研究人员发现，生物体对饥饿或寒冷环境的成功适应取决于一个名为E2F1的蛋白质，新成果发表在8月在线出版的《自然—细胞生物学》期刊上。新发现指出了一种重要方法，表明当被暴露在压力环境中时，细胞能够在分子水平上应付处理。
Lluis Fajas和同事发现，缺失E2F1蛋白质的小鼠不太能适应因运动导致的疲劳，在禁食或寒冷的环境中保持了更高的体温。
这些结果表明E2F1蛋白质调控了身体内的新陈代谢。Fajas等发现，E2F1蛋白质的缺失增加了对氧化代谢有重要意义的基因的表达，显示E2F1蛋白质的正常功能抑制了这种类型的新陈代谢。
Fajas等分析了E2F1蛋白质的功能如何被整合到细胞周期进程中。新发现支持了E2F1蛋白质在细胞繁殖和代谢相互关系中的关键地位。
生物探索推荐英文论文摘要：
E2F transcription factor-1 regulates oxidative metabolism
Cells respond to stress by coordinating proliferative and metabolic pathways. Starvation restricts cell proliferative (glycolytic) and activates energy productive (oxidative) pathways. Conversely, cell growth and proliferation require increased glycolytic and decreased oxidative metabolism levels. E2F transcription factors regulate both proliferative and metabolic genes. E2Fs have been implicated in the G1/S cell-cycle transition, DNA repair, apoptosis, development and differentiation. In pancreatic β-cells, E2F1 gene regulation facilitated glucose-stimulated insulin secretion. Moreover, mice lacking E2F1 (E2f1−/−) were resistant to diet-induced obesity. Here, we show that E2F1 coordinates cellular responses by acting as a regulatory switch between cell proliferation and metabolism. In basal conditions, E2F1 repressed key genes that regulate energy homeostasis and mitochondrial functions in muscle and brown adipose tissue. Consequently, E2f1−/−mice had a marked oxidative phenotype. An association between E2F1 and pRB was required for repression of genes implicated in oxidative metabolism. This repression was alleviated in a constitutively active CDK4 (CDK4R24C) mouse model or when adaptation to energy demand was required. Thus, E2F1 represents a metabolic switch from oxidative to glycolytic metabolism that responds to stressful conditions.
