Ran Chen

This study shows that MLL3 and MLL4 maintain hematopoietic stem cell multipotency by opposing a B-cell default state through distinct enhancer regulation mechanisms.

The paper shows fetal exposure to MLL::ENL creates a heritable leukemia-resistant state by altering hematopoietic progenitor behavior, which can be overcome by MLL3 inactivation or cooperating mutations.

The paper investigates the roles of canonical and alternative RPA in CAG repeat diseases, finding that Alt-RPA antagonizes RPA's suppression of CAG expansions, contributing to disease pathogenesis.