ABCG2 Knockout Cell Line (HEK293)

The choice depends on whether you are studying ABCG2 (BCRP, breast cancer resistance protein)'s role as a multidrug efflux transporter or modeling its functions in drug resistance, pharmacokinetics, and uric acid transport. The Knockout line is the standard tool for asking whether ABCG2/BCRP is required for these processes — ABCG2 is an ATP-binding cassette (ABC) half-transporter that functions as a homodimer to efflux a broad range of substrates including chemotherapeutics (mitoxantrone, topotecan, methotrexate, tyrosine kinase inhibitors), dietary xenobiotics, and urate; ABCG2 is highly expressed at the blood-brain barrier, placenta, intestine, and liver, critically influencing drug absorption, distribution, and resistance. Overexpression is useful for studying ABCG2 gain-of-function effects. For drug resistance and pharmacokinetics research, the EDITGENE ABCG2 Knockout in HEK293 is uniquely valuable — ABCG2/BCRP is one of the three major drug-efflux ABC transporters (with ABCB1/P-gp and ABCC1/MRP1). Rescue with wild-type, transport-deficient, or the common Q141K polymorphism (reduced function, associated with gout and altered drug pharmacokinetics) ABCG2 enables comprehensive structure-function and pharmacogenomic studies. The knockout is a critical specificity tool for studying multidrug resistance, BCRP-mediated drug efflux at the blood-brain barrier, ABCG2-mediated chemotherapy resistance, and ABCG2-related hyperuricemia/gout (the Q141K variant is one of the strongest genetic risk factors for gout).

Primary applications: • Multidrug efflux: substrate (mitoxantrone, Hoechst 33342, topotecan) efflux and accumulation analysis in ABCG2-null cells. • Drug resistance: chemotherapy resistance analysis given BCRP's role in cancer multidrug resistance. • BCRP inhibitor specificity: critical genetic control for Ko143, fumitremorgin C, and emerging BCRP inhibitors. • Gout/hyperuricemia: rescue with Q141K polymorphism for urate transport and gout pharmacogenomic studies — Q141K is one of the strongest genetic risk factors for gout. • BBB/placenta pharmacokinetics: in heterologous barrier-relevant contexts, BCRP-mediated drug efflux studies. EDITGENE recommends this model as a critical specificity control for multidrug resistance, drug pharmacokinetics, and ABCG2-related gout research.

Yes. ABCG2/BCRP rescue experiments are well-established for drug transporter research: • Construct design: use a codon-modified ABCG2 sequence with a small intracellular tag (FLAG, HA) — ABCG2 is an ABC half-transporter (single nucleotide-binding domain + transmembrane domain) functioning as a homodimer; tag placement should preserve dimerization and transport. • Surface localization validation: confirm plasma membrane localization by cell surface staining (5D3 antibody) before efflux assays. • Transport-deficient rescue: K86M Walker A mutation abolishes ATP-dependent transport. • Q141K polymorphism rescue: the common Q141K reduced-function variant enables gout and drug pharmacokinetics pharmacogenomic studies. • Functional readout: rescue should restore substrate efflux measured by mitoxantrone/Hoechst 33342 accumulation assays. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.