CCR6 Knockout HEPG2 Cell Line

The choice depends on whether you are studying CCR6 (CC chemokine receptor 6)'s role as the principal Th17 and B-cell chemokine receptor or modeling its functions in inflammatory disease and hepatic biology. The Knockout line is the standard tool for asking whether CCR6 is required for these processes — CCR6 is a Gαi-coupled seven-transmembrane GPCR uniquely activated by CCL20/MIP-3α (and human β-defensins as alternative ligands), with predominant expression on Th17 cells, regulatory T cells (Tregs), B cells, and dendritic cells; CCR6 mediates mucosal homing especially to gut and skin. Overexpression is useful for studying CCR6 in heterologous expression contexts. For hepatic inflammation and IBD research, the EDITGENE CCR6 Knockout in Hep-G2 is relevant — Hep-G2 provides a hepatocellular context, and CCR6-CCL20 has been characterized in liver disease and inflammatory bowel disease pathology. Rescue with wild-type or signaling-deficient CCR6 enables structure-function studies. The knockout is a critical specificity tool for emerging CCR6 antagonists (CCX507 in clinical development for ulcerative colitis, PF-07054894, vidofludimus calcium with CCR6 effects) and CCR6-targeted approaches in psoriasis, IBD, and rheumatoid arthritis.

Primary applications: • CCL20-induced signaling: Ca²⁺ mobilization and ERK activation following CCL20/MIP-3α stimulation in CCR6-null cells. • IBD biology: in heterologous IBD-relevant contexts, CCR6-mediated Th17 and Treg trafficking studies. • CCR6 antagonist specificity: critical genetic control for ⭐ CCX507 (in clinical development for ulcerative colitis), PF-07054894, and other emerging CCR6-targeted compounds. • Hepatic inflammation: in Hep-G2 context, characterization of CCR6 in liver disease pathology. EDITGENE recommends this model for researchers investigating Th17-associated inflammatory disease and emerging CCR6-targeted therapeutic development.

Yes. CCR6 rescue experiments require attention to GPCR architecture: • Construct design: use a codon-modified CCR6 sequence with a small intracellular C-terminal tag (FLAG, HA). CCR6 is a seven-transmembrane Gαi-coupled GPCR — preserve membrane topology; C-terminal tags may affect β-arrestin recruitment. • Surface localization validation: confirm plasma membrane localization before CCL20 binding studies. • Signaling-deficient rescue: DRY motif mutations disrupt Gαi-coupling. • Functional readout: rescue should restore CCL20-induced Ca²⁺ mobilization and ERK activation. Hep-G2-specific considerations: • Hep-G2 is a human hepatocellular carcinoma cell line widely used for hepatocyte differentiation, drug metabolism, and liver biology research. • Lentiviral transduction is supported with moderate efficiency. • Hep-G2 retains many hepatocyte features and serves as a complementary HCC model to Huh-7.