A study for an essential metabolic shift in glycolytic pathway observed during the transition from cellular senescence to carcinogenesis

最近，应激诱导的衰老被认为是防止致癌的屏障。我们先前克隆了磷酸甘油变位酶(PGM)的cDNAs，作为衰老旁路克隆。我们解决了为什么以及如何增强糖酵解可以影响细胞衰老的问题。我们计划阐明PGM的调控和生理影响的分子机制。在这些尝试中，我们克隆了一个PGM结合蛋白作为一种新的泛素连接酶，称为UBLX1。并建立了PGM转基因小鼠模型。

Stress-induced senescence is recently thought to be a barrier against carcinogensis. We previously cloned the phosphoglycerate mutase (PGM) cDNA as senescence bypassing clone. We addressed the question why and how enhanced glycolysis could affect cellular senescence. We planned to clarify the molecular mechanism of regulation and physiological impact of PGM. During these attempt, we cloned a PGM binding protein as a novel ubiquitin ligase, called UBLX1. Also we established PGM transgenic mice model.