SLC13A5 Knockout HuH-7 Cell Line

The choice depends on whether you are studying SLC13A5 (INDY, Citrate Transporter)'s role in hepatic citrate uptake or modeling early infantile epileptic encephalopathy 25. The Knockout line is the standard tool for asking whether SLC13A5 is required for cellular citrate uptake — SLC13A5 is the principal hepatic plasma membrane citrate importer, mediating sodium-coupled citrate uptake for cytoplasmic acetyl-CoA generation and de novo lipogenesis. Overexpression is useful for studying SLC13A5 as a metabolic disease target. For metabolic disease research, the EDITGENE SLC13A5 Knockout in Huh-7 is highly relevant — Huh-7 has hepatocellular origin matching SLC13A5's physiological context. SLC13A5 mutations cause EIEE25 (autosomal recessive early infantile epileptic encephalopathy with elevated CSF citrate) — disease variant rescue enables genotype-function studies. SLC13A5 is also a metabolic disease therapeutic target (mINDY): inhibition is investigated for fatty liver disease and type 2 diabetes. Rescue with wild-type or transport-deficient SLC13A5 is the standard specificity control.

Primary applications: • Citrate uptake: ³H-citrate or ¹⁴C-citrate uptake under sodium-replete conditions to quantify SLC13A5 transport activity. • De novo lipogenesis: ¹⁴C-acetate incorporation into lipids to assess SLC13A5-dependent citrate-derived acetyl-CoA flux. • EIEE25 disease modeling: rescue with patient-derived SLC13A5 mutations for genotype-function correlation studies. • mINDY therapeutic development: critical genetic specificity control for SLC13A5 inhibitors in development for fatty liver disease and type 2 diabetes. EDITGENE recommends this model for researchers investigating hepatic citrate metabolism, EIEE25 disease mechanisms, and SLC13A5-targeted metabolic disease therapeutics.

Yes. SLC13A5 rescue experiments are well-established for hepatic citrate biology: • Construct design: use a codon-modified SLC13A5 sequence with a small C-terminal tag (FLAG, HA). The 11-transmembrane SLC13 architecture must be preserved. • EIEE25 mutation rescue: patient-derived SLC13A5 mutations enable disease genotype-function correlation studies. • Transport-deficient rescue: substrate-binding pocket mutations enable structure-function studies and inhibitor specificity research. • Functional readout: rescue should restore sodium-dependent citrate uptake and downstream lipogenesis from citrate-derived acetyl-CoA. Huh-7 transduces efficiently with lentivirus and supports stable rescue line generation in a hepatocyte-relevant context.