Your browser doesn't support javascript.
loading
Role of the interferon-stimulated response elements I/II in expression regulation of the retinoic acid induced gene G / 中华医学遗传学杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-349002
Responsible library: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the regulatory role of interferon-stimulated response elements (ISREs) located on the retinoic acid-induced gene G (RIG-G) promoter in RIG-G expression.</p><p><b>METHODS</b>By using point mutation technique, the authors constructed the wide type and site mutant reporter gene plasmids according to the ISRE sequence on RIG-G promoter, and detected the functional activities by luciferase reporter assay.</p><p><b>RESULTS</b>Mutation in ISRE II alone had no obvious effect on the expression of the reporter gene, whereas mutation in ISRE I dramatically inhibited the transactivity of RIG-G promoter. Mutation in both ISRE I and ISRE II resulted in complete loss of its response to the transcription factors for the reporter gene.</p><p><b>CONCLUSION</b>Both ISRE I and ISRE II on the RIG-G promoter are the binding sites for the complex of transcription factors. They are required for RIG-G expression, and ISRE I has a preferential role over ISRE II.</p>
Subject(s)
Full text: Available Database: WPRIM (Western Pacific) Main subject: Interferons / Promoter Regions, Genetic / Response Elements / Cell Line, Tumor / Intracellular Signaling Peptides and Proteins / STAT2 Transcription Factor / Interferon Regulatory Factor-1 / Genetics / Metabolism / Mutation Limits: Humans Language: Chinese Journal: Chinese Journal of Medical Genetics Year: 2010 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Main subject: Interferons / Promoter Regions, Genetic / Response Elements / Cell Line, Tumor / Intracellular Signaling Peptides and Proteins / STAT2 Transcription Factor / Interferon Regulatory Factor-1 / Genetics / Metabolism / Mutation Limits: Humans Language: Chinese Journal: Chinese Journal of Medical Genetics Year: 2010 Document type: Article
...