GPBAR1 Knockout SK-N-AS Cell Line

The choice depends on whether you are studying GPBAR1 (TGR5, M-BAR)'s role as the principal bile acid-sensing GPCR or its emerging functions in neural and metabolic biology. The Knockout line is the standard tool for asking whether TGR5 is required for these processes — GPBAR1/TGR5 is a Gs-coupled seven-transmembrane receptor activated by bile acids (particularly lithocholic acid, taurolithocholic acid, deoxycholic acid), with established roles in energy metabolism, glucose homeostasis, and emerging functions in cancer and CNS biology. Overexpression is useful for studying TGR5 in heterologous expression contexts. For TGR5 research, the EDITGENE GPBAR1 Knockout in SK-N-AS enables study of TGR5 biology — SK-N-AS is a non-MYCN-amplified neuroblastoma cell line providing a neural-derived background. Rescue with wild-type or signaling-deficient TGR5 enables structure-function studies. The knockout is a critical specificity control for TGR5 agonists (INT-777, cilofexor for cholestatic liver disease, semaglutide-related bile acid pharmacology) and emerging TGR5-targeted metabolic disease therapeutics.

Primary applications: • Bile acid-induced signaling: cAMP elevation following lithocholic acid, taurolithocholic acid, or other TGR5 agonist stimulation in TGR5-null cells. • Neural TGR5 biology: in heterologous neural contexts, characterization of TGR5's emerging CNS functions. • TGR5 agonist specificity: critical genetic control for INT-777 (TGR5 agonist) and other emerging TGR5-targeting compounds. • Bile acid signaling crosstalk: parallel analysis with FXR signaling for understanding the FXR-TGR5 dual bile acid signaling axis. EDITGENE recommends this neuroblastoma-derived model for researchers investigating TGR5 biology in neural contexts and bile acid signaling biology.

Yes. TGR5 rescue experiments require attention to bile acid binding: • Construct design: use a codon-modified GPBAR1 sequence with a small intracellular C-terminal tag (FLAG, HA). GPBAR1 is a seven-transmembrane Gs-coupled GPCR — preserve bile acid-binding pocket. • Signaling-deficient rescue: DRY motif mutations disrupt Gs-coupling. • Functional readout: rescue should restore bile acid-induced cAMP elevation and downstream PKA signaling. SK-N-AS-specific considerations: • SK-N-AS is a human neuroblastoma cell line (non-MYCN-amplified, derived from bone marrow metastasis) — a relevant model for non-MYCN-amplified neuroblastoma biology. • Lentiviral transduction is supported with moderate efficiency. • SK-N-AS provides a neural-derived background distinct from MYCN-amplified neuroblastoma lines.