ITGB8 Knockout Cell Line (Hela)

The choice depends on whether you are studying ITGB8 (integrin β8)'s role as a TGF-β-activating integrin or its functions in vascular development and immune regulation. The Knockout line is the standard tool for asking whether ITGB8 is required for these processes — ITGB8 partners exclusively with ITGAV (αv) to form the αvβ8 integrin, which uniquely activates latent TGF-β through binding the RGD motif of the latent TGF-β complex without requiring intracellular force, distinct from other αv-integrins. Overexpression is useful for studying ITGB8 gain-of-function effects. For TGF-β and integrin research, the EDITGENE ITGB8 Knockout in HeLa is highly informative — αvβ8 is a major mechanism of latent TGF-β activation in vivo, particularly in dendritic cells, regulatory T cells, and brain pericytes. Rescue with wild-type or RGD-binding-deficient ITGB8 is the standard specificity control. The knockout is a critical specificity tool for anti-αvβ8 antibodies (e.g., 37E1, PF-06940434, BG00011/STX-100 related) in clinical development for cancer immunotherapy — αvβ8 inhibition releases tumor-immunosuppressive TGF-β from latent stores and enhances anti-PD-1 responses.

Primary applications: • Latent TGF-β activation: SMAD2/3 phosphorylation and TGF-β reporter assays following co-culture with latent-TGF-β-presenting cells to characterize αvβ8-dependent TGF-β release. • αvβ8 antibody specificity: critical genetic control for 37E1, PF-06940434, and other anti-αvβ8 antibodies in cancer immunotherapy development. • Tumor immune evasion: in heterologous immune-relevant contexts, characterization of αvβ8-driven TGF-β-mediated Treg expansion and effector T cell suppression. • Combination immunotherapy: αvβ8 inhibition + anti-PD-1/PD-L1 combination studies in tumor immune evasion models. EDITGENE recommends this model for researchers investigating αvβ8 biology, latent TGF-β activation mechanisms, and emerging αvβ8-targeted cancer immunotherapeutic development.

Yes. ITGB8 rescue experiments require attention to αv heterodimer formation: • Construct design: use a codon-modified ITGB8 sequence with a small intracellular C-terminal tag (FLAG, HA). ITGB8 has extracellular β-I domain (RGD binding), single transmembrane span, and short cytoplasmic tail — preserve all elements. • Surface localization validation: confirm plasma membrane αvβ8 heterodimer formation by cell surface staining before functional assays. • RGD-binding-deficient rescue: β-I domain MIDAS site mutations abolish RGD binding and serve as the standard specificity control. • ITGAV partnership: ITGB8 requires ITGAV for surface expression — rescue interpretation considers αv levels. • Functional readout: rescue should restore αvβ8-dependent latent TGF-β activation measured by SMAD2/3 phosphorylation. HeLa transduces efficiently with lentivirus and supports stable rescue line generation.