It was unclear how AP3M1 abundance is controlled within the AP-3 complex; proteomic analysis with experimental confirmation showed AP3B1 is a rate-limiting assembly factor whose loss reduces AP3M1 levels, establishing that AP3M1 stoichiometry is co-regulated by AP3B1.
Evidence Proteomics across CPTAC/TCGA datasets combined with experimental confirmation of the AP3B1–AP3M1 interaction and co-regulation
- Specific orthogonal methods confirming the interaction are not detailed
- Cargo selectivity and vesicle-trafficking function of AP3M1 not addressed
- Subcellular localization of AP3M1 not established in this finding