Updated project metadata. Misfolded or unfolded proteins from the endoplasmic reticulum (ER) are sent to proteasomal degradation via the Endoplasmic Reticulum Associated Degradation (ERAD) pathway. We provide here a proteomic analysis of the interaction partners for one of the ER mannosidases involved in ERAD, ER degradation-enhancing alpha-mannosidase-like protein 1 (EDEM1) and its mutant, a previously described version of EDEM, lacking its N-terminal disordered region (Δ-EDEM1). Moreover, we also performed a whole proteome analysis for cells overexpressing both, WT and Δ-EDEM1 and investigated the proteins which co-fractionate in a sucrose gradient for both EDEM1 and Δ-EDEM1 and their associated proteins.