Activation of human GPR35 splice variant a (GPR35a) blocks LXR‑induced lipid accumulation in hepatocytes. A humanized knock-in mouse expressing hGPR35a‑HA in place of mouse Gpr35 demonstrated ligand-dependent suppression of hepatic lipid accumulation, overcoming species pharmacology mismatch seen in wild-type mice.
hGPR35a‑HA hepatocytes respond to lodoxamide (EC₅₀ ~17 nM) by blocking and reversing LXR‑induced lipid storage; wild-type mouse GPR35 was unresponsive due to ortholog pharmacological differences
Humanized GPR35a‑HA Knockin mouse (mouse Gpr35 replaced with human splice variant a) — genOway-developed, C57BL/6 background
Non-alcoholic fatty liver disease (NAFLD); GPCR pharmacology; hepatocyte lipid metabolism; species mismatch; humanization strategy
Human gene Knockin; replacement of mouse Gpr35; hepatocyte lipid assay; Oil Red O staining; ligand response profiling (lodoxamide, ML‑145)
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