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2 thelial growth factor receptor-3) and VLA-1 (very late antigen-1) promotes high-risk transplant survi
3 AQC2 to the alpha1 chain of human and sheep very late antigen-1, given 30 minutes before challenge,
4 on, but an increase in p150,95 (CD11c/CD18), very late antigen-1, or ICAM-1 expression was not observ
8 eater glycoprotein (GP) IIb/IIIa (p = 0.04), very late antigen-2 (p = 0.04) and platelet/endothelial
10 tes matrix metalloproteinase-9 secretion and very late antigen 4 (VLA-4)-mediated adhesion to vascula
14 To provide further insights into the anti-very late antigen 4 (VLA4)/anti-vascular cell adhesion m
15 e detected the active conformational form of very late antigen 4 after stimulation with a peptide mim
16 s of beta1 phosphorylation and a decrease in very late antigen 4 binding to its ligand vascular cell
20 hocytes that expressed low or high levels of very late antigen-4 (VLA-4) and non-antigen-specific act
21 rs to stromal cells is primarily mediated by very late antigen-4 (VLA-4) and vascular cell adhesion m
23 nction-associated antigen (LFA-1) and VCAM-1/very late antigen-4 (VLA-4) at select time points compar
24 rsor cells were transiently transfected with very late antigen-4 (VLA-4) binding to vascular cell adh
26 later, GVHD-associated increase in CD25 and very late antigen-4 (VLA-4) expression on donor T cells
27 lar endothelial growth factor receptor-1 and very late antigen-4 (VLA-4) have been shown to arrive at
28 ell adhesion molecule-1 (VCAM-1), LFA-1, and very late antigen-4 (VLA-4) have relatively little effec
29 esent study was to determine the role of the very late antigen-4 (VLA-4) integrin/ligand interaction
30 te function-associated antigen-1 (LFA-1) and very late antigen-4 (VLA-4) on adhesion of influenza hem
32 scular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integral role in t
34 ion, we show that MBP-primed T cells express very late antigen-4 (VLA-4), and functional blocking ant
35 the adhesion molecules CD11a, CD11b, CD11c, very late antigen-4 (VLA-4), and L-selectin, as assessed
37 portance of VCAM-1, and its leukocyte ligand very late antigen-4 (VLA-4), in such leukocyte migration
39 he affinity of the alpha(4)beta(1) integrin, very late antigen-4 (VLA-4), measured with an LDV-contai
40 lasts within the bone marrow is adhesion via very late antigen-4 (VLA-4), the alpha(4)beta(1) integri
41 D49d), in complex with integrin beta1, forms very late antigen-4 (VLA-4), which interacts with vascul
42 cular cell adhesion molecule-1 (VCAM-1)- and very late antigen-4 (VLA-4)-mediated localization of CXC
45 une cells from patients under long-term anti-very late antigen-4 (VLA-4)/natalizumab therapy (LTNT) a
46 skin fibroblasts, making it unlikely that a very late antigen-4 (VLA-4)/VCAM-1 interaction is requir
48 duced by IL-3 in a dose-dependent manner via very late antigen-4 (VLA-4; alpha4beta1 integrins) and V
50 ascular cell adhesion molecule-1 (VCAM1) and very late antigen-4 (VLA4) using monoclonal antibodies.
51 cule antagonist, compound A, to nonactivated very late antigen-4 (VLA4) was examined in lung inflamma
52 BL1(+) progenitors had similar expression of very late antigen-4 (VLA4), VLA5, leukocyte functional a
53 elated protein ligand, resulting in enhanced very late antigen-4 [VLA-4] directed adhesion and motili
55 irway inflammation and was prevented by anti-very late antigen-4 and anti-interleukin-5 treatments, w
57 and natalizumab (Tysabri/Antegren) targeting very late antigen-4 for the treatment of relapsing-remit
58 ncrease expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenit
59 dent mechanism to increase CD11c expression, very late antigen-4 function, and integrin coclustering
61 ction by 50%, whereas blocking L-selectin or very late antigen-4 showed significant but smaller effec
62 te function-associated antigen-1) and VLA-4 (very late antigen-4) is essential for T-cell trafficking
66 al cells, and mild expression of its ligand, very late antigen-4, was apparent in perivascular lympho
67 imilar to, but more restricted than, current very late antigen-4-directed approaches that have signif
70 tion of the interaction between the integrin very-late antigen-4 (VLA-4; alpha 4 beta 1) and vascular
74 otif that has homology to the alpha-chain of very late antigen (a known ligand for VCAM-1), was shown
77 eceptors on Tc1 and Tc2 cells, we found that very late antigen (VLA)-4 (a heterodimer of CD49d and CD
78 tinct kinetic patterns for the regulation of very late antigen (VLA)-4 (alpha 4 beta 1) and VLA-5 (al
79 sp (RGD) sensitive and partially mediated by very late antigen (VLA)-4 and VLA-5 but not alpha(v) or
86 adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC2s from tum
88 vious study showed that the cross-linking of very late antigen (VLA)/beta1 with anti-CD29 monoclonal
90 investigated the role of adhesion molecules (very late antigen [VLA]-4 [ alpha 4 beta 1 integrin] and
91 odies (MoAbs) enhanced integrin alpha4beta1 (very late antigen [VLA]-4) and alpha5 beta1 (VLA-5)-depe
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