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RIP将Toll样受体4（TLR4）与蛋白激酶B（Akt）连接起来，并且在应对脂多糖（LPS）刺激时对细胞存活至关重要。

RIP links TLR4 to Akt and is essential for cell survival in response to LPS stimulation.

作者信息

Vivarelli Marina S, McDonald Douglas, Miller Mendy, Cusson Nicole, Kelliher Michelle, Geha Raif S

机构信息

Division of Immunology, Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.

出版信息

J Exp Med. 2004 Aug 2;200(3):399-404. doi: 10.1084/jem.20040446. Epub 2004 Jul 26.

DOI:10.1084/jem.20040446
PMID:15280422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2211984/
Abstract

Receptor-interacting protein (RIP) has been reported to associate with tumor necrosis-associated factor (TRAF)2 and TRAF6. Since TRAF2 and TRAF6 play important roles in CD40 signaling and TRAF6 plays an important role in TLR4 signaling, we examined the role of RIP in signaling via CD40 and TLR4. Splenocytes from RIP(-/-) mice proliferated and underwent isotype switching normally in response to anti-CD40-IL-4 but completely failed to do so in response to LPS-IL-4. However, they normally up-regulated TNF-alpha and IL-6 gene expression and CD54 and CD86 surface expression after LPS stimulation. RIP(-/-) splenocytes exhibited increased apoptosis and impaired Akt phosphorylation after LPS stimulation. These results suggest that RIP is essential for cell survival after TLR4 signaling and links TLR4 to the phosphatidylinositol 3 kinase-Akt pathway.

摘要

据报道，受体相互作用蛋白（RIP）与肿瘤坏死相关因子（TRAF）2和TRAF6相关联。由于TRAF2和TRAF6在CD40信号传导中起重要作用，且TRAF6在TLR4信号传导中起重要作用，因此我们研究了RIP在通过CD40和TLR4进行信号传导中的作用。来自RIP（-/-）小鼠的脾细胞在抗CD40-IL-4刺激下正常增殖并发生同种型转换，但在LPS-IL-4刺激下则完全无法进行。然而，在LPS刺激后，它们通常会上调TNF-α和IL-6基因表达以及CD54和CD86表面表达。LPS刺激后，RIP（-/-）脾细胞表现出凋亡增加和Akt磷酸化受损。这些结果表明，RIP对于TLR4信号传导后的细胞存活至关重要，并将TLR4与磷脂酰肌醇3激酶-Akt途径联系起来。

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Mechanisms of the TRIF-induced interferon-stimulated response element and NF-kappaB activation and apoptosis pathways.
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