Anwesha Dey

TL;DR: It is shown that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS), and Knockin mice expressing B AP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor–1, O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL

TL;DR: The Hippo pathway is an evolutionarily conserved signalling pathway with key roles in organ development, epithelial homeostasis, tissue regeneration, wound healing and immune modulation, and is an attractive target for therapeutic intervention.

TL;DR: Loss of Asxl1 results in myelodysplastic syndrome, whereas concomitant deletion of Tet2 restores HSC self-renewal and triggers a more severe disease phenotype distinct from that seen in single-gene knockout mice.

TL;DR: The Hippo pathway remains a central focus in both basic and translational research and is a key modulator of developmental biology and there are multiple efforts to target key components of the pathway for disease intervention.

TL;DR: It is shown that human TEADs are palmitoylated at a universally conserved cysteine, and it is demonstrated that this modification is required for proper TEAD folding and stability, indicating a potential new avenue for pharmacologically regulating the Hippo pathway through the modulation of TEADPalmitoylation.