CCR5 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying CCR5 (CC chemokine receptor 5, CD195)'s role as the principal HIV co-receptor or modeling its functions in T cell trafficking and HIV-cure strategies. The Knockout line is the standard tool for asking whether CCR5 is required for these processes — CCR5 is a Gαi-coupled seven-transmembrane GPCR activated by CCL3 (MIP-1α), CCL4 (MIP-1β), and CCL5 (RANTES), expressed on effector/memory T cells, monocytes, macrophages, and DCs; CCR5 is the principal co-receptor for R5-tropic HIV-1 strains (which represent ~90% of new infections), and the CCR5Δ32 homozygous mutation confers HIV resistance — this is the basis of the Berlin, London, and Düsseldorf patients (cured of HIV by CCR5Δ32 allogeneic HSC transplantation). Overexpression is useful for studying CCR5 in heterologous expression contexts. For HIV research, the EDITGENE CCR5 Knockout in HEK293 is uniquely valuable — HEK293 supports systematic structure-function studies. Rescue with wild-type or signaling-deficient CCR5 enables structure-function studies. The knockout is a critical specificity tool for ⭐⭐ maraviroc (Selzentry, FDA-approved 2007 CCR5 antagonist for HIV-1), leronlimab (PRO 140, anti-CCR5 antibody in development), CCR5-modifying gene therapy approaches for HIV cure (sangamo's SB-728, allogeneic CCR5Δ32 HSCT, CRISPR-based CCR5 disruption), and emerging CCR5-targeted approaches in cancer (CCR5 on Tregs and TAMs).

Primary applications: • HIV co-receptor function: R5-tropic HIV-1 envelope-mediated entry analysis in CCR5-null cells. • Maraviroc specificity: critical genetic control for maraviroc (Selzentry, FDA-approved CCR5 antagonist for HIV). • HIV cure strategy validation: CCR5-disruption-based gene therapy vector validation (CRISPR-CCR5 disruption, ZFN-based SB-728, etc.). • Chemokine signaling: CCL3 (MIP-1α), CCL4 (MIP-1β), CCL5 (RANTES)-induced signaling analysis. • Anti-CCR5 antibody specificity: leronlimab (PRO 140) and other anti-CCR5 antibody compound specificity testing. EDITGENE recommends this model as the gold-standard genetic specificity control for HIV co-receptor research and CCR5-targeted HIV cure strategies.

Yes. CCR5 rescue experiments are well-established for HIV co-receptor research: • Construct design: use a codon-modified CCR5 sequence with a small intracellular C-terminal tag (FLAG, HA). CCR5 is a seven-transmembrane Gαi-coupled GPCR with N-terminal sulfated tyrosines (HIV gp120 binding) — preserve all elements. • Surface localization validation: confirm plasma membrane localization by cell surface staining before HIV envelope binding studies. • CCR5Δ32 rescue: rescue with CCR5Δ32 (frameshift mutation, no surface expression) compared to wild-type recapitulates the HIV-resistant phenotype. • Maraviroc-resistant rescue: gp120-binding-pocket mutations can confer resistance for on-target validation. • Functional readout: rescue should restore R5-tropic HIV envelope-mediated entry and maraviroc sensitivity. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation for HIV research.