Sahar Keshvari

This study shows that CEP55 promotes tumorigenesis in cancer models and its deletion suppresses tumor growth and improves survival, especially in PTEN-deficient cancers.

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 shows that CSF1R-dependent macrophages are essential for hematopoiesis but many functions of tissue resident macrophages are redundant or strain-specific in mice.

This study shows that myeloid HDAC7 promotes liver inflammation and glucose dysregulation in obesity, using mouse models and human data.

This paper tests whether perisurgical CSF1 treatment reduces liver I/R injury in rats by enhancing macrophage activity and liver regeneration.

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.

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.