SLC4A4 Knockout HuH-7 Cell Line

The choice depends on whether you are studying SLC4A4 (NBCe1)'s role in sodium-bicarbonate cotransport or its specific functions in pH homeostasis and bicarbonate handling. The Knockout line is the standard tool for asking whether NBCe1 is required for these activities — NBCe1 is the principal electrogenic sodium-bicarbonate cotransporter in kidney, eye, and pancreas. Overexpression is useful for studying NBCe1 splice variants (NBCe1-A, -B, -C, -D) or for modeling proximal renal tubular acidosis mutations. For bicarbonate transport research, the EDITGENE SLC4A4 Knockout in Huh-7 enables study of hepatic bicarbonate handling and pH regulation. SLC4A4 mutations cause autosomal recessive proximal renal tubular acidosis with ocular abnormalities — disease variant rescue enables genotype-function studies. Rescue with wild-type, splice variant-specific, or transport-deficient NBCe1 enables comprehensive structure-function analysis.

Primary applications: • Sodium-bicarbonate cotransport: BCECF-based intracellular pH measurement following bicarbonate addition to quantify NBCe1 activity. • Splice variant studies: rescue with NBCe1-A, -B, -C, or -D variants to dissect tissue-specific functional differences. • Disease mutation modeling: rescue with autosomal recessive proximal renal tubular acidosis-associated SLC4A4 mutations. • Electrogenicity studies: patch-clamp electrophysiology where electrogenic cotransport can be directly measured. EDITGENE recommends this model for researchers investigating bicarbonate transport, pH homeostasis, and proximal renal tubular acidosis mechanisms.

Yes. NBCe1 rescue experiments require attention to splice variant biology: • Construct design: use a codon-modified SLC4A4 sequence with a small C-terminal tag (FLAG, HA). The 14 transmembrane SLC4 architecture must be preserved. • Splice variant-specific rescue: NBCe1-A (kidney), -B (eye/pancreas/heart), -C (brain), and -D (gastrointestinal) variants enable tissue-specific function dissection. • Disease mutation rescue: autosomal recessive proximal renal tubular acidosis-associated mutations enable disease modeling. • Functional readout: rescue should restore sodium-bicarbonate cotransport measured by intracellular pH dynamics and short-circuit current where applicable. Huh-7 transduces efficiently with lentivirus and supports stable rescue line generation.