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1 n the C-terminal region of the protein human lymphotactin.
2 be essential for the biological activity of lymphotactin.
6 s of M3 in complex with C chemokine ligand 1/lymphotactin and CC chemokine ligand 2/monocyte chemoatt
7 -5, IL-13, and IFN-gamma, and the chemokines lymphotactin and RANTES, in stimulated thymocyte culture
9 including RANTES, IFN-inducible protein-10, lymphotactin, and IL-1R antagonist, as well as altered l
10 mokine interleukin-8, the murine C chemokine lymphotactin, and the murine CX(3)C chemokine fractalkin
11 duced in the presence of a neutralizing anti-lymphotactin antiserum and to a lesser extent by neutral
12 affinity identified two arginine residues of lymphotactin as critical for glycosaminoglycan binding.
13 -1alpha (MIP-1alpha) and -1beta (MIP-1beta), lymphotactin), b) type-2-dominant (eotaxin, monocyte che
14 , granulocyte colony-stimulating factor, and lymphotactin by live P. gingivalis, but not by P. gingiv
16 e mRNAs was increased, and low expression of lymphotactin, C10, MIP-2, and MIP-1alpha mRNAs was detec
17 ttin, human beta defensin 1, truncated human lymphotactin, Cytochrome C, holo hemoglobin-alpha, ovalb
21 ocyte recruitment assay, suggesting that the lymphotactin-glycosaminoglycan interactions detected in
29 bcutaneous injections of a vaccine combining lymphotactin (Lptn)- and interleukin-2 (IL-2)-secreting
35 As encoding a lymphocyte-specific chemokine, lymphotactin (Ltn), were isolated from mouse pro-T cell
36 so quantified the effects of acute stress on lymphotactin- (LTN; a predominantly lymphocyte-specific
37 10-kDa interferon-inducible protein, RANTES, lymphotactin, macrophage inflammatory protein 1beta (MIP
38 K receptor induced high levels of IFN-gamma, lymphotactin, macrophage-inflammatory protein (MIP)1alph
39 cell-derived and chemokine-related cytokine/lymphotactin, macrophage-inflammatory protein 1alpha, ma
42 were observed, and levels of RANTES, MCP-1, lymphotactin, MIP-1alpha, MIP-1beta, and MIP-2 mRNAs wer
43 synthesize several chemokines that included lymphotactin, monocyte chemoattractant protein-1 (MCP-1)
47 ta, IL-4, IL-6, TNF-alpha, and the chemokine lymphotactin, mRNAs for IL-1beta, TNF-alpha, and lymphot
48 ain at least some regions of disorder (human lymphotactin, N-terminal p53, alpha-Synuclein, N-termina
49 Second, allografts demonstrated sustained lymphotactin, RANTES, and IP-10 expression, beginning at
50 TNF-alpha and IFN-gamma mRNA and chemokines lymphotactin, RANTES, and macrophage inflammatory protei
52 -2), and CXCL10 (inducing protein-10), XCL1 (lymphotactin/single C motif-1alpha/activation-induced, T
55 ults demonstrate that like other chemokines, lymphotactin utilizes highly specific glycosaminoglycan-
56 otein (MIP)-1 alpha, MIP-1 beta, RANTES, and lymphotactin was inducible in DETC 7-17 cells, whereas m
57 itions used for the structure determination, lymphotactin was predominantly monomeric; however, pulse
59 hotactin, mRNAs for IL-1beta, TNF-alpha, and lymphotactin were down-modulated in the presence of alph
60 luding chemokines such as MIP-1beta (CCL-4), lymphotactin (XCL-1), IFN-gamma-inducible protein 10 (IP
61 crophage colony-stimulating factor (GM-CSF); lymphotactin (XCL1); tumor necrosis factor receptor supe
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