Induction of a prenylated 65-kd protein in macrophages by interferon or lipopolysaccharide.
Induction of a prenylated 65-kd protein in macrophages by interferon or lipopolysaccharide.
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通过干扰素或脂多糖在巨噬细胞中诱导异戊二烯化 65-kd 蛋白。
DOI：
10.1002/jlb.58.5.607
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发表时间：
1995
影响因子：
5.5
通讯作者：
Buss,JE
中科院分区：
文献类型：
--
作者：
Vestal,DJ;Maki,RA;Buss,JE
用干扰素-γ (IFN-γ) 和/或脂多糖 (LPS) 处理小鼠骨髓来源的巨噬细胞，导致许多异戊烯化蛋白的丰度发生变化。最显着的变化涉及 65 kd (p65) 的蛋白质，该蛋白质在处理后成为最丰富的异戊二烯化蛋白质之一。 65-kd 蛋白是由刺激巨噬细胞活化的物质（IFN 或 LPS）诱导的，但不是由促进巨噬细胞增殖的细胞因子诱导的，例如粒细胞巨噬细胞集落刺激因子 (GM-CSF)、M-CSF 或白细胞介素 3。大多数 p65 定位于含有内膜和质膜的亚细胞部分，但在核膜中未检测到。法呢基转移酶抑制剂 BZA-5B 导致 p65 异戊二烯化显着减少，表明该蛋白可能被 C15 类异戊二烯法呢基修饰。这些观察结果提供了第一个直接证据，证明干扰素和脂多糖会导致巨噬细胞中特定类异戊二烯修饰蛋白的丰度发生变化。
Treatment of murine bone marrow-derived macrophages with interferon-γ (IFN-γ) and/or lipopolysaccharide (LPS) resulted in changes in the abundance of a number of prenylated proteins. The most significant change involved a protein of 65 kd (p65) that became one of the most abundant prenylated proteins following treatment. The 65-kd protein was induced by agents that stimulate macrophage activation (IFNs or LPS) but not by cytokines that promote macrophage proliferation, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), M-CSF, or interleukin-3. The majority of p65 was localized to subcellular fractions containing internal and plasma membranes but was not detected in nuclear membranes. The farnesyltransferase inhibitor BZA-5B caused a dramatic decrease in p65 prenylation, suggesting that this protein may be modified by the C15isoprenoid farnesyl. These observations provide the first direct evidence that interferons and LPS cause changes in the abundance of specific isoprenoid-modified proteins in macrophages.