SLC39A4 Knockout Cell Line (HCT 116)

The choice depends on whether you are studying SLC39A4 (ZIP4)'s role in intestinal zinc absorption or modeling acrodermatitis enteropathica. The Knockout line is the standard tool for asking whether ZIP4 is required for cellular zinc uptake — ZIP4 is the principal apical zinc transporter in intestinal epithelium and is essential for systemic zinc homeostasis. Overexpression is useful for testing whether elevated ZIP4 enhances zinc uptake or for studying cancer-associated ZIP4 upregulation (pancreatic cancer, others). For ZIP4 research, the EDITGENE Knockout in HCT 116 is particularly relevant for intestinal zinc absorption biology in a colorectal cancer-derived background. SLC39A4 mutations cause acrodermatitis enteropathica (autosomal recessive zinc deficiency syndrome) — disease variant rescue enables genotype-function correlation studies. Rescue with wild-type or transport-deficient ZIP4 is the standard specificity control.

Primary applications: • Intestinal zinc uptake: FluoZin-3 imaging or ⁶⁵Zn uptake assays to quantify ZIP4-dependent zinc transport in a colorectal-relevant context. • Acrodermatitis enteropathica modeling: rescue with patient-derived SLC39A4 mutations for disease genotype-function correlation studies. • Cancer biology: studies of ZIP4 contribution to pancreatic and colorectal cancer where ZIP4 upregulation has been reported. • Apical surface localization: rescue with epitope-tagged ZIP4 to study trafficking determinants in an intestinal-derived background. EDITGENE recommends this model for researchers investigating intestinal zinc absorption, acrodermatitis enteropathica mechanisms, and ZIP4-related cancer biology.

Yes. ZIP4 rescue experiments are well-established for zinc biology research: • Construct design: use a codon-modified SLC39A4 sequence with a small C-terminal tag (FLAG, HA). ZIP4 has 8 transmembrane domains and an N-terminal extracellular ectodomain — preserve both elements. • Disease mutation rescue: acrodermatitis enteropathica-associated SLC39A4 mutations (e.g., G643R, P200L) enable disease genotype-function studies. • Surface localization validation: confirm plasma membrane localization of exogenous ZIP4 by cell surface staining before zinc uptake assays. • Functional readout: rescue should restore zinc uptake activity measured by FluoZin-3 imaging or ⁶⁵Zn uptake. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.