Omkar L. Patkar

This study shows that mice with a germ-line deletion of a Csf1r enhancer lack specific macrophages but maintain normal physiology and can be replenished by donor cells.

This study examines the effects of a loss-of-function mutation in the rat Il34 gene on macrophage development, homeostasis, and inflammation in both the brain and periphery.

This study shows that wild-type bone marrow cells can restore macrophage populations and reverse developmental defects in Csf1rko rats, but not in the brain.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.

This study shows that Csf1r mutation in mice, rats, and humans causes developmental defects, and bone marrow transfer can reverse some phenotypes by restoring macrophages.