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1.
PLoS One ; 7(7): e41092, 2012.
Artículo en Inglés | MEDLINE | ID: mdl-22844427

RESUMEN

Interferon (IFN)-induced Janus kinase (Jak)/signal transducer and activator of transcription (Stat) pathway is important in controlling immune responses and is negatively response-regulated by the suppressor of cytokine signaling (SOCS) proteins. However, several viruses have developed various strategies to inhibit this pathway to circumvent the anti-viral immunity of the host. The infectious spleen and kidney necrosis virus (ISKNV) is the type species of the genus Megalocytivirus in the family Iridoviridae and a causative agent of epizootics in fish. ISKNV ORF103R encodes a predicted viral SOCS (vSOCS) with high homology to the vertebrate SOCS1, but lacks a SOCS-box domain. Interestingly, vSOCS only exists in the genus Megalocytivirus. ISKNV-vSOCS can block the IFN-α-induced Jak/Stat pathway in HepG2 cells. Over-expression of ISKNV-vSOCS inhibited the activities of IFN-stimulated response element (ISRE) promoter; however, the inhibitions by ISKNV-vSOCS were dose-dependent. ISKNV-vSOCS interacted with Jak1 protein and inhibited its tyrosine kinase activity in vitro. ISKNV-vSOCS also impaired the phosphorylation of Stat1 and Stat3 proteins and suppressed their activations. The point mutations (F18D, S66A, S85A, and R64K) of ISKNV-vSOCS significantly impaired the inhibition of IFN-α-induced ISRE-promoter activation. In conclusion, vSOCS inhibits IFN-α-induced Stat1/Stat3 signaling, suggesting that Megalocytivirus has developed a novel strategy to evade IFN anti-viral immunity via vSOCS protein.


Asunto(s)
Interferón-alfa/farmacología , Janus Quinasa 1/metabolismo , Riñón/virología , Factores de Transcripción STAT/metabolismo , Proteínas Supresoras de la Señalización de Citocinas/metabolismo , Virus de la Necrosis Esplénica del Pato de Trager , Proteínas Virales/metabolismo , Secuencia de Aminoácidos , Animales , Biología Computacional , Genes Reporteros/genética , Células Hep G2 , Humanos , Ratones , Datos de Secuencia Molecular , Fosforilación/efectos de los fármacos , Mutación Puntual , Unión Proteica , Factor de Transcripción STAT1/metabolismo , Factor de Transcripción STAT3/metabolismo , Transducción de Señal/efectos de los fármacos , Proteínas Supresoras de la Señalización de Citocinas/química , Proteínas Supresoras de la Señalización de Citocinas/genética , Proteínas Virales/química , Proteínas Virales/genética
2.
Vet Immunol Immunopathol ; 139(1): 61-6, 2011 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-20817314

RESUMEN

The IκB kinase ß (IKKß) plays crucial roles in regulating activation of nuclear factor-kappa B (NF-κB) in response to proinflammatory factors and microbial and viral infections. Here, we report the cloning of an IKKß cDNA (named SicIKKß) from the mandarin fish Siniperca chuatsi. The full-length cDNA is 4052bp and contains an ORF that encodes a predicted protein of 743-amino acid residues. The deduced amino acid sequence of SicIKKß has the same domain organization as human IKKß, which consists of a serine/threonine kinase domain, a leucine zipper motif and a putative helix-loop-helix motif. Quantitative RT-PCR showed that SicIKKß was ubiquitously expressed in tissues of mandarin fish, and its expression in mandarin fish fry (MFF-1) cells was up-regulated during the course of ISKNV infection.


Asunto(s)
Infecciones por Virus ADN/veterinaria , Enfermedades de los Peces/enzimología , Quinasa I-kappa B/genética , Perciformes/inmunología , Animales , Clonación Molecular , Infecciones por Virus ADN/enzimología , Infecciones por Virus ADN/genética , Infecciones por Virus ADN/inmunología , Enfermedades de los Peces/genética , Enfermedades de los Peces/inmunología , Iridoviridae/inmunología , FN-kappa B/metabolismo , Perciformes/genética , Perciformes/metabolismo , Filogenia , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/veterinaria , Análisis de Secuencia de ADN/veterinaria , Regulación hacia Arriba
3.
Fish Shellfish Immunol ; 27(2): 349-59, 2009 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-19539032

RESUMEN

The JAK/STAT signal transduction pathway plays a critical role in host defence against viral and bacterial infections. In the present study, we report cDNA cloning and characterization of the JAK family (mJAK1-3 and mTYK2) and STAT family members (mSTAT1, mSTAT3-6) from the mandarin fish Siniperca chuatsi. To our knowledge, JAK2, TYK2 and STAT6 genes were cloned from fish for the first time. The mJAK family proteins consist of 1112-1177 residues with a FERM domain, an SH2 domain, a pseudokinase domain, and a tyrosine kinase domain. The mSTAT family members contain 716-786 residues with similar architecture, including an N-terminal domain, a coiled coil domain, a DNA binding domain, a linker domain, an SH2 domain, and a transcription activation domain. Multiple sequence alignments of mJAKs/mSTATs and phylogenetic analysis showed that mJAK1 was closed to mTYK2, and mJAK2 was closed to mJAK3. Quantitative real-time PCR results revealed that mJAK/mSTAT family members were expressed in most tissues examined except muscle. In mandarin fish fry cells, the expressions of IRF-1, Mx, SOCS1 and SOCS3 genes were significantly induced by poly(I:C) stimulation, indicating that the mJAK/mSTAT signal pathway is activated by poly(I:C). Furthermore, expressions of all four mJAKs and four mSTATs were all up-regulated after poly(I:C) stimulation, but expression of mSTAT5 was inhibited by poly(I:C). These results suggest that mandarin fish has the JAK/STAT signal transduction pathways similar to those in mammals, and these signalling pathways may play an important role in regulation of antiviral responses in fish.


Asunto(s)
Regulación de la Expresión Génica , Quinasas Janus/genética , Quinasas Janus/inmunología , Perciformes/genética , Perciformes/inmunología , Factores de Transcripción STAT/genética , Factores de Transcripción STAT/inmunología , Adyuvantes Inmunológicos/farmacología , Secuencia de Aminoácidos , Animales , Clonación Molecular , Perfilación de la Expresión Génica , Regulación de la Expresión Génica/efectos de los fármacos , Janus Quinasa 2/genética , Janus Quinasa 2/inmunología , Quinasas Janus/química , Datos de Secuencia Molecular , Filogenia , Poli I-C/farmacología , Factores de Transcripción STAT/química , Factor de Transcripción STAT6/genética , Factor de Transcripción STAT6/inmunología , Alineación de Secuencia , Transducción de Señal/efectos de los fármacos , TYK2 Quinasa/genética , TYK2 Quinasa/inmunología
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