RIP links TLR4 to Akt and is essential for cell survival in response to LPS stimulation.
J Exp Med
; 200(3): 399-404, 2004 Aug 02.
Article
em En
| MEDLINE
| ID: mdl-15280422
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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Glicoproteínas de Membrana
/
Proteínas
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Lipopolissacarídeos
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Proteínas Proto-Oncogênicas
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Proteínas Serina-Treonina Quinases
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Receptores de Superfície Celular
Limite:
Animals
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
2004
Tipo de documento:
Article
País de afiliação:
Estados Unidos