SLC40A1 Knockout Cell Line (HEK293)

The choice depends on whether you are studying ferroportin's role as the principal cellular iron exporter or modeling hemochromatosis type 4 and ferroportin disease. The Knockout line is the standard tool for asking whether ferroportin is required for iron efflux — ferroportin is the only known mammalian cellular iron export transporter, expressed on enterocytes, macrophages, and hepatocytes. Overexpression is useful for studying ferroportin in heterologous expression systems and for testing hepcidin-mediated regulation. For iron homeostasis research, the EDITGENE Ferroportin Knockout in HEK293 is the standard mechanistic platform — HEK293 has been extensively used for ferroportin biochemistry and structural studies. Rescue with wild-type, hepcidin-resistant (C326S), or ferroportin disease-associated mutant SLC40A1 enables comprehensive disease modeling. SLC40A1 mutations cause autosomal dominant hemochromatosis type 4/ferroportin disease — disease variant rescue is a standard genotype-function approach.

Primary applications: • Iron efflux assays: ⁵⁹Fe efflux from preloaded cells to quantify ferroportin transport activity. • Hepcidin-mediated regulation: hepcidin-induced ferroportin internalization and degradation assays — the primary regulatory mechanism for systemic iron homeostasis. • Disease mutation modeling: rescue with autosomal dominant hemochromatosis type 4-associated SLC40A1 variants (e.g., A77D 'loss-of-function', N144H 'hepcidin-resistant'). • Hepcidin-resistant rescue: C326S mutation creates a hepcidin-resistant ferroportin useful for studying iron export independent of hepcidin regulation. EDITGENE recommends this model for researchers investigating iron homeostasis, hereditary hemochromatosis, and ferroportin-targeting therapeutic development.

Yes. Ferroportin rescue experiments are well-established in iron biology research: • Construct design: use a codon-modified SLC40A1 sequence with a small C-terminal tag (FLAG, HA). Ferroportin has 12 transmembrane domains — N-terminal tags must not disrupt topology. • Hepcidin-resistant rescue: the C326S mutation prevents hepcidin binding and creates a hepcidin-insensitive ferroportin — invaluable for studying iron export independent of hepcidin regulation. • Disease mutation rescue: A77D (classical 'loss-of-function'), N144H, and other hemochromatosis type 4-associated mutations enable disease genotype-function studies. • Functional readout: rescue should restore ⁵⁹Fe efflux from preloaded cells and hepcidin-induced ferroportin internalization (where wild-type protein is used). HEK293 transduces efficiently with lentivirus and is the standard heterologous expression background for ferroportin biochemistry and disease modeling.