SLC4A11 Knockout Cell Line (HCT 116)

The choice depends on whether you are studying SLC4A11 (NaBC1)'s role in sodium-borate cotransport, ammonia transport, or its emerging functions in mitochondrial uncoupling and corneal endothelial dystrophy. The Knockout line is the standard tool for asking whether SLC4A11 is required for these activities — SLC4A11 is genetically linked to congenital hereditary endothelial dystrophy 2 (CHED2), Harboyan syndrome, and Fuchs endothelial corneal dystrophy. Overexpression is useful for studying disease-associated SLC4A11 mutations or for testing transport activity in heterologous systems. For SLC4A11 research, the EDITGENE Knockout in HCT 116 enables mechanistic studies of NH₃/H⁺ transport and emerging mitochondrial functions, though corneal endothelial physiology requires corneal endothelial cell models. Rescue with wild-type, transport-deficient, or CHED2-associated mutant SLC4A11 is the standard approach for genotype-function correlation studies and mechanistic dissection.

Primary applications: • Transport activity assays: ammonia transport (NH₃/H⁺) and borate transport assays to characterize SLC4A11 substrate handling. • Mitochondrial function: Seahorse OCR/ECAR measurements and mitochondrial uncoupling assessment given SLC4A11's reported inner mitochondrial membrane functions. • CHED2/Harboyan syndrome modeling: rescue with disease-associated SLC4A11 variants for genotype-function correlation in a controlled background. • Corneal endothelial-relevant biochemistry: SLC4A11 substrate handling in HCT 116 background, complementing physiological studies in corneal endothelial models. EDITGENE recommends this model for researchers investigating SLC4A11 transporter biology and corneal endothelial dystrophy disease mechanisms.

Yes. SLC4A11 rescue experiments require attention to membrane targeting and CHED2 disease biology: • Construct design: use a codon-modified SLC4A11 sequence with a small C-terminal tag (FLAG, HA). SLC4A11 has 14 transmembrane domains in the SLC4 family architecture — N-terminal tags must not disrupt membrane topology. • Disease mutation rescue: CHED2-associated mutations (e.g., R109H, G583R) and Harboyan syndrome variants enable comprehensive disease genotype-function correlation. • Surface localization validation: many CHED2 mutations cause ER retention rather than transport defects — surface biotinylation distinguishes trafficking from transport defects. • Functional readout: rescue should restore NH₃/H⁺ transport activity measured by intracellular pH dynamics. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.