ライフサイエンスコーパス: very late antigen-4

1 nocyte chemoattractant protein-1) and VLA-4 (very-late antigen-4).

2 r by chemokines leads to the inactivation of very late antigen 4.

3 tide affinity ligand, VHPKQHR, homologous to very late antigen-4, a known ligand for VCAM-1.

4 lymphocyte adhesion but partially conserved very late antigen-4 adhesiveness.

5 e detected the active conformational form of very late antigen 4 after stimulation with a peptide mim

6 The leukocyte integrin very late antigen-4 (alpha(4)beta(1), CD49d/CD29) is an

7 Activated T cells use very late antigen-4/alpha4beta1 integrin for capture, ro

8 irway inflammation and was prevented by anti-very late antigen-4 and anti-interleukin-5 treatments, w

9 Very late antigen-4 and CD11/CD18 integrins mediated pas

10 s of beta1 phosphorylation and a decrease in very late antigen 4 binding to its ligand vascular cell

11 imilar to, but more restricted than, current very late antigen-4-directed approaches that have signif

12 and natalizumab (Tysabri/Antegren) targeting very late antigen-4 for the treatment of relapsing-remit

13 ncrease expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenit

14 dent mechanism to increase CD11c expression, very late antigen-4 function, and integrin coclustering

15 te function-associated antigen-1) and VLA-4 (very late antigen-4) is essential for T-cell trafficking

16 lymphocyte function-associated antigen-1 and very late antigen-4) on splenocytes.

17 for the integrin alpha4beta1 (also known as very late antigen-4 or VLA-4).

18 ction by 50%, whereas blocking L-selectin or very late antigen-4 showed significant but smaller effec

19 The optimization and validation of the very late antigen-4/vascular cell adhesion molecule-1 as

20 Very late antigen 4 (VLA-4) and CD11/CD18 integrins medi

21 tes matrix metalloproteinase-9 secretion and very late antigen 4 (VLA-4)-mediated adhesion to vascula

22 e function-associated antigen 1 (LFA-1), and very late antigen 4 (VLA-4).

23 s mediated by a single integrin heterodimer, very late antigen 4 (VLA-4).

24 Anti-very late antigen 4 (VLA-4; on neutrophils) inhibited ad

25 The leukocyte integrin very late antigen-4 (VLA-4) (alpha 4 beta 1, CD49d/CD29)

26 hocytes that expressed low or high levels of very late antigen-4 (VLA-4) and non-antigen-specific act

27 rs to stromal cells is primarily mediated by very late antigen-4 (VLA-4) and vascular cell adhesion m

28 Extremely potent very late antigen-4 (VLA-4) antagonists with picomolar,

29 nction-associated antigen (LFA-1) and VCAM-1/very late antigen-4 (VLA-4) at select time points compar

30 rsor cells were transiently transfected with very late antigen-4 (VLA-4) binding to vascular cell adh

31 As very late antigen-4 (VLA-4) can exist in different funct

32 later, GVHD-associated increase in CD25 and very late antigen-4 (VLA-4) expression on donor T cells

33 lar endothelial growth factor receptor-1 and very late antigen-4 (VLA-4) have been shown to arrive at

34 ell adhesion molecule-1 (VCAM-1), LFA-1, and very late antigen-4 (VLA-4) have relatively little effec

35 esent study was to determine the role of the very late antigen-4 (VLA-4) integrin/ligand interaction

36 te function-associated antigen-1 (LFA-1) and very late antigen-4 (VLA-4) on adhesion of influenza hem

37 The expression of very late antigen-4 (VLA-4) on the surface of MBP-primed

38 scular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integral role in t

39 Interaction of very late antigen-4 (VLA-4) with its ligand vascular cel

40 ion, we show that MBP-primed T cells express very late antigen-4 (VLA-4), and functional blocking ant

41 the adhesion molecules CD11a, CD11b, CD11c, very late antigen-4 (VLA-4), and L-selectin, as assessed

42 The alpha(4)beta(1)-integrin (very late antigen-4 (VLA-4), CD49d/CD29) is an adhesion

43 portance of VCAM-1, and its leukocyte ligand very late antigen-4 (VLA-4), in such leukocyte migration

44 Natalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for mul

45 he affinity of the alpha(4)beta(1) integrin, very late antigen-4 (VLA-4), measured with an LDV-contai

46 lasts within the bone marrow is adhesion via very late antigen-4 (VLA-4), the alpha(4)beta(1) integri

47 D49d), in complex with integrin beta1, forms very late antigen-4 (VLA-4), which interacts with vascul

48 cular cell adhesion molecule-1 (VCAM-1)- and very late antigen-4 (VLA-4)-mediated localization of CXC

49 and human monoblastoid U937 cells expressing Very Late Antigen-4 (VLA-4).

50 ascular cell adhesion molecule-1 (VCAM-1) or very late antigen-4 (VLA-4).

51 une cells from patients under long-term anti-very late antigen-4 (VLA-4)/natalizumab therapy (LTNT) a

52 skin fibroblasts, making it unlikely that a very late antigen-4 (VLA-4)/VCAM-1 interaction is requir

53 ion of one of the major leukocyte integrins, very late antigen-4 (VLA-4, CD49d/CD29).

54 duced by IL-3 in a dose-dependent manner via very late antigen-4 (VLA-4; alpha4beta1 integrins) and V

55 Very late antigen-4 (VLA-4; also called integrin alpha4b

56 tion of the interaction between the integrin very-late antigen-4 (VLA-4; alpha 4 beta 1) and vascular

57 , a ligand for the alpha(4)beta(1) integrin, very-late-antigen-4 (VLA-4 or CD49d).

58 Very-late-antigen-4 (VLA-4, alpha4beta1 integrin, CD49d/

59 elated protein ligand, resulting in enhanced very late antigen-4 [VLA-4] directed adhesion and motili

60 The antigen alpha4beta1 (very late antigen-4, VLA-4) plays an important role in t

61 To provide further insights into the anti-very late antigen 4 (VLA4)/anti-vascular cell adhesion m

62 ascular cell adhesion molecule-1 (VCAM1) and very late antigen-4 (VLA4) using monoclonal antibodies.

63 cule antagonist, compound A, to nonactivated very late antigen-4 (VLA4) was examined in lung inflamma

64 BL1(+) progenitors had similar expression of very late antigen-4 (VLA4), VLA5, leukocyte functional a

65 al cells, and mild expression of its ligand, very late antigen-4, was apparent in perivascular lympho