Regulatory mechanism of PML body function by MORC3

PML-RARα融合蛋白引起急性早幼粒细胞白血病（APL）。PML蛋白在正常细胞中形成称为PML小体的核灶。然而，APL细胞中pml核体被破坏。我们关注MORC3作为APL药物靶点的定位机制，因为在APL细胞中，MORC3在pml核体上的定位也会被破坏。在这项研究中，我们发现MORC3通过两步分子机制与PML共定位。

The PML-RARα fusion proteins cause acute promyelocytic leukemia(APL). The PML proteins form nuclear foci called PML-body in normal cells. However, PML-nuclear body is disrupted in APL cells. We focus on the localization mechanisms of MORC3 as a drug target of APL because the localization of MORC3 on PML-nuclear body is also disrupted in APL cells. In this study, we show that MORC3 colocalizes with PML by a two-step molecular mechanism.