I coordinated research efforts in Proteomics of human lysosomal storage disorders (LSD's), including implementation of ICAT-like techniques. I optimized the in gel digestion protocol and colloidal Coomassie staining to get routine identification at very low protein abundancies. I collaborated with many different groups (in and outside of the AMC) in Proteomic studies. In the context of my own research (a.o. Proteomics of HIV-Tcell interaction), I initiated the reproducible large scale DIGE approach in our lab (together with Jeffrey Ringrose and Rienk Jeeninga) and used this to monitor changes in cellular proteins induced by HIV-1 infection. In several collaborations I analysed changes in protein PTM's, identified several biologically important proteins, tested peptidomimetics for biological activities and was involved in immunologcal work. Lately, I have published several theoretical articles regarding the mitochondrial respiratory chain, genome architecture and (eukaryotic) evolution. I am also trying to start research to monitor oxidative damage of proteins, comparing conditions under which most energy is either derived from Fatty Acid or from Glucose breakdown, to test an hypothesis I first formulated in BioEssays 33, pp. 88-94. Last but not least, I have been extending this hypothesis, which might explain the evolution of peroxisomes and the absence of Fatty Acid oxidation in neurons, in several further publications focussing on the source of electrons entering the mitochondrial respiratory chain via NADH (complex I) or FADH₂ (linked to several different complexes) and the resulting differences in ROS (reactive oxygen species) formation. I am currently collaborating with Antoine van Kampen (Medische Bioinformatica) to model these processes mathematically.