FXYD6 Knockout Cell Line (HEK293)

The choice depends on the experimental question. FXYD6 (FXYD domain containing ion transport regulator 6) is a member of the FXYD family of small transmembrane proteins that modulate Na⁺/K⁺-ATPase activity and have emerging associations with schizophrenia susceptibility. The Knockout line is appropriate for asking whether FXYD6 is required for predicted activities — FXYD family proteins (FXYD1/phospholemman, FXYD2/γ-subunit, FXYD4/CHIF, FXYD6) bind Na⁺/K⁺-ATPase α-subunits to modulate enzyme kinetics, Na⁺/K⁺ affinity, and tissue-specific function; FXYD6 is principally expressed in cochlea and brain, and has been associated with schizophrenia by GWAS. Overexpression is useful for studying FXYD6 in heterologous expression contexts. For FXYD family research, the EDITGENE FXYD6 Knockout in HEK293 enables clean genetic background studies — HEK293 supports systematic structure-function studies. Other FXYD family member expression analysis aids interpretation given partial functional overlap. Rescue with wild-type or Na⁺/K⁺-ATPase-binding-deficient FXYD6 enables structure-function studies. This product complements the parallel FXYD6 Knockout in HCT 116 (also available) for cross-background validation. The knockout is valuable for studying FXYD6's role in Na⁺/K⁺-ATPase regulation and emerging schizophrenia susceptibility biology.

Primary applications: • Na⁺/K⁺-ATPase modulation: in vitro Na⁺/K⁺-ATPase kinetic analysis (Na⁺ K0.5, K⁺ K0.5, Vmax) with FXYD6 reconstitution. • Schizophrenia susceptibility studies: rescue with FXYD6 polymorphic variants associated with schizophrenia for genotype-function studies. • FXYD family comparative studies: FXYD1, FXYD2, FXYD3, FXYD4, FXYD5, FXYD7 expression analysis for family-wide regulation studies. • Co-immunoprecipitation with Na⁺/K⁺-ATPase α-subunits: ATP1A1, ATP1A2, ATP1A3 binding analysis. EDITGENE recommends this HEK293-based model for biochemical FXYD6 research; the parallel FXYD6 Knockout in HCT 116 (also available) is useful for cross-background validation.

Yes. FXYD6 rescue experiments require attention to small transmembrane protein architecture: • Construct design: use a codon-modified FXYD6 sequence with a small intracellular C-terminal tag (FLAG, HA) — FXYD6 is a small (~95 aa) protein with N-terminal signal peptide, FXYD-motif-containing extracellular region, single transmembrane span, and short cytoplasmic tail; preserve membrane topology. • Surface localization validation: confirm plasma membrane localization by cell surface staining before functional assays. • Na⁺/K⁺-ATPase-binding-deficient rescue: FXYD motif mutations (the conserved PFXYD core) disrupt α-subunit binding and serve as the standard specificity control. • Functional readout: rescue should restore FXYD6-dependent Na⁺/K⁺-ATPase kinetic modulation. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.