SLC2A2 Knockout HuH-7 Cell Line

The choice depends on whether you are studying SLC2A2 (GLUT2)'s role as the principal hepatic glucose transporter or modeling Fanconi-Bickel syndrome and diabetes-related glucose handling. The Knockout line is the standard tool for asking whether GLUT2 is required for bidirectional glucose transport — GLUT2 is the major glucose transporter in hepatocytes, pancreatic β-cells, and enterocytes, mediating both glucose uptake and release. Overexpression is useful for studying GLUT2 substrate selectivity (it transports glucose, fructose, galactose, and glucosamine). For hepatic glucose research, the EDITGENE GLUT2 Knockout in Huh-7 is highly relevant — Huh-7 has hepatocellular origin and supports physiologically meaningful glucose transport studies. SLC2A2 mutations cause Fanconi-Bickel syndrome (hepatomegaly, renal Fanconi syndrome, glucose intolerance) — disease variant rescue enables genotype-function correlation studies. Rescue with wild-type or transport-deficient GLUT2 is the standard specificity control.

Primary applications: • Glucose uptake/release assays: ³H-2-deoxyglucose uptake and ³H-glucose efflux to characterize bidirectional GLUT2 transport. • Substrate specificity: comparative uptake of glucose, fructose, galactose, and glucosamine to assess GLUT2's broad substrate scope. • Fanconi-Bickel syndrome modeling: rescue with patient-derived SLC2A2 mutations for genotype-function correlation studies. • Glucose sensing biology: studies of GLUT2's role in glucose-sensing functions in hepatocyte-derived contexts. EDITGENE recommends this model for researchers investigating hepatic glucose transport biology, Fanconi-Bickel syndrome mechanisms, and GLUT family substrate specificity.

Yes. GLUT2 rescue experiments are well-established in hepatic glucose biology: • Construct design: use a codon-modified SLC2A2 sequence with a small C-terminal tag (FLAG, HA). GLUT2 has 12 transmembrane domains — preserve plasma membrane targeting determinants. • Surface localization validation: confirm plasma membrane localization by cell surface biotinylation before glucose transport assays. • Disease mutation rescue: Fanconi-Bickel syndrome-associated SLC2A2 mutations enable genotype-function studies. • Functional readout: rescue should restore glucose, fructose, and galactose transport activities measured by radiolabel or LC-MS uptake assays. Huh-7 transduces efficiently with lentivirus and supports stable rescue line generation in a hepatocyte-derived background appropriate for GLUT2 functional studies.