Yang H, et al. (2022) TNFα-induced IDH1 hyperacetylation reprograms redox homeostasis and promotes the chemotherapeutic sensitivity. Oncogene 36352097

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K115-ac - IDH1 (human) ▲

Modsite: FREAIICkNIPRLVS SwissProt Entrez-Gene Orthologous residues IDH1 (human): K115‑ac, IDH1 (mouse): K115‑ac, IDH1 (rat): K115‑ac Characterization Methods used to characterize site in vivo:  immunoassay, immunoprecipitation, modification-specific antibody, mutation of modification site, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  colon, HCT116 (intestinal), HCT8 (intestinal), SW480 (intestinal) Cellular systems studied:  cell lines, tissue Species studied:  human, mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes DEACETYLASE SIRT1 (human) transfection of wild-type enzyme, co-immunoprecipitation, pharmacological inhibitor of upstream enzyme, microscopy-colocalization Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes TNF increase nicotinamide increase Necrostatin-1 decrease Z-IETD-fmk decrease selisistat increase SRT2104 decrease selisistat increase Downstream Regulation Effect of modification (function):  intracellular localization, protein degradation, ubiquitination Effect of modification (process):  apoptosis, induced, carcinogenesis, inhibited, cell growth, inhibited Associated Diseases Diseases Alterations Comments colorectal cancer decreased