机译:通过靶向组蛋白甲基转移酶Suv39h1,增强糖尿病db / db小鼠血管平滑肌细胞中microRNA-125b的水平,导致炎症基因表达增加。
From the Department of Diabetes, Beckman Research Institute of City of Hope, Duarte, California.Corresponding author: Rama Natarajan, RNatarajan@coh.org.Received 10 February 2010 and accepted 13 July 2010. Published ahead of print at http://diabetes.diabetesiiounials.org on 10 August 2010, DOL 10.2337^10-0208.© 2010 by the American Diabetes Association, Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommon5.org/liceiises/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in pan by tiie payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.;
机译:通过靶向组蛋白甲基转移酶Suv39h1,增强糖尿病db / db小鼠血管平滑肌细胞中microRNA-125b的水平,导致炎症基因表达增加。
机译:源自糖尿病db / db小鼠的巨噬细胞和血管平滑肌细胞中增强的促动脉粥样硬化反应。
机译:糖尿病DB / DB小鼠中内皮和平滑肌细胞中的胰高血糖素样肽1受体表达:TCF7L2是血管胰高血糖素样肽1受体的可能调节剂
机译:流体剪切应力和机械应变对血管平滑肌细胞基因表达的调控
机译:Leiomodin1,一种新型SRF / MYOCD靶基因,优先在血管平滑肌细胞中表达。
机译:通过靶向组蛋白甲基转移酶Suv39h1增强糖尿病db / db小鼠血管平滑肌细胞中microRNA-125b的水平导致炎症基因表达增加。
机译:通过靶向组蛋白甲基转移酶Suv39h1,增强糖尿病db / db小鼠血管平滑肌细胞中microRNA-125b的水平,导致炎症基因表达增加。