A Crosstalk Between Inflammation and Epigenetics in Regulating HSC Fitness

造血干细胞(HSC)的功能取决于静止和激活之间有限的可逆平衡。终止激活和重新进入休眠所需的细胞内在机制的识别，以及介导这一转变的信号通路，仍然是尚未解决的关键问题。基于我们的数据，我们提出，通过在MYD88或SETD2降解中起作用的E3泛素连接酶斑点类型POZ蛋白(SPOP)的核质穿梭，“炎症和表观遗传学之间的串扰控制HSC的适合性”。

The functionality of hematopoietic stem cell (HSC) compartment hinges on the limited reversible balance between quiescence and activation. The identity of cell-intrinsic mechanisms required to terminate activation and re-enter dormancy, and the signaling pathways that mediate this transition, remain unresolved key questions. Based on our data, we propose that “A crosstalk between inflammation and epigenetics controls HSC fitness” through nucleocytoplasmic shuttling of an E3 ubiquitin ligase Speckle-type POZ protein (SPOP) functioning in MYD88 or SETD2 degradation.