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Protein-based virtual screening: SIRT-1 as modulator maturation of circulating endothelial progenitor cells

机译:基于蛋白质的虚拟筛选:SIRT-1作为循环内皮祖细胞的调节剂成熟

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Circulating endothelial progenitor cells (cEPCs) are having involvement in the replacing vascular endothelial cells damaged or detachment from the basement membrane. cEPC needs to fulfill both quantity and quality requirements in order to play this important role. After efflux from bone marrow to circulation, niche EPC necessary of maturation to reach the potential for re-endothelialization. Risk factors exposure for cardiovascular disease not only affect the quantity and quality of cEPC, but it is also to be involved in downregulation of SIRT1. SIRT1 downregulation is mostly associated with the mechanism of senescence. Objective. to predict the direction of SIRT-1 interaction with cEPC maturation that is validated with cEPC marker surface using the STRING DB method of protein interaction. Result. SIRT1 interacts with two proteins, inhibiting VEGFA and activating and inhibiting P53. P53 inhibits the expression of p16ink4a, a protein involved in cellular senessence and P53 through AKT involved in CD 309 and ITGA2B expression. Whereas there was a direct interaction of the expression of CD 309 through the VEGFA line; CD117; TIE-2; CD 144; CD62a. Conclusion. SIRT-1 is an intracellular protein that is involved in cellular anti-aging processes but is not directly involved in the expression of EPC marker surfaces.
机译:循环内皮祖细胞(Cepcs)涉及替代血管内皮细胞的血管内皮细胞受损或从基底膜脱离的脱离。 CEPC需要满足数量和质量要求,以便发挥这种重要作用。在从骨髓流出到循环后,利基EPC成熟必要的,以达到重新内皮化的潜力。心血管疾病的风险因素不仅影响CEPC的数量和质量,而且还涉及SIRT1的下调。 SIRT1下调主要与衰老机制相关。客观的。预测使用CEPC标记表面验证的CEPC成熟的SIRT-1的方向,使用蛋白质相互作用的串联DB方法验证。结果。 SIRT1与两种蛋白质相互作用,抑制VEGFA并激活和抑制P53。 P53抑制P16ink4a的表达,涉及CD 309和ITGA2B表达中涉及蜂窝壮大的蛋白质和P53的蛋白质。而CD 309的表达通过VEGFA线的直接相互作用; CD117; TIE-2; CD 144; CD62A。结论。 SIRT-1是参与细胞抗衰老过程的细胞内蛋白质,但不直接参与EPC标记表面的表达。

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