RHBDF2 Knockout Cell Line (HEK293)

The choice depends on whether you are studying RHBDF2 (iRhom2)'s role as a tissue-specific regulator of ADAM17/TACE-mediated ectodomain shedding or its emerging functions in inflammatory disease and cancer. The Knockout line is the standard tool for asking whether iRhom2 is required for ADAM17 maturation and substrate selection — iRhom2 is critical for TNF-α release from immune cells and EGFR ligand shedding in epithelial contexts. Overexpression is useful for studying iRhom2's tissue-specific TACE regulation. For inflammation and EGFR signaling research, the EDITGENE RHBDF2 Knockout in HEK293 is a mechanistic platform — HEK293 has been extensively used for iRhom-ADAM17 biochemistry and structure-function studies. This product complements the parallel RHBDF2 Knockout in A-549 and the RHBDF1 & RHBDF2 Double Knockouts (also available); HEK293 is preferred for biochemistry and rescue studies given its high transfection efficiency. RHBDF2 mutations cause tylosis with esophageal cancer (TOC) and curly coat syndrome — disease variant rescue enables genotype-function studies.

Primary applications: • ADAM17 maturation: pro-ADAM17 versus mature ADAM17 Western blot analysis to assess iRhom2's contribution to TACE Golgi maturation. • ADAM17 substrate shedding: TNF-α, TGF-α, amphiregulin, heparin-binding EGF, and other ADAM17 substrate shedding assays. • Tylosis with esophageal cancer modeling: rescue with disease-associated RHBDF2 mutations (e.g., I186T, P189L) for genotype-function studies. • Structure-function studies: rescue with iRhom2 variants in HEK293's high-transfection background for systematic functional dissection. EDITGENE recommends this HEK293-based model for biochemical iRhom2-ADAM17 research; the parallel knockouts in A-549 and double knockouts complement this for paralog and cancer studies.

Yes. iRhom2 rescue experiments are well-established for ADAM17 regulation research: • Construct design: use a codon-modified RHBDF2 sequence with a small C-terminal tag (FLAG, HA). iRhom2 has the rhomboid family 7-transmembrane architecture but lacks catalytic activity (pseudoenzyme) — preserve all elements. • N-terminal cytoplasmic domain mutant rescue: phospho-resistant or phospho-mimetic mutations at key sites in the N-terminal cytoplasmic domain enable studies of 14-3-3-regulated activation. • Tylosis-associated mutation rescue: TOC-associated RHBDF2 mutations (I186T, P189L, D188N) introduced for disease genotype-function studies. • Functional readout: rescue should restore ADAM17 Golgi maturation (mature ADAM17 Western blot) and substrate ectodomain shedding activity. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.