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Intrinsic Cellular Defenses against Virus Infection by Antiviral Type I Interferon
Yonsei Medical Journal ; : 9-17, 2010.
Artículo en Inglés | WPRIM | ID: wpr-39516
ABSTRACT
Intrinsic cellular defenses are non-specific antiviral activities by recognizing pathogen-associated molecular patterns (PAMPs). Toll-like receptors (TLRs), one of the pathogen recognize receptor (PRR), sense various microbial ligands. Especially, TLR2, TLR3, TLR4, TLR7, TLR8 and TLR9 recognize viral ligands such as glycoprotein, single- or double-stranded RNA and CpG nucleotides. The binding of viral ligands to TLRs transmits its signal to Toll/interleukin-1 receptor (TIR) to activate transcription factors via signal transduction pathway. Through activation of transcription factors, such as interferon regulatory factor-3, 5, and 7 (IRF-3, 5, 7) or nuclear factor-kappaB (NF-kappaB), type I interferons are induced, and antiviral proteins such as myxovirus-resistance protein (Mx) GTPase, RNA-dependent Protein Kinase (PKR), ribonuclease L (RNase L), Oligo-adenylate Synthetase (OAS) and Interferon Stimulated Gene (ISG) are further expressed. These antiviral proteins play an important role of antiviral resistancy against several viral pathogens in infected cells and further activate innate immune responses.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Virosis / Interferón Tipo I / FN-kappa B / Proteínas de Unión al GTP / EIF-2 Quinasa / Factores Reguladores del Interferón / Receptores Toll-Like / Modelos Biológicos Tipo de estudio: Estudio pronóstico Límite: Animales / Humanos Idioma: Inglés Revista: Yonsei Medical Journal Año: 2010 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Virosis / Interferón Tipo I / FN-kappa B / Proteínas de Unión al GTP / EIF-2 Quinasa / Factores Reguladores del Interferón / Receptores Toll-Like / Modelos Biológicos Tipo de estudio: Estudio pronóstico Límite: Animales / Humanos Idioma: Inglés Revista: Yonsei Medical Journal Año: 2010 Tipo del documento: Artículo