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1                    The alpha1beta1 integrin, very late antigen-1 (VLA-1), is a collagen receptor expr
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
5                    The integrin alpha1beta1 (very late antigen-1; CD49a/CD29) is a major adhesion rec
6               These findings establish human very late antigen 2 transgenic mice as a model for echov
7                 Production of human integrin very late antigen 2, a receptor for echovirus type 1, in
8 eater glycoprotein (GP) IIb/IIIa (p = 0.04), very late antigen-2 (p = 0.04) and platelet/endothelial
9                                              Very late antigen 4 (VLA-4) and CD11/CD18 integrins medi
10 tes matrix metalloproteinase-9 secretion and very late antigen 4 (VLA-4)-mediated adhesion to vascula
11 e function-associated antigen 1 (LFA-1), and very late antigen 4 (VLA-4).
12 s mediated by a single integrin heterodimer, very late antigen 4 (VLA-4).
13                                         Anti-very late antigen 4 (VLA-4; on neutrophils) inhibited ad
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
17 r by chemokines leads to the inactivation of very late antigen 4.
18                       The leukocyte integrin very late antigen-4 (alpha(4)beta(1), CD49d/CD29) is an
19                       The leukocyte integrin very late antigen-4 (VLA-4) (alpha 4 beta 1, CD49d/CD29)
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
22                             Extremely potent very late antigen-4 (VLA-4) antagonists with picomolar,
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
25                                           As very late antigen-4 (VLA-4) can exist in different funct
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
31                            The expression of very late antigen-4 (VLA-4) on the surface of MBP-primed
32 scular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integral role in t
33                               Interaction of very late antigen-4 (VLA-4) with its ligand vascular cel
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
36                The alpha(4)beta(1)-integrin (very late antigen-4 (VLA-4), CD49d/CD29) is an adhesion
37 portance of VCAM-1, and its leukocyte ligand very late antigen-4 (VLA-4), in such leukocyte migration
38                     Natalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for mul
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
43 and human monoblastoid U937 cells expressing Very Late Antigen-4 (VLA-4).
44 ascular cell adhesion molecule-1 (VCAM-1) or very late antigen-4 (VLA-4).
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
47 ion of one of the major leukocyte integrins, very late antigen-4 (VLA-4, CD49d/CD29).
48 duced by IL-3 in a dose-dependent manner via very late antigen-4 (VLA-4; alpha4beta1 integrins) and V
49                                              Very late antigen-4 (VLA-4; also called integrin alpha4b
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
54  lymphocyte adhesion but partially conserved very late antigen-4 adhesiveness.
55 irway inflammation and was prevented by anti-very late antigen-4 and anti-interleukin-5 treatments, w
56                                              Very late antigen-4 and CD11/CD18 integrins mediated pas
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
60  for the integrin alpha4beta1 (also known as very late antigen-4 or VLA-4).
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
63 lymphocyte function-associated antigen-1 and very late antigen-4) on splenocytes.
64 tide affinity ligand, VHPKQHR, homologous to very late antigen-4, a known ligand for VCAM-1.
65                     The antigen alpha4beta1 (very late antigen-4, VLA-4) plays an important role in t
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
68                        Activated T cells use very late antigen-4/alpha4beta1 integrin for capture, ro
69       The optimization and validation of the very late antigen-4/vascular cell adhesion molecule-1 as
70 tion of the interaction between the integrin very-late antigen-4 (VLA-4; alpha 4 beta 1) and vascular
71 nocyte chemoattractant protein-1) and VLA-4 (very-late antigen-4).
72 , a ligand for the alpha(4)beta(1) integrin, very-late-antigen-4 (VLA-4 or CD49d).
73                                              Very-late-antigen-4 (VLA-4, alpha4beta1 integrin, CD49d/
74 otif that has homology to the alpha-chain of very late antigen (a known ligand for VCAM-1), was shown
75                           The human integrin very late antigen (VLA)-2 (CD49b/CD29) mediates interact
76                  Despite the higher level of very late antigen (VLA)-2, VLA-4, and VLA-5 on Sca-1(+)c
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
80                  The transient regulation of very late antigen (VLA)-4 avidity by CC chemokines may p
81        This study tested the hypothesis that very late antigen (VLA)-4 mediates CD18-independent neut
82 lar endothelial growth factor (VEGF)-induced very late antigen (VLA)-4.
83 s subset depends on the alpha4beta1 integrin very late antigen (VLA)-4.
84 n to be important in hematopoiesis, CD44 and very late antigen (VLA)-4.
85                Cross-linking of adherent PMN very late antigen (VLA)-5 and VLA-6 receptors resulted i
86  adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC2s from tum
87 ing that stem cells may express the integrin very late antigen (VLA)-5.
88 vious study showed that the cross-linking of very late antigen (VLA)/beta1 with anti-CD29 monoclonal
89       In this study, we investigated whether very late antigen (VLA)4 and VLA-6 integrins, which play
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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