Journal: Cancer Genomics & Proteomics

Article Title: ATIC Knockdown Reduces B7-H3 Expression and Oncogenic Signaling in Upper Tract Urothelial Carcinoma Cells

doi: 10.21873/cgp.20575

Figure Lengend Snippet: Functional characterization of ATIC downstream targets in BFTC909 cells. (A, B) Western blot validation of siRNA-mediated knockdown efficiency for B7-H3, prion protein, RAC2, and NT5E in BFTC909 cells (n=3). (C) Silencing of B7-H3, RAC2, or NT5E significantly reduced cell proliferation, as assessed using cell viability assays (n=4). (D, E) Knockdown of B7-H3, prion protein, RAC2, or NT5E markedly suppressed BFTC909 cell migration and invasion (n=3). (F) Knockdown of B7-H3 decreased fibronectin 1, slug, cyclin A2, and cyclin B1 expression while increasing p57 levels (n=3). (G) Silencing of prion protein reduced fibronectin 1 and cyclin A2 expression while upregulating p57 expression (n=3). (H) Suppression of RAC2 diminished fibronectin 1 and slug expression with a concomitant increase in p57 levels (n=3). (I) Depletion of NT5E decreased fibronectin 1 and elevated p57 expression levels (n=3). The results are shown as the mean±standard deviation (SD); *p<0.05, **p<0.01, and ***p<0.001; NS: Nonsignificant using two‐tailed t‐test for (B), (F), (G), (H) and (I), and ANOVA followed by Fisher’s LSD test for (C), (D) and (E).

Article Snippet: Membranes were incubated overnight at 4°C with anti-ATIC (MA1-086, Invitrogen, Waltham, MA, USA), β-actin (#3700, Cell Signaling Technology, Danvers, MA, USA), α-tubulin (NB100-690, Novus Biologicals, Centennial, CO, USA), B7-H3 (#14058, Cell Signaling Technology), Prion Protein (A18058, ABclonalbio, New Taipei, Taiwan, ROC), RAC2 (A1139, ABclonalbio), NT5E (A25914, ABclonalbio), Fibronectin 1 (#26836, Cell Signaling Technology), Slug (NBP2-52570, Novus), Cyclin A2 (#4656, Cell Signaling Technology), Cyclin B1 (#4138, Cell Signaling Technology), p57 (NBP1-89917, Novus), phospho-mTOR (Ser2448) (SAB4504476, Sigma-Aldrich), mTOR (#2983, Cell Signaling Technology), phospho-AKT (Thr308) (#9275, Cell Signaling Technology), AKT (#9272, Cell Signaling Technology), phospho-p38 MAPK (Thr180/Tyr182) (#9211, Cell Signaling Technology), p38 MAPK (#9212, Cell Signaling Technology), phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (#9101, Cell Signaling Technology), and p44/42 MAPK (Erk1/2) (#9102, Cell Signaling Technology).

Techniques: Functional Assay, Western Blot, Biomarker Discovery, Knockdown, Migration, Expressing, Standard Deviation, Two Tailed Test

Journal: bioRxiv

Article Title: A single cell atlas of mouse podocytes upon injury identifies kidney zone-dependent responses

doi: 10.64898/2026.02.26.708349

Figure Lengend Snippet: (A) Mouse breeding schema showing the crosses of Podocin rtTA, p53 fl/fl and tetO-cre mice used to establish mice with doxycycline inducible podocyte specific ablation of p53. ( B ) Kidney function. Bar Graph of albumin creatinine ratios(ACR) at baseline and day 14 of FSGS in p53 +/+ (light gray) and p53 fl/fl (dark gray) mice. ACR was higher in p53 +/+ compared with p53 fl/fl mice ( C ) Podocyte number . Representative images of p57 staining in the OC and JM and bar graphs of quantification of the number of p57 positive cells per glomerular cross section. Podocyte number was lower in p53 +/+ compared with p53 fl/fl mice ( D ) Glomerulosclerosis. Representative images of Jones silver staining in the OC and JM and bar graphs of quantification of the percentage of the glomerular area stained with silver. Silver staining was higher in p53 +/+ compared with p53 fl/fl mice indicating matrix expansion and more scarring.

Article Snippet: To identify podocyte injury and determine glomerulosclerosis, p57/PAS staining was performed, the following antibody was applied: rabbit anti-p57 (#sc-56341, 1:1000, Santa Cruz Biotechnology).

Techniques: Staining, Silver Staining