ITGB7 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying ITGB7 (integrin β7)'s role as the principal gut-homing integrin or modeling its functions in mucosal immunity and inflammatory bowel disease. The Knockout line is the standard tool for asking whether ITGB7 is required for these processes — ITGB7 partners with ITGA4 (forming α4β7, the gut-homing integrin binding MAdCAM-1) and ITGAE (forming αEβ7, the intraepithelial lymphocyte integrin binding E-cadherin). Overexpression is useful for studying ITGB7 in heterologous expression contexts. For mucosal immunity research, the EDITGENE ITGB7 Knockout in HEK293 enables study of β7-integrin biology — α4β7 is the molecular basis of gut-homing lymphocyte trafficking. Rescue with wild-type or ligand-binding-deficient ITGB7 is the standard specificity control. The knockout is a critical specificity tool for vedolizumab (anti-α4β7, FDA-approved for IBD), etrolizumab (anti-β7, investigated for IBD/colitis), and emerging β7-integrin-targeted IBD therapeutics.

Primary applications: • α4β7-MAdCAM-1 binding: in heterologous co-culture systems, characterization of α4β7-dependent lymphocyte adhesion to MAdCAM-1-expressing cells. • Gut-homing biology: in heterologous lymphocyte-relevant contexts, characterization of β7-integrin-dependent gut-homing receptor function. • Vedolizumab specificity: critical genetic control for vedolizumab (anti-α4β7, FDA-approved for IBD) — the antibody should have no effect in ITGB7-null cells. • Etrolizumab studies: critical genetic control for etrolizumab (anti-β7, investigated for ulcerative colitis and Crohn's disease). EDITGENE recommends this model for researchers investigating mucosal immunity, gut-homing receptor biology, and β7-integrin-targeted IBD therapeutic development.

Yes. ITGB7 rescue experiments require attention to integrin heterodimer formation: • Construct design: use a codon-modified ITGB7 sequence with a small intracellular C-terminal tag (FLAG, HA). ITGB7 has the canonical β-integrin architecture — preserve extracellular and cytoplasmic regions. • Surface localization validation: confirm α4β7 and αEβ7 heterodimer surface expression before functional assays. • Ligand-binding-deficient rescue: β-I domain MIDAS site mutations abolish MAdCAM-1/E-cadherin binding. • ITGA4 and ITGAE partnership: ITGB7 partners with ITGA4 (forming α4β7) and ITGAE (forming αEβ7) — rescue interpretation considers α-subunit availability. • Functional readout: rescue should restore MAdCAM-1 and E-cadherin binding-dependent cell adhesion. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.