rabbit anti cldn3  (Proteintech)

Journal: Fluids and barriers of the CNS

Article Title: SARS-CoV-2 causes dysfunction in human iPSC-derived brain microvascular endothelial cells potentially by modulating the Wnt signaling pathway.

doi: 10.1186/s12987-024-00533-9

Figure Lengend Snippet: Fig. 4 Analysis of human iPSC-BMELC barrier disruption based on RNA-seq. A Comprehensive RNA-seq was performed using total RNA with or without SARS-CoV-2 infection. Heatmap shows screened up- and downregulated genes by using cut-off values of fold change of ≥ 1.5 followed by second selection based on KEGG pathway analysis and references. B After SARS-CoV-2 infection for 24 h, tight junction marker genes (CLDN3, CLDN5, CLDN11, and CLDN12) were analyzed by RT-qPCR. C After SARS-CoV-2 infection for 24 h, expression of CLDN3 and CLDN11 was analyzed by western blot. Cropped blots were shown and the full-length blots were indicated in Fig. S5. The relative band densities were analyzed using ImageJ software and normalized to β-actin. Data are represented as mean ± SD (n = 3). *P < 0.05

Article Snippet: The membranes were probed with anti-CLDN3 monoclonal antibodies (D7A3O, #83609S, 1:1000; Cell Signaling Technology), anti-CLDN11 monoclonal antibodies (E7E9U, #38062S, 1:1000; Cell Signaling Technology), anti-β-catenin polyclonal antibodies (#9562, 1:1000; Cell Signaling Technology), anti-β-actin monoclonal antibodies (AC-15, #A5441, 1:5000; SigmaAldrich), and anti-histone H3 monoclonal antibodies (D1H2, #4499S, 1:2000; Cell Signaling Technology).

Techniques: Disruption, RNA Sequencing, Infection, Selection, Marker, Quantitative RT-PCR, Expressing, Western Blot, Software