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Mechanism of RUNX1 targeted AKT3 regulated alveolar procoagulant fibrinolytic inhibition in ARDS

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Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury and one of the serious life-threatening forms of respiratory failure. Alveolar procoagulation and fibrinolytic inhibition constitute the core part of the pathophysiology of ARDS, RUNX1 plays an important role in this pathogenesis. We screened for AKT3, the target gene of RUNX1, using CHIP-seq and verified its binding target by a dual luciferase assay.

急性呼吸窘迫综合征(ARDS)属于急性炎症性肺损伤,亦是一类危及生命的重症呼吸衰竭类型。肺泡促凝与纤溶抑制是ARDS病理生理过程的核心环节,RUNX1在该发病机制中发挥重要作用。本研究通过染色质免疫沉淀测序(CHIP-seq)筛选得到RUNX1的靶基因AKT3,并借助双荧光素酶报告基因检测验证了其结合靶点。

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