of human Annexin II receptor (AXIIR) mRNA, there are two upstream
137 body raised against the putative recombinant annexin II receptor also recognized the same 26-kDa prot
139 HEK 293 cells transformed with the cloned annexin II receptor cDNA showed a similar binding affini
140 expression library, we identified a putative annexin II receptor clone, which encoded a novel 26-kDa
142 emonstrated that there was a single class of annexin II receptors with a Kd of 5.79 nm and Bmax of 2.
143 Direct physical evidence showed that the annexin II-S100A10 complex, which regulates exocytosis,
144 lin and IGF-1 receptor, was shown to inhibit annexin II secretion along with reduced receptor phospho
145 in kinase C had no effect on insulin-induced annexin II secretion, suggesting a possible direct link
148 um-dependent phospholipid-binding ability of annexin II since some annexin II was dissociated from vi
151 acrophages, there was a 2.4-fold increase in annexin II-specific mRNA, and a 7.9-fold increase in sur
153 displayed an additional 3.8-fold increase in annexin II surface expression compared with resident cel
156 ion of two of these receptors in MS lesions, annexin II tetramer (AIIt) and low-density lipoprotein r
158 itric oxide (NO) donors on the activities of annexin II tetramer (AIIt), a member of the Ca2+- depend
159 aken together, our results indicate that the annexin II tetramer can serve as a binding protein for p
161 more, procathepsin B could interact with the annexin II tetramer in vivo as demonstrated by coimmunop
163 chain (p11), one of the two subunits of the annexin II tetramer, was one of the proteins identified.
164 act as a neural cytokine, signaling through annexin II to activate microglia in settings of disease
168 uced transport of the membrane-bound form of annexin II to the outside layer of the cell membrane and
169 cells was confirmed by the observations that annexin II-transfected HEK 293 cells bound approximately
173 hese findings indicate that the formation of annexin II, V, and VI Ca(2+) channels in MV together wit
174 urthermore, K-201 inhibited up-regulation of annexin II, V, and VI gene expression in these cells.
175 concentration, followed by up-regulation of annexin II, V, and VI gene expression, and release of an
176 ntration leads to a further up-regulation of annexin II, V, and VI gene expression, the release of an
177 channel blocker, or antibodies specific for annexin II, V, or VI inhibited the increases in cytosoli
179 a-2-loaded PS-enriched liposomes mediated by annexin II, V, or VI, but also inhibited Ca(2+) uptake b
181 ch contained significantly higher amounts of annexins II, V, and VI as well as APase activity than ve
183 I, V, and VI gene expression, the release of annexin II-, V-, VI- and alkaline phosphatase-containing
184 I, V, and VI gene expression, and release of annexin II-, V-, VI- and alkaline phosphatase-containing
185 pid-binding ability of annexin II since some annexin II was dissociated from virions with chelating a
186 lization studies revealed that in NHP cells, annexin II was distributed both in the cytosol and under
188 plasminogen activator binding to immobilized annexin II was inhibited by intact fluid phase annexin I
190 substantial proportion of virion-associated annexin II was resistant to chelation, which suggested a
191 , we used coimmunoprecipitation to show that Annexin-II was bound to insulin and insulin-like growth
192 embryonic endocardial-derived cells express annexin II which promotes plasminogen activation in vitr
193 L cells contained abundant messenger RNA for annexin II, which disappeared through a transcriptional
194 ll substrate phosphorylation, in particular, annexin II, which is strongly phosphorylated by the gag-
195 the possibility that increased expression of annexin II, which promotes the generation of plasmin, is
197 thods to inhibit the interaction of tPA with annexin II would offer a new and selective approach to i
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