The ubiquitin ligase c-Cbl preferentially targets unique-region phosphorylated LynA for rapid degradation, regulating its expression and differentially tuning signaling responsiveness in macrophages and mast cells.
In the pancreas, reciprocal interactions between epithelial cells and myeloid cells determine the balance between tissue repair and carcinogenesis by regulating acinar cell plasticity through differential activation of EGFR/MAPK signaling.
Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.
Age-specific transcriptional responses to Flt3-ITD and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult, but not fetal/neonatal, stages of development.
A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.
The signaling lipid PI(3,5)P2 supports the formation of the myelin sheath, by regulating trafficking of myelin building blocks within oligodendrocytes and communication between oligodendrocytes and neuronal axons.