SLC37A4 Knockout Cell Line (HEK293)

The choice depends on whether you are studying SLC37A4 (glucose-6-phosphate translocase/G6PT)'s role in hepatic and renal glucose-6-phosphate transport or modeling glycogen storage disease type Ib. The Knockout line is the standard tool for asking whether G6PT is required for transporting glucose-6-phosphate across the ER membrane — G6PT partners with glucose-6-phosphatase to enable gluconeogenesis and glycogenolysis. Overexpression is useful for testing rescue with disease-associated mutations or for biochemical reconstitution studies. For glucose metabolism research, the EDITGENE SLC37A4 Knockout in HEK293 is a mechanistic platform, though physiological gluconeogenesis requires hepatic models. SLC37A4 mutations cause glycogen storage disease type Ib (GSD1b), characterized by hypoglycemia, neutropenia, and inflammatory bowel disease — disease variant rescue enables genotype-function studies. Empagliflozin has been shown to treat GSD1b neutropenia, making this knockout relevant for SGLT2 inhibitor mechanism studies in this context.

Primary applications: • Glucose-6-phosphate transport: in vitro G6P transport assays using ER membrane preparations from knockout versus wild-type cells. • GSD1b modeling: rescue with patient-derived SLC37A4 mutations for glycogen storage disease type Ib genotype-function studies. • Empagliflozin mechanism studies: assessment of SGLT2 inhibitor effects in GSD1b context where empagliflozin treats neutropenia. • Glucose-6-phosphatase (G6PC) coupling: combined G6PT-G6PC reconstitution studies in heterologous systems. EDITGENE recommends this model for researchers investigating glucose-6-phosphate transport biology, GSD1b mechanisms, and emerging treatments for this disease.

Yes. G6PT rescue experiments are well-established for GSD1b research: • Construct design: use a codon-modified SLC37A4 sequence with a small cytoplasmic C-terminal tag (FLAG, HA). G6PT is an ER membrane protein with 10 transmembrane domains — preserve ER targeting determinants. • ER localization validation: confirm ER localization by calnexin co-staining before functional assays. • GSD1b mutation rescue: patient-derived SLC37A4 mutations (e.g., R28H, W118R, common deletions) enable comprehensive disease genotype-function studies. • Functional readout: rescue should restore glucose-6-phosphate translocation activity measured in microsomal preparations. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.