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Yusuke Kawashima

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Open access Jul 2026

Enrichment-free deep proteomics enables proteome-scale analysis of methionine oxidation

Abstract Advances in mass spectrometry (MS)-based proteomics have enabled the large-scale characterization of posttranslational modifications (PTMs) through affinity-based enrichment. However, this technique introduces a bias towards selectively enrichable modifications, thus leaving oxidative modifications underexplored. Methionine oxidation (methionine sulfoxide) is an important indicator of cellular redox status, but its systematic analysis remains challenging because no enrichment method is available and artifactual oxidation can occur during sample preparation. Here, we developed an enrichment-free proteomic strategy for large-scale detection of methionine oxidation using a deep LC-MS platform. By optimizing acquisition conditions, we identified more than 260k precursors in a single-shot analysis. Under these conditions, methionine oxidation was efficiently detected, whereas many other PTMs remained poorly detected. To improve data reliability, we established a sample preparation workflow that minimized artifactual oxidation. Accordingly, we identified more than 3,500 methionine-oxidized proteins. Integration of methionine oxidation and expression proteomics across subcellular compartments revealed redox patterns under low-serum conditions, including increased mitochondrial oxidation and decreased endoplasmic reticulum oxidation. These changes are associated with metabolic reprogramming and altered antioxidant capacity. Overall, this study established an enrichment-free framework for the proteome-scale methionine oxidation analysis, and demonstrated that integrating oxidation and expression data enables the spatially resolved interpretation of cellular redox states.

Hiromasa Mitsui, Yusei Okuda, R. Konno et al. · DNA Research · 0 citations

Open access Aug 2026

Disruption of de novo fatty acid biosynthesis rewires cellular lipid metabolism toward mTOR-associated compensatory fatty acid uptake

Upon antigen stimulation, naïve CD4⁺ T cells undergo rapid metabolic remodeling that supports immune responses. Lipid metabolism has emerged as a critical regulator of T-cell proliferation, effector function, and memory formation, and has been proposed as a potential therapeutic target in immune-related diseases. However, how T cells adapt to perturbation in lipid metabolism remains unclear. To address this question, we performed integrative multi-omics analyses in EL4 T cells, including transcriptomics, proteomics, phosphoproteomics, and lipidomics, to investigate metabolic adaptation under conditions of impaired fatty acid biosynthesis. In EL4 T cells, disruption of acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid biosynthesis, reduced lipid droplet abundance and enhanced fatty acid uptake. Transcriptomic and proteomic analyses revealed upregulation of fatty acid transporters such as CD36 and SLC27A4, and functional disruption of these transporters attenuated the increased fatty acid uptake. Lipidomic analysis further showed widespread reductions in neutral lipid species and increased phospholipid unsaturation. Moreover, phosphoproteomic analysis implicated the mTOR signaling pathway, and pharmacological inhibition of mTOR suppressed the elevated fatty acid uptake in ACC1-deficient cells. Collectively, these findings reveal unrecognized mechanisms of lipid metabolic adaptation and highlight a regulatory network that coordinates fatty acid uptake in response to impaired lipid synthesis.

Takeru Endo, T. Kanno, R. Konno et al. · Scientific Reports · 0 citations