PTGER4 Knockout RT4 Cell Line

The choice depends on whether you are studying PTGER4 (EP4)'s role as the principal Gs-coupled PGE2 receptor or its functions in bladder cancer biology and inflammation. The Knockout line is the standard tool for asking whether EP4 is required for PGE2-induced cAMP elevation and downstream PKA signaling — EP4 has the lowest Km for PGE2 among the four EP receptors and dominates PGE2 responses in many contexts. Overexpression is useful for studying EP4 in cancer contexts where it is upregulated. For bladder cancer research, the EDITGENE EP4 Knockout in RT-4 is highly relevant — RT-4 is a well-differentiated urothelial papilloma cell line, and EP4 has been implicated in bladder cancer progression, invasion, and immune evasion. Rescue with wild-type or signaling-deficient EP4 enables structure-function studies. The knockout is a critical specificity control for EP4 antagonists (grapiprant, ONO-AE3-208) in oncology and inflammation drug development.

Primary applications: • PGE2-cAMP signaling: cAMP measurement following PGE2 stimulation to quantify EP4-dependent Gs signaling. • Bladder cancer biology: proliferation, invasion, and migration assays in RT-4 to assess EP4's contribution to urothelial cancer phenotypes. • Anti-EP4 specificity: critical genetic control for grapiprant, ONO-AE3-208, and other EP4 antagonists in cancer and inflammation drug development. • EP receptor selectivity: comparison with other EP receptor knockouts for EP4-specific PGE2 response characterization. EDITGENE recommends this model for researchers investigating PGE2-EP4 signaling, bladder cancer biology, and EP4-targeted therapeutic development.

Yes. EP4 rescue experiments are well-established for GPCR pharmacology research: • Construct design: use a codon-modified PTGER4 sequence with a small intracellular C-terminal tag (FLAG, HA). EP4 is a seven-transmembrane GPCR — N-terminal tags after the signal peptide are tolerated. • Signaling-deficient rescue: DRY motif mutations or other intracellular loop mutations separate ligand binding from intracellular signaling. • EP4-selective response: rescue with wild-type EP4 restores PGE2-induced cAMP elevation distinguishable from EP2 (also Gs-coupled but lower affinity). • Functional readout: rescue should restore PGE2-induced cAMP signaling and bladder cancer-relevant phenotypes. RT-4 is a urothelial papilloma cell line — transduction with lentivirus is supported at standard efficiency.