Lipopolysaccharide and serum cause the translocation of G-protein to the membrane and prime neutrophils via CD14.

Lipopolysaccharide and serum cause the translocation of G-protein to the membrane and prime neutrophils via CD14.
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脂多糖和血清导致 G 蛋白易位至细胞膜并通过 CD14 启动中性粒细胞。

DOI:
10.1016/s0006-291x(05)80329-8
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发表时间:
1992
影响因子:
3.1
通讯作者:
Sha'afi,RI
Sha'afi,RI
中科院分区:
生物学4区
文献类型:
--
作者:
Yasui,K;Becker,EL;Sha'afi,RI

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脂多糖(LPS)与人血清结合,在没有第二刺激的情况下,引起与膜相关的鸟嘌呤核苷酸结合蛋白(gi2)的α -亚基(Giα2)的数量增加。脂多糖-血清复合体在趋化因子(meet - leu - phe)的刺激下,也启动人中性粒细胞产生O2−。添加血清因子对于低浓度LPS的启动是必不可少的。在血清存在的情况下,LPS浓度低至0.1 ng/ml时,可以观察到显著的增强作用。启动与剂量和时间有关。此外,观察到的lps -血清复合物的作用是不可逆的,因为它们不能通过洗涤来克服。抗CD14单克隆抗体抑制lps -血清复合物的直接和引物作用。另一方面,抗CD11b抗体和抗TNF-α抗体均不能抑制该复合物的作用。
Lipopolysaccharide (LPS) in combination with human serum, in the absence of a second stimulus, causes an increase in the amount of the α -subunit (Giα2) of the guanine nucleotide binding protein Gi2associated with the membrane. The LPS-serum complex also primes human neutrophils for O2−production in response to stimulation by the chemotactic factor fMet-Leu-Phe. Added serum factor is essential for priming at low concentrations of LPS. In the presence of serum, significant potentiation can be observed at LPS concentration as low as 0.1 ng/ml. The priming is dose and time dependent. Furthermore, the observed actions of the LPS-serum complex are not reversible since they cannot be overcome by washing. Monoclonal antibody against CD14 inhibits both the direct and priming actions of the LPS-serum complex. On the other hand, neither the antibody against CD11b nor the antibody against TNF-α inhibits the action of this complex.
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发表时间: 1990-09-21
期刊: SCIENCE
影响因子: 56.9
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