SLC15A4 Knockout Cell Line (HCT 116)

The choice depends on whether you are studying SLC15A4 (PHT1)'s role as an endolysosomal histidine/peptide transporter or its emerging functions in innate immunity and SLE pathogenesis. The Knockout line is the standard tool for asking whether SLC15A4 is required for endolysosomal nucleotide delivery to TLR7/TLR9 and NOD1/NOD2 — SLC15A4 transports histidine and small peptides into the endolysosomal lumen and is required for nucleic acid sensor activation. Overexpression is useful for studying SLC15A4 in TLR signaling or autoimmunity contexts. For autoimmunity research, the EDITGENE SLC15A4 Knockout in HCT 116 is particularly valuable — SLC15A4 has been identified as a systemic lupus erythematosus (SLE) susceptibility gene through GWAS, and Slc15a4-deficient mice are protected from lupus models. TLR7/TLR9 signaling readouts (IFN-α, IRF7 activation) characterize SLC15A4's adaptor-like role. Rescue with wild-type or transport-deficient SLC15A4 enables structure-function studies. SLC15A4 is being investigated as a therapeutic target for SLE.

Primary applications: • TLR7/TLR9 signaling: IFN-α production, IRF7 activation following endosomal TLR ligand stimulation (CpG, R848, imiquimod). • Histidine/peptide transport: ³H-histidine and dipeptide uptake assays in endolysosomal preparations. • NOD-like receptor signaling: NOD1 and NOD2 activation following intracellular bacterial product delivery. • SLE therapeutic development: SLC15A4 inhibitor specificity testing in this lupus susceptibility gene knockout — critical for emerging SLE drug development. EDITGENE recommends this model for researchers investigating endosomal innate immunity, autoimmune disease mechanisms, and SLC15A4-targeted SLE therapeutic development.

Yes. SLC15A4 rescue experiments are well-established for immune signaling research: • Construct design: use a codon-modified SLC15A4 sequence with a small C-terminal tag (FLAG, HA). SLC15A4 has 12 transmembrane domains with endolysosomal targeting determinants. • Endolysosomal localization validation: confirm endolysosomal localization by LAMP1 co-staining before functional assays. • Transport-deficient rescue: substrate-binding pocket mutations enable distinguishing histidine/peptide transport from adaptor/scaffolding functions in TLR signaling. • Functional readout: rescue should restore endosomal TLR7/TLR9 signaling activity and histidine/peptide transport. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.