stat3 antibody  (Bioss)

Journal: Journal of Translational Autoimmunity

Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

doi: 10.1016/j.jtauto.2025.100341

Figure Lengend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Article Snippet: Membranes were stripped and re-probed for total AKT, NFκB p65, p38 MAPK, STAT1, STAT3, and β-actin (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA) as a loading control.

Techniques: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

Journal: Journal of Translational Autoimmunity

Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

doi: 10.1016/j.jtauto.2025.100341

Figure Lengend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Article Snippet: Membranes were blocked with 5 % non-fat milk in TBS-T and incubated overnight at 4 °C with primary antibodies against phospho-AKT (Thr308), phospho-NFκB p65 (Ser536), phospho-p38 MAPK (Thr180/Tyr182), phospho-STAT1 (Tyr701), and phospho-STAT3 (Tyr705) (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

Journal: Genes & Diseases

Article Title: MFAP2 promotes metastasis and drug resistance by regulating epithelial-to-mesenchymal transition through EGFR signaling pathway in colorectal cancer cells

doi: 10.1016/j.gendis.2025.101800

Figure Lengend Snippet: MFAP2 promotes epithelial–mesenchymal transition (EMT) through the EGFR-AKT-STAT3 signaling pathway in colorectal cancer (CRC) cells. (A, B) The top 20 enrichment signaling pathways regulated by MFAP2 knockdown. (C, D) VEGFR2 signaling pathway was enriched in the MFAP2 knockdown cells, shown by Gene Set Enrichment Analysis (GSEA) and essential genes in this enrichment. (E) MFAP2 knockdown affected the EGFR-AKT-STAT3 axis.

Article Snippet: Following blocking with 5% non-fat milk in PBS with 0.02% Tween 20 detergent (PBST) at room temperature for 2 h, the membranes were incubated with primary antibodies, including MFAP2 (Solarbio, China), GAPDH (BBI Co., Ltd., China), epidermal growth factor receptor (EGFR; Proteintech, China), protein kinase B (AKT) (Proteintech), signal transducer and activator of transcription 3 (STAT3) (Proteintech), and vascular endothelial growth factor A (VEGFA) (Proteintech), p-EGFR (Cell Signaling Technology, USA), p-STAT3 (Cell Signaling Technology), and p-AKT ser473 (Cell Signaling Technology) antibodies, at 4 °C overnight.

Techniques: Protein-Protein interactions, Knockdown

Journal: Redox Biology

Article Title: Astrocytic GSTM2-STAT3 interaction ameliorates the diabetes associated cognitive dysfunction via targeting mitochondrial defects and oxidative stress

doi: 10.1016/j.redox.2026.104137

Figure Lengend Snippet: Inhibition of STAT3/Drp1 signaling defends HG-induced oxidative stress and mitochondrial defects. (A) Western blotting of STAT3 protein levels in primary cultured astrocytes, and quantification data. n = 3. (B) Representative images of ROS content by flow cytometry analysis, and quantification data. n = 5. (C-E) MDA, GSH and SOD contents in primary cultured astrocytes. n = 5. (F) Representative images of the morphology of mitochondria by TEM in primary cultured astrocytes. Scale bar, 500 nm. (G) Mitochondrial aspect ratio, n = 3. (H) Mitochondrial cristae density, n = 3. (I) Western blotting of Mfn1, p -Drp1 and Drp1 protein levels in primary cultured astrocytes. (J) Representative images of JC-1 staining by flow cytometry analysis used to assess mitochondrial membrane potential. (K–N) OCR, ATP production, Basal respiration and Maximal respiration in primary cultured astrocytes. n = 5. si-NC (scrambled negative control siRNA); si-STAT3 (si-STAT3 primer). (High glucose, 50 mmol/L treated 48 h). Data are shown as mean ± SEM or SD. Statistical significance was defined as ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001.

Article Snippet: The OE-GSTM2 and si-STAT3 constructs utilized in this study were custom-designed and procured from OBio Technology Co. Ltd. (Shanghai, China).

Techniques: Inhibition, Western Blot, Cell Culture, Flow Cytometry, Staining, Membrane, Negative Control