ライフサイエンスコーパス: VLA-5

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1 was found to bind directly to purified human VLA-5.

2 ficient to ensure proteolytic degradation of VLA-5.

3 ecific and can be inhibited by antibodies to VLA-5.

4 d resulted from activation of both VLA-4 and VLA-5.

5 Chinese hamster ovary cells transfected with VLA-5.

6 signaling pathway of IL-3-induced VLA-4 and VLA-5 activation in Baf3 cells.

7 ry late antigen (VLA)-4 (alpha 4 beta 1) and VLA-5 (alpha 5 beta 1) avidity by the CC chemokines mono

8 on of the monocyte fibronectin (FN) receptor VLA-5 (alpha(5)beta(1) integrin, CD49e/CD29).

9 antigen-4 (VLA-4; alpha4beta1 integrins) and VLA-5 (alpha5beta1 integrins) activation.

10 fragments selectively reduced expression of VLA-5, an effect suppressed by specific immunoadsorption

11 uring hypoxia; cross-linking of adherent PMN VLA-5 and and VLA-6 receptors resulted in a progressive

12 tion of IL-1 beta and TNF-alpha receptors by VLA-5 and VLA-6 required protein tyrosine kinase activat

13 activation of VLA-4, whereas upregulation of VLA-5 avidity occurred later and persisted.

14 These domains included the VLA-5- binding sequence RGD, the VLA-4-binding site CS1,

15 hereas anti-VLA-6 but not anti-VLA-1 through VLA-5 blocked the effect of Ln on IL-1 beta receptors.

16 ly mediated by very late antigen (VLA)-4 and VLA-5 but not alpha(v) or beta(2) integrins.

17 locked in vivo by RGD peptides and VLA-4 and VLA-5 but not beta(2) blocking antibodies.

18 ion to fibronectin via integrin alpha5beta1 (VLA-5), but not alpha4beta1 (VLA-4) in both cell lines.

19 Anti-VLA-5 (CD49e) but not anti-VLA-1 through VLA-4 and VLA-6

20 integrins alpha(4) (VLA-4/CD49d), alpha(5) (VLA-5/CD49e), and CD11b (alpha(M)).

21 very late antigen [VLA]-4) and alpha5 beta1 (VLA-5)-dependent adhesion of human cord blood CD34(+) ce

22 ding FN fragments (FN120) likewise decreased VLA-5 expression, and did so by inducing a serine protei

23 We postulated that changes in VLA-5 expression, which were induced by interactions wit

24 ith cell-binding FN fragments also modulates VLA-5/FN adhesive interactions, and this causes monocyte

25 ained activation of the adhesive strength of VLA-5 for the 120-kD fragment of fibronectin (FN120).

26 Stimulation of VLA-5 function directly correlated with induction of Bcr

27 cellular matrix protein FN by using integrin VLA-5 in vitro.

28 e effect was due to enhanced function of the VLA-5 integrin fibronectin receptor and not to increased

29 ne Bcr/Abl has positive effects on VLA-4 and VLA-5 integrin function.

30 ce of cytokines, the engagement of VLA-4 and VLA-5 integrins to the fibronectin fragment CH-296 prese

31 ligand for DC VLA-5, that binding of CypA to VLA-5 is at a site different from FN, and that there is

32 In summary, our data demonstrate that VLA-5 is expressed on primitive mouse and human hematopo

33 Alpha5beta1 (VLA-5) is one of two major FN receptors on T cells.

34 The VLA-5 ligand vascular-cell adhesion molecule-1 mediated

35 is, whereas late and prolonged activation of VLA-5 may mediate subsequent interactions with the basem

36 rs, whereas late and prolonged activation of VLA-5 may mediate subsequent localization in the extrace

37 sponses generated though adhesive VLA-4- and VLA-5-mediated contacts.

38 Thus, PIM interacts directly with VLA-5 on CD4+ T lymphocytes, inducing activation of the

39 vel of very late antigen (VLA)-2, VLA-4, and VLA-5 on Sca-1(+)c-kit(+) cells from FL compared to BM,

40 DC recognize Hc yeasts via the VLA-5 receptor, whereas Mphi recognize yeasts via CD18.

41 VLA-5 recognized a 20-kDa protein, identified as cycloph

42 onstrate that CypA serves as a ligand for DC VLA-5, that binding of CypA to VLA-5 is at a site differ

43 n that engagement of the integrins VLA-4 and VLA-5 to the fibronectin fragment CH-296 in combination

44 o identify ligand(s) on Hc recognized by DC, VLA-5 was used to probe a Far Western blot of a yeast fr

45 n without IL-3 stimulation through VLA-4 and VLA-5, whereas dominant-negative H-Ras-transfected Baf3

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