DDR2 Knockout HCT116 Cell Line

The choice depends on whether you are studying DDR2 (discoidin domain receptor 2)'s role as a collagen-activated receptor tyrosine kinase or modeling its functions in fibrosis, cancer, and skeletal dysplasia. The Knockout line is the standard tool for asking whether DDR2 is required for these processes — DDR1 and DDR2 constitute the discoidin domain receptor family, unique among RTKs in being activated by fibrillar collagens (DDR1 binds collagens I-V, VIII; DDR2 binds collagens I, II, III) rather than soluble growth factors; collagen binding induces slow, sustained DDR2 autophosphorylation. Overexpression is useful for studying DDR2 gain-of-function effects. For DDR2 research, the EDITGENE DDR2 Knockout in HCT 116 enables study of DDR2 biology in colorectal cancer context. DDR2 activating mutations are characteristic of squamous cell lung carcinoma (~4% of cases, e.g., L63V, S768R, I638F kinase domain mutations); DDR2 loss-of-function mutations cause spondylo-meta-epiphyseal dysplasia (SMED-SL/Al-Awadi-Teebi syndrome). Rescue with wild-type, kinase-dead, or disease-mutant DDR2 enables comprehensive structure-function studies. The knockout is a critical specificity tool for DDR2 inhibitors (dasatinib, imatinib have DDR2 activity; selective DDR2 inhibitors in development) and emerging anti-fibrosis therapeutics.

Primary applications: • Collagen-induced activation: type I/II/III collagen-induced phospho-DDR2 (Y740) Western blot analysis. • Lung cancer mutation modeling: rescue with squamous cell lung carcinoma DDR2 mutations (L63V, S768R, I638F) for genotype-function studies. • Skeletal dysplasia modeling: rescue with SMED-SL patient-derived DDR2 mutations for autosomal recessive dysplasia studies. • DDR2 inhibitor specificity: critical genetic control for selective DDR2 inhibitors and pan-RTK inhibitors with DDR2 activity (dasatinib). EDITGENE recommends this model for researchers investigating DDR2 collagen-receptor biology, squamous lung cancer mutation pharmacology, and SMED-SL disease modeling.

Yes. DDR2 rescue experiments are well-established for collagen receptor research: • Construct design: use a codon-modified DDR2 sequence with a small intracellular C-terminal tag (FLAG, HA). DDR2 has extracellular discoidin-like domain (collagen binding), discoidin-like domain 2, single transmembrane span, juxtamembrane region, and intracellular kinase domain — preserve all elements. • Surface localization validation: confirm plasma membrane localization before collagen binding studies. • Kinase-dead rescue: K608E mutation in the ATP-binding lysine abolishes catalytic activity. • Lung cancer mutation rescue: L63V, S768R, I638F mutations enable squamous cell lung carcinoma disease modeling. • Functional readout: rescue should restore collagen-induced phospho-DDR2 (Y740) signaling. HCT 116 transduces efficiently with lentivirus and supports stable rescue line generation.