Nofar Mor

Patient-derived neuronal models and mouse models reveal that truncated ASXL3 drive epigenetic dysregulation through a gain-of-function mechanism.

The paper shows ASXL3 truncating variants cause disease via gain-of-function, not loss-of-function, and demonstrates antisense oligonucleotides can reverse the transcriptional effects.

This study identifies signaling pathways that enable the expansion of human naive pluripotent stem cells in defined conditions and highlights differences between mouse and human naive pluripotency.

The paper investigates functional compensation among Ythdf m6A readers in mouse gametogenesis and embryonic stem cells, revealing dosage-dependent redundancy and distinct roles.

This study identifies the Gatad2a-Chd4-Mbd3 subcomplex of the NuRD complex as a key inhibitor of naive pluripotency, showing that its disruption enables deterministic reprogramming of somatic cells to iPSCs.

This paper maps high-resolution epigenetic and biosynthetic changes during reprogramming of fibroblasts to iPSCs, identifying two gene modules regulated by different mechanisms.