【摘 要】
：
To date, the biological function of FAM3A, the first member of FAM3 gene family, remains unknown.The current study aimed to investigate whether the expression of FAM3A in liver cells is regulated by n
【机 构】
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Department of Physiology and Pathophysiology,Peking University Health Science Center Beijing,China
【出 处】
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International Conference for Physiological Sciences 2012(201
论文部分内容阅读
To date, the biological function of FAM3A, the first member of FAM3 gene family, remains unknown.The current study aimed to investigate whether the expression of FAM3A in liver cells is regulated by nuclear receptor peroxisome proliferator activated receptors (PPARγs).In HepG2 cells, PPARγ agonists induced FAM3A expression, which was repressed by PPARγantagonist T007090.PPARγ overexpression also upregulated FAM3A expression.In contrast, agonists of PPARα and PPARβ failed to affect FAM3A expression.Rosiglitazone also induced FAM3A expression in primary cultured mouse hepatocytes.The activities of both the human and mouse FAM3A promoter luciferase reporters were significantly stimulated by PPARγ activation, but not by PPARα and PPARβ activation.Chromatin immunoprecipitation assay revealed a direct binding of PPARγ to the PPRE-1-ike site (-1258 to-1246) in the human FAM3A promoter.Mutation of this PPRE-like motif abolished PPARγs stimulation on the activity of human FAM3A promoter.In vivo, oral rosiglitazone treatment upregulated FAM3A expression in the liver of C57BL/6 mice and db/db mice.Notably, upregulation of FAM3A by PPARγ activation was associated with Akt acitvation in liver cells.In conclusion, FAM3A is a novel target gene of PPARγ.Upregulation of FAM3A by PPARy was associated with Akt activation in liver cells.
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