CD74 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying CD74 (invariant chain, Ii, MHC class II invariant chain)'s role as the MHC class II chaperone or modeling its functions as the macrophage migration inhibitory factor (MIF) receptor and emerging cancer immunotherapy applications. The Knockout line is the standard tool for asking whether CD74 is required for these processes — CD74 has dual functions: (1) as the MHC class II invariant chain in APCs, where the CD74 CLIP region occupies the MHC II peptide groove during ER-to-MIIC trafficking; (2) as the cell surface MIF receptor (with CD44 co-receptor) that mediates pro-inflammatory and pro-survival MIF signaling in macrophages, B cells, and cancer cells. Overexpression is useful for studying CD74 gain-of-function effects. For immunology and cancer therapy research, the EDITGENE CD74 Knockout in HEK293 is highly valuable — HEK293 supports systematic structure-function studies of CD74. Rescue with wild-type or CLIP-deficient CD74 enables structure-function studies. The knockout is a critical specificity tool for ⭐ milatuzumab (anti-CD74 antibody in clinical development for hematologic malignancies), STRO-001 (CD74-ADC), ISB 1442 (CD74×CD47 bispecific), MIF-targeted therapies (ibudilast affects MIF signaling), and emerging CD74-targeted approaches in B-cell lymphomas and inflammatory diseases.

Primary applications: • MHC class II chaperone: in heterologous APC-relevant contexts, MHC II-CD74 trafficking through ER-Golgi-MIIC compartments. • MIF receptor signaling: MIF-induced phospho-ERK, phospho-AKT, and NF-κB activation analysis in CD74-null cells. • Anti-CD74 antibody specificity: critical genetic control for ⭐ milatuzumab, STRO-001 (CD74-ADC), ISB 1442 (CD74×CD47 bispecific) in B-cell lymphoma and inflammatory disease development. • MIF antagonist studies: ibudilast and MIF-targeted compound mechanism studies. EDITGENE recommends this model as a critical specificity control for CD74-targeted therapeutics in hematologic malignancies and inflammatory diseases.

Yes. CD74 rescue experiments require attention to type II membrane topology and dual functions: • Construct design: use a codon-modified CD74 sequence with a small intracellular N-terminal tag (FLAG, HA) — CD74 is a type II transmembrane protein with intracellular N-terminus and extracellular C-terminus (with CLIP and trimerization regions); N-terminal tag preserves extracellular regions. • Surface localization validation: confirm plasma membrane CD74 by cell surface staining for MIF receptor assays. • CLIP-deficient rescue: CLIP region mutations affect MHC II peptide loading but may preserve MIF receptor function — useful for separating CD74's two functions. • Functional readout: rescue should restore MHC II maturation (in APC-relevant contexts) and MIF-induced signaling. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.