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Fig. 4 | Molecular Brain

Fig. 4

From: Long non-coding RNA lncC11orf54-1 modulates neuroinflammatory responses by activating NF-κB signaling during meningitic Escherichia coli infection

Fig. 4

MgU2-30 promotes meningitic E. coli-induced activation of NF-κB signaling. A Western blot analysis of NF-κB p65 and phosphorylated p65 in hBMECs transfected with multiple dosages of lncC11orf54-1 (0, 100, 500, 1000, and 20,000 ng) under E. coli infection. β-actin was used as the loading control. B hBMECs were transfected with control construct (pcDNA3.1), overexpression constructs of lncC11orf54-1, mgU2-19, or mgU2-30, and infected with E. coli; the protein levels of NF-κB p65 and phosphorylated p65 were determined by Western blotting. β-actin was used as the loading control. C Western blot analysis of NF-κB p65 and phosphorylated p65 in hBMECs transfected with multiple dosages of mgU2-30 (0, 100, 500, 1000, and 2000 ng) under E. coli infection. β-actin was used as the loading control. D Schematic diagram of CRISPR/Cas9 knockout strategies at the mgU2-30 loci. A deletion of 48 bp was validated by sequencing. The red rectangle outlines the deletion region, the blue arrows indicate genotyping PCR primers for identifying knocked-out cell clones. E Gel image shows PCR identification results for wildtype hBMECs, and mgU2-30 knockout hBMECs. F Effects of mgU2-30 knock out on the expression of NF-κB p65 and phosphorylated p65 in E. coli treated hBMECs, as determined by Western blotting. β-actin was used as the loading control

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