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Body weight, serum biochemistry (ALT, AST, TC, TG), liver histopathology (H&E, Sirius Red), hepatic mRNA expression ( Tlr4, Tnf-α, and α-SMA ), gut microbiota (16S rRNA sequencing), and serum metabolites (untargeted metabolomics) were assessed

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Since the ANKIB1-RBR but not its RING2 was required, we next generated ANKIB1-deficient cells expressing a RING1-mutant ANKIB1 (ANKIB1-RING1 mut ) with mutations in several conserved residues (C333A/I335A/C336A/C351A/H353A) and, indeed, TLR3 stimulation failed to activate TBK1 in these cells (Fig