Fig. 3: HERV-K expression activates nucleotide sensing pathways in proximal tubule cells. | Nature Communications

Fig. 3: HERV-K expression activates nucleotide sensing pathways in proximal tubule cells.

From: Increased levels of endogenous retroviruses trigger fibroinflammation and play a role in kidney disease development

Fig. 3: HERV-K expression activates nucleotide sensing pathways in proximal tubule cells.The alternative text for this image may have been generated using AI.

a Experimental hypothesis. b Relative mRNA levels of cytosolic RNA sensors (Rigi, Mda5, Mavs, Tlr3, Tlr4, and Tlr7) and DNA sensors Cgas, Sting, and Aim2 in WT PTECs transfected with HERV-K (red) or Vector control (blue) (n = 3 in each). c Western blot showing representative images of RIG-I, cGAS, STING, pTBK1, TBK1, pIRF3, and IRF3 protein levels in WT, RIG KO, and STING KO PTECs transfected with HERV-K/Vector. ACTIN was used as a loading control. d Ifnb, Ifne, and Ifnk RNA expression in WT (Vector: blue, HERV-K: red), RIG KO (Vector: yellow, HERV-K: green), and STING KO (Vector: black, HERV-K: magenta) PTECs transfected with HERV-K or Vector control (n = 3 in each). e Relative mRNA levels of Interferon-stimulated genes (Mx1, Isg20, Rsad2, Oas1, and Bst2) in WT, RIG KO, and STING KO PTECs transfected with HERV-K/Vector (n = 3 in each). Data were presented as mean ± s.e.m. and all data were analyzed using a one-way ANOVA followed by Tukey post hoc test for multigroup comparison (b, d, e). Data were representative of two independent experiments (c). Source data are provided as a Source Data file.

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