Journal: Redox Biology

Article Title: NRF2 controls a diverse network of antiviral effectors with p62 acting as a central restriction factor effective across virus families

doi: 10.1016/j.redox.2026.104135

Figure Lengend Snippet: NRF2 restricts SARS-CoV-2 replication (A-B) SARS-CoV-2 permissive 786-O cell clone deficient in NRF2 (NRF2-KO) and control cells were infected with SARS-CoV-2 at MOI 0.01 for 24 h. Cell lysates were then prepared for qPCR for viral RNA or for immunoblotting against viral protein NC, NRF2, and loading control VCL (Vinculin). (C–D) SARS-CoV-2 permissive 786-O cells were used for CRISPR-Cas9-mediated elimination of NRF2. Cells were then infected with SARS-CoV-2 at MOI 0.01 for 24 h before cell lysates were prepared for qPCR and cell supernatants harvested for TCID50 analysis. (E–F) SARS-CoV-2 permissive Huh-7 cells were treated with dCas9 alone or dCas9 along with sgRNAs targeting the promoter region of NRF2 or IRF1. Cells were then infected with SARS-CoV-2 at MOI 0.01 for 24 h before cell lysates were prepared for immunoblotting and cell supernatants harvested for TCID50. (G) Graphic representation of CRISPRa for NRF2-driven genes. (H–J) CRISPRa was used to induce endogenous expression of indicated NRF2-driven genes in SARS-CoV-2 permissive Huh-7 cells. Cells were then infected with SARS-CoV-2 at MOI 0.01 for 8 h before lysates were collected for qPCR or immunoblotting. (H) Displays immunoblots for viral protein NC and loading control VCL. (I) Displays expression levels of NC normalized to VCL expression levels for each tested gene based on densitometric quantification of immunoblots. (J) Displays mean SARS-CoV-2 RNA levels by qPCR normalized to beta actin expression levels for each gene tested from two independent experiments. (K) TCID50 was established from cell supernatants harvested from Huh-7 cells where indicated genes were induced by CRISPRa before infection with SARS-CoV-2 at MOI 0.02 for 8 h. (A–F) Are representative of two independent experiments. Each data point represents one biological replicate with bars indicating mean ± s.e.m. (H–I) represents data from one experiment. (K) Each data point indicates mean of three biological replicates. Bars indicate mean ± s.e.m. of two or three independent experiments. p-values were established using Graphpad Prism 10 using the Student's t -test with “∗” indicating p < 0.05.

Article Snippet: 786-O NRF2-KO and control cells were purchased from ATCC.

Techniques: Control, Infection, Western Blot, CRISPR, Expressing

Journal: Translational Oncology

Article Title: Integrated spatial and single‑cell transcriptomics maps disulfidptosis in renal cell carcinoma and reveals PDLIM1 as a prognostic biomarker and potential therapeutic target

doi: 10.1016/j.tranon.2026.102765

Figure Lengend Snippet: PDLIM1 knockdown reduces proliferation, clonogenicity, and migration in renal cancer cells in vitro. (A) qPCR validation of siRNA/shRNA‑mediated PDLIM1 knockdown in renal cancer cell lines (786‑O and OSRC-2). (B) CCK‑8 proliferation/viability curves comparing control and PDLIM1‑depleted cells over time. (C-D) Representative images (C) and quantification (D) of wound‑healing assays. (E) Transwell migration assays showing decreased motility/invasiveness after PDLIM1 depletion. (F) Quantification of transwell migration assays. Data are presented as mean ± SEM; statistical significance was determined by two‑sided Student’s t‑test (two groups) or one‑way ANOVA with Tukey’s post hoc test (multiple groups), unless otherwise specified. ns, not significant; * FDR < 0.05; ** FDR < 0.01; *** FDR < 0.001.

Article Snippet: 786O cells and OSRC2 cells were provided by ATCC.

Techniques: Knockdown, Migration, In Vitro, Biomarker Discovery, Control