Proteomic data from TMT based analysis of synapses biochemically isolated from Sfxn3-KO mice (http://www.mousephenotype.org/data/genes/MGI:2137679). See attached word/.txt description for further information. Briefly - Synapses are a primary pathological target in neurodegenerative diseases. Identifying therapeutic targets at the synapse could delay progression of numerous conditions. The mitochondrial protein SFXN3 is a neuronally-enriched protein expressed in synaptic terminals and regulated by key synaptic proteins, including alpha-synuclein (previously reported in Amorim et al., 2017 [PMID:28049726] and Graham et al., 2017 [PMID: 29078798]). Applying high-resolution proteomics to synapses biochemically isolated from Sfxn3-KO mice (http://www.mousephenotype.org/data/genes/MGI:2137679), we sought to identify what the molecular consequences of altered SFXN3 expression are in vivo. Analysis of the data contained within this submission suggest that Sfxn3 regulates proteins and pathways associated with neurodegeneration and cell death (including CSP alpha and caspase-3), as well as cascades altered in other neurological conditions (including Parkinson’s disease and Alzheimer’s disease).Attached are two documents describing the rational, methodology employed and confirming ethical approval are in place (1 x word and 1 x .txt). The data set comprises an xl file with multiple tabs: Tab 1 - Molecular tag identification numbers. Tab 2- Raw proteomic data Tab 3 - Filtered by number of unique peptides Tab 4 - Filtered by fold change Tab 5 - Molecules involved in Iron Homeostasis - derived from Ingenuity Pathway Analysis Tab 6 - Molecules involved in Iron Synthesis - derived from Ingenuity Pathway Analysis