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1 -related factors, inducers of cytokines, and chemotaxins).
2 induce the production of IL-6 and neutrophil chemotaxins.
3 irways epithelial cells to induce neutrophil chemotaxins.
4 ich specifically cleaves mouse and human C5a chemotaxins.
5  hepatic amyloidosis, leukocyte cell-derived chemotaxin 2 (LECT2) amyloidosis (ALect2) accounted for
6 ke chemotactic factor leukocyte cell-derived chemotaxin 2 (LECT2) and invariant NKT (iNKT) cells were
7        Aggregation of leukocyte cell-derived chemotaxin 2 (LECT2) causes ALECT2, a systemic amyloidos
8 e circulating protein leukocyte-cell-derived chemotaxin 2 (LECT2) causes amyloidosis of LECT2 (ALECT2
9                       Leukocyte cell-derived chemotaxin 2 (LECT2) is a cytokine and preferentially ex
10                       Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine that
11  that we must now add leukocyte cell-derived chemotaxin 2 (LECT2) to the list of proteins that can ca
12    Here, we show that leukocyte cell-derived chemotaxin 2 (LECT2), a hepatokine and ligand of the MET
13 ologous to vertebrate leukocyte cell-derived chemotaxin 2 (LECT2)/Chondromodulin II.
14  S-transferase A1 and leukocyte cell-derived chemotaxin 2, could potentially assist in clinical diagn
15 mine synthetase (GS), leukocyte cell-derived chemotaxin 2, Regucalcin, and Cyclin-D1 and of K-Ras eff
16 CT-2, the ortholog of leukocyte cell-derived chemotaxin-2 (LECT2), is secreted from the muscles and r
17 hrombin protein), and leukocyte cell-derived chemotaxin-2.
18 leukin-8 (IL-8) is the major lung neutrophil chemotaxin, and we have shown that Ad7 induces IL-8 rele
19 al of those occurring in cells stimulated by chemotaxins, and that the nucleotides ADP, ATP, and UTP
20 e conclude that some of the effects of these chemotaxins are mediated by translocation of an intracel
21  (SCPA) specifically cleaves the human serum chemotaxin C5a at the polymorphonuclear leukocyte (PMNL)
22 s, including IL-1, IL-36, and the neutrophil chemotaxins CXCL1 and CXCL8.
23               Anaphylatoxin C5a was a potent chemotaxin (EC50 approximately 0.5 nM) for J774 monocyte
24 n from lamina propria to lumen caused by the chemotaxin, FMLP, and that LTB4-induced eosinophil migra
25 ponsiveness both to C5a and to the bacterial chemotaxin, fMLP.
26                               ADP was also a chemotaxin for murine J774 monocytes.
27 ally cleaves the complement component C5a, a chemotaxin for polymorphonuclear leukocytes.
28             Intralumenal instillation of the chemotaxin, formyl-met-leu-phe (FMLP) caused migration o
29 d virus-induced expression of the neutrophil chemotaxin IL-8, previously implicated in adenoviral pat
30 sely related chemokines are major neutrophil chemotaxins in experimental gout.
31 stals induce different classes of neutrophil chemotaxins, including certain chemokines (e.g., interle
32 5a promoted the production of the neutrophil chemotaxin interleukin-8, and recruitment of neutrophils
33 kotriene A4 (LTA4) and subsequently into the chemotaxin LTB4, which has no direct bronchoconstrictor
34 le derivatives of ADP and ATP were effective chemotaxins, obviating a role for adenosine receptors.
35 ng the SDF-1-CXCR4-axis by cleaving SDF-1, a chemotaxin recruiting CXCR4(+) SC.
36   These findings highlight the complexity of chemotaxin signaling pathways and offer one mechanism by
37  by which neutrophils may spatially organize chemotaxin signaling within the plasma membrane.
38  their role in recognition systems for other chemotaxins such as leukotriene B4 (LTB4) and fMLP is un
39  peptide-78 (ENA-78), is a potent neutrophil chemotaxin whose expression is increased in inflamed syn