mouse monoclonal anti c fos e 8  (Santa Cruz Biotechnology)

Journal: Bioactive Materials

Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

doi: 10.1016/j.bioactmat.2026.05.005

Figure Lengend Snippet: In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

Article Snippet: Anti-Ki67 mouse mAb (Cat# GB121141-100), anti-CD3 mouse mAb (Cat# GB15014-100), FITC-conjugated goat anti-mouse IgG (H + L) (Cat# GB22301), and Cy5-conjugated goat anti-mouse IgG (H + L) (Cat# GB27301) for immunofluorescence assays, and DAB (SA-HRP) TUNEL apoptosis detection kit were supplied by Servicebio (Wuhan, China).

Techniques: In Vivo, Drug discovery, Staining, TUNEL Assay, Immunofluorescence

Journal: Cancer Pathogenesis and Therapy

Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target

doi: 10.1016/j.cpt.2025.08.002

Figure Lengend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

Article Snippet: Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA).

Techniques: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction