TGFBR2 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying TGF-β signaling cascade biology or modeling TGFBR2 loss-of-function in disease contexts (Loeys-Dietz syndrome, microsatellite-instable cancers). The Knockout line is the standard tool for asking whether TGFBR2 is required for SMAD2/3 phosphorylation and downstream TGF-β responses. Overexpression is useful for studying disease-associated TGFBR2 missense mutations or constitutively active variants. For TGF-β pathway research, the EDITGENE TGFBR2 Knockout in HEK293 is a mechanistic platform — HEK293 has a long history in TGF-β signaling research, supporting SMAD reporter assays and rescue with structural variants. Rescue with wild-type, kinase-dead, or disease-mutant TGFBR2 enables structure-function studies and disease modeling.

Primary applications: • SMAD signaling: phospho-SMAD2/3 Western blot and SMAD-responsive reporter (CAGA-luc) assays to assess TGFBR2-dependent canonical TGF-β signaling. • TGF-β responsive gene expression: analysis of canonical TGF-β target genes (PAI-1, SMAD7, p15/CDKN2B) following TGF-β stimulation. • Disease mutation rescue: introduction of Loeys-Dietz syndrome-associated TGFBR2 mutations or MSI-associated truncating mutations for genotype-function studies. • Non-canonical TGF-β signaling: TAK1, MAPK, and PI3K activation analysis to assess TGFBR2-dependent non-SMAD pathways. EDITGENE recommends this model for researchers investigating TGF-β signaling biology, Loeys-Dietz syndrome, and TGFBR2-related cancer biology.

Yes. TGFBR2 rescue experiments are well-established in TGF-β pathway research: • Construct design: use a codon-modified TGFBR2 sequence with a cytoplasmic C-terminal tag (FLAG, HA). TGFBR2 is a type I membrane serine/threonine kinase — extracellular ligand-binding domain and intracellular kinase domain must both be preserved. • Kinase-dead rescue: the K277R mutation in the active site lysine abolishes kinase activity and is the standard control for distinguishing kinase from receptor-binding functions. • Disease mutation rescue: Loeys-Dietz syndrome-associated TGFBR2 mutations or MSI-associated frameshift mutations enable genotype-function studies. • Functional readout: rescue should restore TGF-β-induced SMAD2/3 phosphorylation (Western blot) and CAGA-luc reporter activity. HEK293 transduces efficiently with lentivirus and has established protocols for TGF-β pathway rescue experiments.