Proteomic analysis of Lineage negative bone marrow cells from wild-type and Dcaf8 knockout mice

To explore the mechanisms by which DCAF8 deficiency induces functional defects in hematopoietic stem cells with an aging-like phenotype, and given DCAF8’s role as a substrate receptor in the E3 ubiquitin ligase complex, we conducted proteomic analysis on Lineage negative bone marrow cells from wild-type and Dcaf8 knockout mice. This analysis aimed to identify protein alterations, providing insights into potential substrates of DCAF8 in murine hematopoietic cells.