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首页> 外文期刊>The Journal of Biochemistry >CEL-I, an N-acetylgalactosamine (GalNAc)-specific C-type lectin, induces nitric oxide production in RAW264.7 mouse macrophage cell line.
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CEL-I, an N-acetylgalactosamine (GalNAc)-specific C-type lectin, induces nitric oxide production in RAW264.7 mouse macrophage cell line.

机译:CEL-1是一种N-乙酰半乳糖胺(GalNAc)特异的C型凝集素,可诱导RAW264.7小鼠巨噬细胞细胞系产生一氧化氮。

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摘要

We found that CEL-I, a GalNAc-specific C-type lectin isolated from the marine invertebrate Holothuroidea (Cucumaria echinata), induces inducible nitric oxide synthase (iNOS) expression and NO production in RAW264.7 cells. The NO production was inhibited by an iNOS inhibitor, L-NAME, but was not by a lipopolysaccharide (LPS) inhibitor, polymyxin B. In the presence of 0.1-M GalNAc, increased NO production by CEL-I-treated RAW264.7 cells was observed rather than the inhibition. Bovine serum albumin (BSA) significantly inhibited the CEL-I-induced NO production as well as the binding of FITC-labelled CEL-I on RAW264.7 cells. Three MAP kinase inhibitors (specific to extra-cellular regulated kinase, c-jun NH(2)-terminal kinase and p38 MAP kinase) inhibited CEL-I-induced NO production with different extents. Heat-treatment of CEL-I resulted in a decreased activity of CEL-I depending on the temperature. These results suggest that CEL-I induces NO production in RAW264.7 cells through the protein-cell interaction rather than the binding to the specific carbohydrate chains on the cell surface.
机译:我们发现,CEL-I,一种从海洋无脊椎动物无脊椎动物(Cucumaria echinata)分离出来的GalNAc特异性C型凝集素,在RAW264.7细胞中诱导诱导型一氧化氮合酶(iNOS)表达和NO产生。 NO的产生受到iNOS抑制剂L-NAME的抑制,但脂多糖(LPS)抑制剂多粘菌素B却没有。在存在0.1-M GalNAc的情况下,经CEL-1处理的RAW264.7细胞的NO产生增加被观察到而不是抑制。牛血清白蛋白(BSA)显着抑制CEL-1诱导的NO生成以及FITC标记的CEL-1在RAW264.7细胞上的结合。三种MAP激酶抑制剂(特异于细胞外调节激酶,c-jun NH(2)-末端激酶和p38 MAP激酶)在不同程度上抑制CEL-1诱导的NO产生。 CEL-1的热处理导致CEL-1活性降低,具体取决于温度。这些结果表明,CEL-1通过蛋白质-细胞相互作用而不是与细胞表面上特定碳水化合物链的结合诱导RAW264.7细胞中NO的产生。

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