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1 gingivalis invasion of cells is mediated by alpha5 integrin.
2 lls were more resistant to the inhibition of alpha5 integrin.
3 by supporting Akt-dependent upregulation of alpha5 integrin.
4 ally altered in the genes for fibronectin or alpha5 integrin.
5 ization identifies this second protein to be alpha5-integrin.
6 ntegrins, particularly those associated with alpha5 integrins.Activation of beta1 by antibody 8A2 als
8 f constitutively active or dominant negative alpha5 integrin also resulted in alterations in the numb
9 tern blots revealed significant induction of alpha5 integrin and Fn expression by HEp-2 cells in resp
10 1 receptor I and antibodies directed against alpha5 integrin and Fn, indicating that increased invasi
12 ; an increase in the pool of ubiquitinylated alpha5 integrin and its lysosome-dependent degradation;
14 d with gene and surface expression levels of alpha5 integrin and urokinase plasminogen activator rece
15 , we show that EWS/FLI-induced repression of alpha5 integrin and zyxin expression promotes tumor prog
16 ggesting a functional link between sEGFR and alpha5-integrin and a role of the calf-1 domain in cell
18 We have analyzed embryos lacking alpha4- or alpha5-integrins and show here that these integrins cont
20 ntibodies to human beta4, beta1, alpha6, and alpha5 integrins; and sera from patients with pemphigus
23 ), similar to removal of the endothelium and alpha5 integrin blockade, inhibited the vasoconstriction
25 egulation and mislocalization of alpha3- and alpha5-integrins by immunohistochemistry but, surprising
26 adhesion to FN was blocked with mAbs against alpha5 integrin chain and with RGD-containing peptides.
30 s conditional knockout of another RCP cargo, alpha5 integrin, does not suppress pancreatic cancer met
31 ce with reduced expression of the alpha3 and alpha5 integrins exhibit a defect in paired-pulse facili
36 pression was associated with upregulation of alpha5 integrin (fibronectin receptor component), the an
38 to GRGDNP (2.1 mM) was inhibited by blocking alpha5 integrin function, and was intensified by blockin
39 gressive phenotype in brain tumors, and high alpha5 integrin gene expression was associated with decr
43 ntial targets of the inhibitor, did not have alpha5 integrin immunoreactivity in inflamed airways.
45 ing proliferation, ectopic expression of the alpha5 integrin in cultures of primary quail myoblasts p
47 F) analysis revealed prominent expression of alpha5 integrin in microglia and macrophages in a supero
49 inistration of a monoclonal antibody against alpha5 integrin increased survival compared to an isotyp
50 findings in mice and in humans suggest that alpha5 integrin is a potential therapeutic target in ALS
51 ibition resulting from ectopic expression of alpha5 integrin is due to induction of autocrine negativ
52 linical ALS phenotypes and disease duration, alpha5 integrin is prominent in motor pathways of the ce
53 coding just two of these proteins, zyxin and alpha5 integrin, is sufficient to restore cell adhesion
57 P-2 expressed on cancer cells interacts with alpha5 integrin on endothelial cells to mediate vascular
58 rs, expressed on cancer cells interacts with alpha5 integrin on endothelial cells to mediate vascular
59 ctivator nutlin-3a, the protective effect of alpha5 integrin on p53 activation and cell survival was
60 -7 breast cancer cells do not express either alpha5 integrin or type II TGF-beta receptor and hence a
61 nd surface protein expression for alpha1 and alpha5 integrin (P < 0.01) but not alpha3 integrin subun
63 inally, we show that reduction of myocardial alpha5 integrin rescues the myocardial proliferation phe
64 26-amino acid peptide in the calf domain of alpha5-integrin (residues 710-735) is 35% identical in s
65 rase cDNA into cells stably transfected with alpha5 integrin resulted in basal promoter activities 5-
66 y terminus of sEGFR and the calf-1 domain of alpha5-integrin share a region of sequence identity, whi
67 vessels, but not all, stained positively for alpha5-integrin, showing that they were host derived.
69 ed with increased proteasomal degradation of alpha5 integrin subunit (ITGA5) and reduced activation o
70 s study, we show that high expression of the alpha5 integrin subunit compromises temozolomide-induced
73 grin in which the cytoplasmic portion of the alpha5 integrin subunit is replaced by the cytoplasmic p
75 ubunit but also an intense expression of the alpha5 integrin subunit particularly in the endothelial
76 p53 background, nutlin-3a downregulated the alpha5 integrin subunit, thereby increasing the cytotoxi
79 IGF-I treatment caused a 73% reduction in alpha5-integrin subunit protein and a 25% increase in al
80 nectin and enhanced expression of alphav and alpha5 integrin subunits together with increased cell mi
81 alpha(v) or beta1, but not beta3, beta5, or alpha5, integrin subunits block Ad infection and viral e
82 t alpha1, alpha2, alpha6, and beta1, but not alpha5, integrin subunits reduced invasion of a reconsti
84 ized to linear, punctate structures, and the alpha5 integrin to some focal complexes and/or vesicle-l
85 osphorylation regulated vesicular traffic of alpha5-integrin to the cell surface and cell attachment
89 inhibition of Akt phosphorylation prevented alpha5 integrin upregulation elicited by survivin overex
90 as inhibited; in parallel, the expression of alpha5 integrin was enhanced, and that of alpha6 integri
91 dhesion to fibronectin, and up-regulation of alpha5 integrin were also dependent on ADAM10 but not AD
92 ) cells-wild-type, heterozygous, or null for alpha5-integrin-were injected ectopically into syngeneic