MLL4 (KMT2D) is a major mammalian H3K4 mono- and di-methyltransferase that is essential for enhancer activation, cell-type-specific gene expression, and cell differentiation.
Changyu Zhu, Yadira M Soto-Feliciano ... Scott W Lowe
Epigenetic regulator MLL3 is mutated and lost in human hepatocellular carcinoma due to its ability to activate a well-defined tumor suppressor and cell death in transformed cells.
The HOXA9 reporter and genetic screens facilitated the functional interrogation of the HOXA9 regulome and advanced our understanding of the molecular regulation network in HOXA9-driven leukemia.
William F Richter, Rohan N Shah, Alexander J Ruthenburg
FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.
The H3K4 methyltransferase Setd1b is intrinsically required for hematopoietic stem and progenitor cell homeostasis and regulates lineage specification in mice.
Lena Tveriakhina, Karin Schuster-Gossler ... Achim Gossler
Regions outside the major receptor binding interface of DLL1 and DLL4 contribute to context-dependent divergence of ligand function in vivo and differential Notch1 and Notch2 activation in vitro.
Stanislao Igor Travisano, Vera Lucia Oliveira ... José Luis de la Pompa
Notch ligands Jag1 and Dll4 and their effector Ephb2 are required in sinus venosus endocardium for primitive coronary vasculature formation and later for arterial differentiation and maturation of coronary endothelium.
PASK phosphorylates Wdr5 to trigger epigenetic changes at lineage specifying promoters resulting in transcriptional derepression and differentiation of stem or progenitor cells.