Involvement of C-Abl tyrosine kinase in lipopolysaccharide-induced macrophage activation.
Involvement of C-Abl tyrosine kinase in lipopolysaccharide-induced macrophage activation.
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DOI：
10.4049/jimmunol.160.7.3330
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发表时间：
1998-04
影响因子：
4.4
通讯作者：
Q. Le;R. Daniel;S. Chung;A. Kang;T. Eisenstein;B. M. Sultzer;H. Simpkins;P. Wong
中科院分区：
文献类型：
--
作者：
Q. Le;R. Daniel;S. Chung;A. Kang;T. Eisenstein;B. M. Sultzer;H. Simpkins;P. Wong
LPS内毒素诱导的巨噬细胞活化被认为是重要的非特异性免疫和内毒素诱导的脓毒症时，发生过度的巨噬细胞刺激。在这项研究中，我们发现，减少c-Abl在巨噬细胞阻止LPS诱导的生长停滞，一氧化氮的生产和TNF-α分泌的ANA-1巨噬细胞。这些细胞继续生长，但后来发生凋亡。这些细胞中c-Abl的减少导致与Ran相关的c-Abl激酶活性降低，Ran最近已被证明是LPS应答基因产物。我们的数据表明，c-Abl酪氨酸激酶是与LPS激活巨噬细胞相关的初始信号转导事件下游的中间产物之一。
LPS endotoxin-induced macrophage activation is recognized to be important in both nonspecific immunity and endotoxin-induced sepsis when excessive macrophage stimulation occurs. In this study, we showed that reduction of c-Abl in macrophages prevented LPS-induced growth arrest, nitric oxide production and TNF-alpha secretion by ANA-1 macrophages. These cells continued to grow but later underwent apoptosis. Reduction of c-Abl in these cells led to reduced c-Abl kinase activity associated with Ran, which recently has been shown to be an LPS-responsive gene product. Our data suggest that c-Abl tyrosine kinase is one of the intermediates downstream of the initial signal transduction event related to activation of macrophages by LPS.