SLC7A5 Knockout Cell Line (Hela)

The choice depends on whether you are studying SLC7A5 (LAT1)'s role in mTORC1-regulating leucine transport or its emerging functions in cancer biology and drug delivery. The Knockout line is the standard tool for asking whether LAT1 is required for large neutral amino acid (leucine, isoleucine, valine, methionine, phenylalanine) uptake — LAT1 is upregulated in many cancers and is a target for both PET imaging (¹⁸F-FDOPA) and therapeutics. Overexpression is useful for testing transport activity (requires 4F2hc partnership) or for studying LAT1 in cancer contexts where it is amplified. For LAT1 research, the EDITGENE Knockout in HeLa is a well-characterized cancer cell line for studying amino acid transporter biology and mTORC1 nutrient signaling. Rescue with wild-type or transport-deficient LAT1 enables structure-function studies, and is particularly valuable as a specificity control for LAT1 inhibitors (JPH203/nanvuranlat, others) in clinical development.

Primary applications: • Large neutral amino acid uptake: ³H-leucine, ³H-phenylalanine, or LC-MS-based uptake assays to quantify LAT1-dependent transport. • mTORC1 nutrient signaling: phospho-S6K1, phospho-4E-BP1 analysis under amino acid replete/depleted conditions in the absence of LAT1. • Cancer phenotype studies: proliferation, autophagy, and cell death assays relevant to LAT1's role in supporting tumor growth. • LAT1 inhibitor specificity: critical genetic control for JPH203/nanvuranlat and other LAT1-targeting compounds in clinical development. EDITGENE recommends this model for researchers investigating LAT1 transporter biology, mTORC1 nutrient signaling, and LAT1-targeted cancer pharmacology.

Yes. LAT1 rescue experiments are well-established in transporter pharmacology research: • Construct design: use a codon-modified SLC7A5 sequence with a small C-terminal tag (FLAG, HA). The 12 transmembrane topology must be preserved. • 4F2hc partnership: LAT1 requires 4F2hc for functional surface expression — HeLa expresses 4F2hc endogenously, but high-level LAT1 rescue may require 4F2hc co-expression for stoichiometric balance. • Transport-deficient rescue: substrate-binding mutations or established inhibitor-binding residue mutations enable structure-function studies. • Functional readout: rescue should restore large neutral amino acid uptake (³H-leucine) and downstream mTORC1 activation under amino acid challenge. HeLa transduces efficiently with lentivirus and is well-validated for LAT1 functional studies.