Study on mechanisms of the expression regulation of interferon-induced gene RIG-G / 中华医学遗传学杂志
Chinese Journal of Medical Genetics
;
(6): 625-628, 2007.
Artigo
em Chinês
| WPRIM
| ID: wpr-229857
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the molecular mechanisms of the expression regulation of retinoic acidinduced gene G (RIG-G) by interferon alpha (IFNalpha).</p><p><b>METHODS</b>RIG-G promoter region was analyzed by bioinformatics. The functional activities of RIG-G promoter with or without IFNalpha were detected by luciferase reporter assay and electrophoretic mobility shift assay (EMSA).</p><p><b>RESULTS</b>RIG-G promoter region contained two well-conserved IFN-stimulated response elements (ISREs). Both ISRE I and ISRE II showed their effective binding abilities with signal transducer and activator of transcription 1 (STAT1). In HT1080 cells, in contrast with the empty plasmid pXP2, pXP2-A reporter construct containing intact ISRE I and ISRE II showed a significant higher baseline expression (1741.2 +/- 517.5) which could be further enhanced up to three-four folds by IFNalpha (5338.7 +/- 1226.9, P < 0.05). However, the luciferase activity of pXP2-A as well as its IFNalpha inducibility could be abrogated in STAT1-deficient U3A cells (from 1741.2 +/- 517.5 to 406.1 +/- 103.2, P < 0.05), indicating that the STAT1 protein was a prerequisite for the activities of ISRE I and ISRE II.</p><p><b>CONCLUSION</b>ISREs present in RIG-G promoter region are molecular basis of IFNalpha induced RIG-G expression. RIG-G is a target gene directly regulated by STAT1 protein and should play a key role in IFNalpha signaling pathways.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Fisiologia
/
Dados de Sequência Molecular
/
Sequência de Bases
/
Células Cultivadas
/
Regulação da Expressão Gênica
/
Interferons
/
Regiões Promotoras Genéticas
/
Interferon-alfa
/
Fator de Transcrição STAT1
Limite:
Humanos
Idioma:
Chinês
Revista:
Chinese Journal of Medical Genetics
Ano de publicação:
2007
Tipo de documento:
Artigo
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