Journal: Journal of Molecular Histology

Article Title: Interleukin-1 Receptor-Associated Kinase 3 Attenuates Chondrocyte Senescence and Osteoarthritis via Inhibition of the TLR7/9–NF-κB Axis

doi: 10.1007/s10735-026-10804-4

Figure Lengend Snippet: illustrates the role of IRAK3 in modulating TLR7/9 signaling and reducing inflammation in chondrocytes. AT791 is a TLR7 and TLR9 inhibitor. The treatment concentration is 3 µM and the treatment time is 48 h. The TLR9 agonist used is ODN 1826, with a concentration of 1 µg/ml and a treatment time of 48 h. The TLR7 agonist used is Resiquimod, with a concentration of 1 µM and a treatment time of 48 h. Both were purchased from MedChemExpress, HY-124,603, HY-146,245 and HY-13,740. Panels A and B show Western blot analysis of TLR7 and TLR9 expression following IRAK3 knockdown and overexpression, respectively. Panels C through E present ELISA results indicating levels of IL-1β, IL-6, and TNF-α after IRAK3 knockdown. Similarly, panels F through H display ELISA findings for IL-1β, IL-6, and TNF-α levels following IRAK3 overexpression. In panel I, chondrocytes were treated with TLR7/9 inhibitors and agonists, and β-galactosidase staining was performed on senescent chondrocytes for statistical analysis. (* p < 0.05, ** p < 0.01)

Article Snippet: The treatment concentration is 3 μM and the treatment time is 48 h. The TLR9 agonist used is ODN 1826, with a concentration of 1 μg/ml and a treatment time of 48 h. The TLR7 agonist used is Resiquimod, with a concentration of 1 μM and a treatment time of 48 h. Both were purchased from MedChemExpress, HY-124,603, HY-146,245 and HY-13,740.

Techniques: Concentration Assay, Western Blot, Expressing, Knockdown, Over Expression, Enzyme-linked Immunosorbent Assay, Staining

Journal: Cancer cell

Article Title: The osteogenic niche is a calcium reservoir of bone micrometastases and confers unexpected therapeutic vulnerability

doi: 10.1016/j.ccell.2018.10.002

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Western Blot Western blots were performed using antibodies against NFAT1(Cell Signalling, 5861S), pS6K(T389) (Cell Signaling, 9234S), pCamKII(T286) (Cell Signalling, 12716S), MeCP2 (Cell Signalling, 3456S), pMeCP2(S421)(Rockland, 600-401-X14), Firefly luciferase (Thermo, PA5-32209).

Techniques: Luciferase, Recombinant, Expressing, In Vivo, Software

Journal: The Journal of infectious diseases

Article Title: Hepatitis C Virus nonstructural 5A protein inhibits lipopolysaccharide-mediated apoptosis of hepatocytes by decreasing expression of Toll-like receptor 4.

doi: 10.1093/infdis/jir381

Figure Lengend Snippet: Figure 1. Hepatitis Cvirus (HCV) nonstructural protein 5 A (NS5A) protects hepatocytes from lipopolysaccharide (LPS)–induced cell death. A, B, HepG2 control (A) and HepG2-NS5A (B) hepatocytes were cultured for 24 hours with ligands of Toll-like receptor (TLR) 1/TLR2 (Pam3CSK4), TLR3 (poly[I:C]), TLR4 (LPS), TLR5 (flagellin), TLR6/TLR2 (macrophage-activating lipopeptide 2), TLR7 (Imiquimod [R-837]), TLR9 (type B CpG oligonucleotide), and control oligonucleotide, as indicated in Materials and Methods. Cells were washed and stained with crystal violet, and experiments were performed 3 times. PBS, phosphate-buffered saline. C, HCV NS5A protects hepatocytes from LPS-induced apoptosis. HepG2 control and HepG2-NS5A hepatocytes were cultured for 24 hours with LPS (5 lg/mL). Cell apoptosis was quantified using the APOPercentage Apoptosis Assay. Data are expressed as means 6 standard deviations of triplicate determinations from 1 experiment represen- tative of 3 independent experiments.

Article Snippet: 3HCL; 100 lg/mL), TLR3 (poly[I:C]; 50 lg/mL), TLR4 (LPS from Escherichia coli; 5 lg/mL), TLR5 (purified flagellin; 100 lg/mL), TLR6/TLR2 (macrophage-activating lipopeptide 2; 100 lg/mL), TLR7 (Imiquimod [R-837]; 2.5 lg/mL), and TLR9 (type B CpG ODN; 0.5 lg/mL) (all purchased from Imgenex).

Techniques: Control, Cell Culture, Staining, Saline, Apoptosis Assay