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 ubiquitin proteomic analysis on bone marrow cells from wild-type and Dcaf8 knockout mice. This analysis aimed to identify ubiquitinated proteins and assess changes in ubiquitination, providing insights into potential substrates of DCAF8 in murine hematopoietic cells.