SLC39A13 Knockout HCT116 Cell Line

The choice depends on whether you are studying SLC39A13 (ZIP13)'s role as a Golgi/ER-localized zinc transporter or modeling spondylocheirodysplastic Ehlers-Danlos syndrome (SCD-EDS). The Knockout line is the standard tool for asking whether ZIP13 is required for zinc release from intracellular compartments — ZIP13 functions in the Golgi/ER rather than at the plasma membrane, distinguishing it from many other ZIP family members. Overexpression is useful for studying ZIP13's role in secretory pathway function and connective tissue biology. For ZIP13 research, the EDITGENE Knockout in HCT 116 enables study of intracellular zinc trafficking and ER/Golgi zinc-dependent processes. SLC39A13 mutations cause SCD-EDS, characterized by connective tissue abnormalities — disease variant rescue enables genotype-function studies in a controlled background. Rescue with wild-type or transport-deficient ZIP13 is the standard specificity control.

Primary applications: • Intracellular zinc trafficking: subcellular zinc distribution analysis using FluoZin-3 imaging and organelle-targeted zinc sensors. • Golgi/ER zinc function: analysis of zinc-dependent secretory pathway processes and collagen processing. • SCD-EDS modeling: rescue with patient-derived SLC39A13 mutations for connective tissue disease genotype-function correlation. • ZIP family compensation: ZIP7 (also Golgi-localized) expression analysis to interpret ZIP13-specific phenotypes. EDITGENE recommends this model for researchers investigating intracellular zinc transport, connective tissue biology, and SCD-EDS disease mechanisms.

Yes. ZIP13 rescue experiments require attention to intracellular targeting: • Construct design: use a codon-modified SLC39A13 sequence with a small C-terminal tag (FLAG, HA). ZIP13 has 8 transmembrane domains with Golgi/ER targeting determinants. • Intracellular localization validation: confirm Golgi/ER localization of exogenous ZIP13 by GM130 or KDEL co-staining before functional assays. • SCD-EDS mutation rescue: patient-derived SLC39A13 mutations (e.g., G64D, frameshift mutations) enable connective tissue disease modeling. • Functional readout: rescue should restore intracellular zinc trafficking and zinc-dependent collagen processing. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.