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GORYO Chemical
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European Directorate for the Quality of Medicines and HealthCare
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InnoChem Inc
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NanoSany Corporation
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Avantor
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Verlag GmbH
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Image Search Results
Journal: Journal of Orthopaedic Translation
Article Title: TRIM59 alleviates neuronal ferroptosis and promotes functional recovery after spinal cord injury by mediating ubiquitination and degradation of ANXA2
doi: 10.1016/j.jot.2026.101070
Figure Lengend Snippet: TRIM59 mitigates ferroptosis in vitro . Neuronal cells were transfected with Lv-shTRIM59 or Lv-TRIM59 and treated with Erastin (5 μM) for 6 h. (A) Experimental group specifications; (B, C) Transfection efficiency was confirmed through western blot analysis (n = 3); (D) Cell viability was determined using CCK-8 assay (n = 6); (E, F) Neuronal survival was examined by Calcein-AM/PI double staining (n = 3); (G-K) ROS, Fe 2+ , MDA, and GSH levels were measured (n = 3); (L, M) Fe 2+ accumulation was visualized with SiRhoNox-1 staining (n = 3); (N) Ferroptosis-related protein expression was assessed by western blot (n = 3); (O, P) Mitochondrial ROS accumulation was measured using MitoSOX immunofluorescence and corresponding statistical analysis (n = 3); (Q, R) Mitochondrial membrane potential was assessed via JC-1 staining, with quantification of JC-1 aggregates and monomers (n = 3); (S) Representative TEM images of mitochondrial ultrastructure in neuronal cells. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001.
Article Snippet: Intracellular labile iron pool (Fe 2+ ) levels were detected using the
Techniques: In Vitro, Transfection, Western Blot, CCK-8 Assay, Double Staining, Staining, Expressing, Immunofluorescence, Membrane
Journal: Journal of Orthopaedic Translation
Article Title: TRIM59 alleviates neuronal ferroptosis and promotes functional recovery after spinal cord injury by mediating ubiquitination and degradation of ANXA2
doi: 10.1016/j.jot.2026.101070
Figure Lengend Snippet: Lv-shANXA2 mitigates the ferroptosis induced by TRIM59 knockdown. Neuronal cells were transfected with either Lv-shANXA2 or Lv-ANXA2 and treated with Erastin (5 μM) for 6 h. (A) Experimental group specifications; (B) Cell viability assessment via CCK-8 assay (n = 6); (C, D) Neuronal survival evaluation through Calcein-AM/PI staining (n = 3); (E, F) Intracellular ROS quantification by flow cytometry with statistical analysis (n = 3); (G-I) Measurement of Fe 2+ , MDA, and GSH levels in neuronal cells (n = 3); (J, K) Fe 2+ accumulation detection using SiRhoNox-1 staining (n = 3); (L) Western blot examination of ferroptosis-associated protein expression in neuronal cells (n = 3); (M, N) Mitochondrial ROS detection and quantification via MitoSOX immunofluorescence in neuronal cells (n = 3); (O, P) Mitochondrial membrane potential assessment through JC-1 staining, including JC-1 aggregate-to-monomer ratio quantification (n = 3); (Q) Transmission electron microscopy visualization of mitochondrial ultrastructure in neuronal cells. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001.
Article Snippet: Intracellular labile iron pool (Fe 2+ ) levels were detected using the
Techniques: Knockdown, Transfection, CCK-8 Assay, Staining, Flow Cytometry, Western Blot, Expressing, Immunofluorescence, Membrane, Transmission Assay, Electron Microscopy