HTLV-1 Tax protein recruitment into IKKε and TBK1 kinase complexes enhances IFN-I expression.
Virology
; 476: 92-99, 2015 Feb.
Article
em En
| MEDLINE
| ID: mdl-25531185
ABSTRACT
The Tax protein expressed by human T-cell leukemia virus type 1 (HTLV-1) plays a pivotal role in the deregulation of cellular pathways involved in the immune response, inflammation, cell survival, and cancer. Many of these effects derive from Tax multiple interactions with host factors, including the subunits of the IKK-complex that are required for NF-κB activation. IKKÉ and TBK1 are two IKK-related kinases that allow the phosphorylation of interferon regulatory factors that trigger IFN type I gene expression. We observed that IKKÉ and TBK1 recruit Tax into cellular immunocomplexes. We also found that TRAF3, which regulates cell receptor signaling effectors, forms complexes with Tax. Transactivation analyses revealed that expression of Tax, in presence of IKKÉ and TBK1, enhances IFN-ß promoter activity, whereas the activation of NF-κB promoter is not modified. We propose that Tax may be recruited into the TBK1/IKKÉ complexes as a scaffolding-adaptor protein that enhances IFN-I gene expression.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vírus Linfotrópico T Tipo 1 Humano
/
Infecções por HTLV-I
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Produtos do Gene tax
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Interferon beta
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Proteínas Serina-Treonina Quinases
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Quinase I-kappa B
Limite:
Humans
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article