SLC43A2 Knockout Cell Line (HEK293)

The choice depends on whether you are studying SLC43A2 (LAT4)'s role in basolateral large neutral amino acid efflux or its specific contributions distinct from LAT1/LAT2. The Knockout line is the standard tool for asking whether LAT4 is required for sodium-independent transport of branched-chain amino acids (leucine, isoleucine, valine), methionine, and phenylalanine — particularly relevant in epithelial transepithelial amino acid handling. Overexpression is useful for transport kinetics studies — notably, LAT4 functions independently of 4F2hc unlike LAT1 and LAT2. For LAT family research, the EDITGENE SLC43A2 Knockout in HEK293 is a mechanistic platform distinct from heterodimeric LAT1/LAT2 — LAT4 is a uniporter that does not require 4F2hc partnership, simplifying transport activity reconstitution. Rescue with wild-type or transport-deficient LAT4 enables structure-function studies and substrate specificity characterization independent of heterodimer assembly considerations.

Primary applications: • Branched-chain amino acid efflux: ³H-leucine, ³H-valine, ³H-isoleucine efflux assays to characterize LAT4-mediated transport without confounding 4F2hc heterodimer considerations. • Comparative LAT family studies: parallel analysis with LAT1 and LAT2 (also available from EDITGENE) to dissect transporter-specific functions. • Cancer metabolism studies: assessment of LAT4 contribution to amino acid handling in cancer contexts. • Inhibitor specificity: critical genetic control for LAT4-selective compound development. EDITGENE recommends this model for researchers investigating large neutral amino acid efflux biology and LAT family transporter pharmacology.

Yes. LAT4 rescue experiments are well-established for amino acid transport research: • Construct design: use a codon-modified SLC43A2 sequence with a small C-terminal tag (FLAG, HA). The 12 transmembrane architecture must be preserved. • 4F2hc independence: unlike LAT1 and LAT2, LAT4 does not require 4F2hc for surface expression — rescue can be performed without co-expression considerations. • Transport-deficient rescue: substrate-binding pocket mutations enable structure-function studies. • Functional readout: rescue should restore branched-chain amino acid uptake measured by radiolabel or LC-MS. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.