SLC30A10 Knockout HuH-7 Cell Line

The choice depends on whether you are studying SLC30A10 (ZnT10)'s role in manganese efflux or modeling parkinsonism with hypermanganesemia. The Knockout line is the standard tool for asking whether SLC30A10 is required for cellular manganese extrusion — despite its SLC30 'zinc transporter' family designation, SLC30A10 is the principal cellular manganese efflux transporter, distinct from other ZnT family members. Overexpression is useful for testing manganese transport activity in heterologous systems and for rescue with disease-associated mutations. For manganese biology research, the EDITGENE SLC30A10 Knockout in Huh-7 is highly relevant — hepatic SLC30A10 mediates biliary manganese excretion, and its loss-of-function causes hepatic cirrhosis, dystonia, parkinsonism, and polycythemia (HMNDYT1, hypermanganesemia with dystonia type 1). Rescue with wild-type, transport-deficient, or patient-derived mutant SLC30A10 enables comprehensive disease modeling. This product is particularly valuable for manganese-related neurodegenerative disease research.

Primary applications: • Manganese efflux assays: ICP-MS-based intracellular manganese measurement or Mn²⁺-sensitive fluorescent probe imaging following Mn²⁺ loading. • Biliary manganese excretion modeling: SLC30A10-dependent Mn²⁺ extrusion in hepatocyte-derived contexts. • HMNDYT1 disease modeling: rescue with patient-derived SLC30A10 mutations (e.g., L89P, T196P) for genotype-function correlation in this autosomal recessive disorder. • Parkinsonism mechanism research: studies of manganese-induced neurotoxicity and disease relevance. EDITGENE recommends this model for researchers investigating manganese homeostasis, hepatic Mn²⁺ excretion, and HMNDYT1/parkinsonism with hypermanganesemia disease mechanisms.

Yes. SLC30A10 rescue experiments are well-established for manganese biology research: • Construct design: use a codon-modified SLC30A10 sequence with a small C-terminal tag (FLAG, HA). The 6 transmembrane ZnT family architecture must be preserved. • Disease mutation rescue: HMNDYT1-associated patient mutations (L89P, T196P, frameshift mutations) enable comprehensive disease genotype-function studies. • Surface localization validation: confirm plasma membrane localization by cell surface biotinylation — many disease mutations cause trafficking defects. • Functional readout: rescue should restore cellular manganese efflux measured by ICP-MS or Mn²⁺ fluorescent probes following manganese loading. Huh-7 transduces efficiently with lentivirus and supports stable rescue line generation in a hepatocyte-derived background appropriate for biliary Mn²⁺ excretion studies.