{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Lei Fang"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0018766000"],"submitter_email":["njfanglei@nju.edu.cn"],"submitter_affiliation":["Nanjing University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"iTraq proteomics of SARM1-OE/HEK293 cells","description":"SARM1 (sterile alpha and Toll/interleukin-1 receptor motif-containing protein 1) is an inducible NAD-consuming enzyme that drives axon degeneration and a form of non-apoptotic cell death termed sarmoptosis. Using SARM1-overexpressing HEK293 cells, we previously showed that the cell-permeant NMN mimetic CZ-48 activates SARM1, depletes cellular NAD and ATP, and induces regulated, propidium iodide (PI)-positive, non-apoptotic cell death that is potently suppressed by the HSP70-family ATP-competitive inhibitor VER-155008 (VER). To investigate the proteome-wide changes underlying CZ-48-induced SARM1 activation and VER-mediated rescue, we performed iTRAQ-based quantitative proteomics on SARM1-overexpressing HEK293 cells treated with vehicle control, 20 μM VER alone, 100 μM CZ-48 alone, or CZ-48 plus VER for 16 h, with biological replicates per group. This dataset was used to identify CZ-48-responsive proteins whose abundance changes were reversed by VER co-treatment, focusing on HSP70/chaperone-related proteostasis proteins, mitochondrial and metabolic proteins, and cell-death-related proteins, in order to elucidate mechanisms of SARM1-driven ATP collapse and mitochondrial dysfunction during sarmoptosis.","dates":{"publication":"Sat Aug 01 00:00:00 GMT+01:00 2026"},"accession":"PXD082054","cross_references":{"TAXONOMY":["9606"]}}