tp53  (Cell Signaling Technology Inc)

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Role of CCNG1 in radiation-induced hepatocyte damage. (A) BRL-3A cells were transfected with empty vector or siCcng1, cultured with or without exogenous interleukin (IL)-6, and then irradiated with a single 10-Gy electron beam. Four hours after irradiation (IR), the apoptotic rate and cell cycle distribution were detected using flow cytometry. (B) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH in BRL-3A cells in these 4 groups. (C) Changes in γH2AX and GAPDH in BRL-3A cells transfected with empty vector or siCcng1 at various time points after a single 10-Gy electron beam IR. (D) Western blot analysis showing CCNG1, γH2AX, and GAPDH expression in BRL-3A cells transfected with empty vector or siTp53 and cultured with or without exogenous IL-6 4 hours after a single 10-Gy electron beam IR. (E) Western blot analysis showing CCNG1, γH2AX, TP53, and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA) or Student’s t test; *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

Article Snippet: The primary antibodies included phosphorylated STAT3 (Tyr705) (p-STAT3; Abcam, #ab308386; 1:1000), cyclin G1 (CCNG1; Santa Cruz Biotechnology, #sc-8016; 1:1000), γH2AX (Abcam, #ab81299; 1:5000), TP53 (Cell Signaling Technology, #32532; 1:1000), and GAPDH (Abcam, #ab8245; 1:10000) antibodies.

Techniques: Transfection, Plasmid Preparation, Cell Culture, Irradiation, Flow Cytometry, Western Blot, Expressing, Isolation

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

Article Snippet: The primary antibodies included phosphorylated STAT3 (Tyr705) (p-STAT3; Abcam, #ab308386; 1:1000), cyclin G1 (CCNG1; Santa Cruz Biotechnology, #sc-8016; 1:1000), γH2AX (Abcam, #ab81299; 1:5000), TP53 (Cell Signaling Technology, #32532; 1:1000), and GAPDH (Abcam, #ab8245; 1:10000) antibodies.

Techniques: Irradiation, Phospho-proteomics, Ubiquitin Proteomics