SLC31A2 Knockout HCT116 Cell Line

The choice depends on whether you are studying SLC31A2 (CTR2)'s role as an intracellular low-affinity copper transporter or its emerging functions in lysosomal copper handling. The Knockout line is appropriate for asking whether CTR2 is required for these activities — CTR2 is distinct from CTR1 (SLC31A1, the high-affinity plasma membrane copper importer) and functions primarily at endosomes/lysosomes. Overexpression is useful for studying CTR2 in heterologous expression systems or for assessing platinum chemotherapy resistance mechanisms. For copper biology research, the EDITGENE SLC31A2 Knockout in HCT 116 enables study of intracellular copper trafficking distinct from CTR1-mediated uptake. CTR2 is implicated in resistance to platinum-based chemotherapy (cisplatin, carboplatin) through reduced drug accumulation. Rescue with wild-type or transport-deficient CTR2 is the standard specificity control.

Yes. CTR2 rescue experiments require attention to intracellular targeting: • Construct design: use a codon-modified SLC31A2 sequence with a small C-terminal tag (FLAG, HA). CTR2 has 3 transmembrane domains and intracellular trafficking determinants. • Endosomal/lysosomal localization validation: confirm intracellular localization by LAMP1 or Rab9 co-staining — CTR2 functions primarily at endosomes/lysosomes. • Transport-deficient rescue: methionine-rich motif mutations enable structure-function studies of copper coordination. • Functional readout: rescue should restore intracellular copper handling and platinum chemotherapy sensitivity profiles. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.