This product is a polyclonal population of CRISPR/Cas9-edited Jurkat cells harboring a disruption of the ITGB8 gene. ITGB8 encodes the integrin ??8 subunit required for ??v??8 integrin heterodimer formation. The polyclonal knockout cells provide a loss-of-function model to interrogate ITGB8-dependent functions in a human T lymphocyte background.
Jurkat cells are an immortalized human T lymphocyte line derived from acute T cell leukemia. They are widely used to study T cell receptor signaling, apoptosis, and intracellular signaling cascades. The Jurkat background is well-suited for examining integrin and cytokine functions in T cells due to its robust signaling networks and genetic tractability.
ITGB8 partners with ITGAV to form integrin ??v??8, which binds the latency-associated peptide (LAP) of TGF-?? and promotes its activation. Mature TGF-?? engages TGFBR1/TGFBR2 receptors, leading to SMAD2/3 phosphorylation and SMAD4 nuclear translocation, which transcriptionally regulate genes such as SERPINE1 and CTGF. Non-SMAD signaling includes FAK/SRC-mediated activation of PI3K/AKT and MAPK/ERK pathways. ITGB8 expression is modulated by TGF-??1, SP1, NOTCH1, IL-1??, and TNF-??. The integrin interacts with extracellular matrix ligands vitronectin and fibronectin and intracellular adaptors talin and kindlin to control adhesion and migration.
In Jurkat T cells, ITGB8-mediated TGF-?? activation influences T cell differentiation, particularly Th17 and Treg subsets, and modulates immune responses. Disruption of ITGB8 impairs ??v??8-dependent SMAD and non-SMAD signaling, altering adhesion and cytokine profiles. This knockout model thus enables dissection of integrin ??v??8 functions in T cell biology and their implications in cancer, fibrosis, and autoimmunity.
Typical applications include analyzing surface ??v??8 expression by flow cytometry, measuring SMAD signaling via phospho-SMAD3 western blotting or SMAD luciferase reporters, and quantifying TGF-?? secretion by ELISA. Adhesion and migration assays on vitronectin or fibronectin assess integrin-dependent motility. Co-immunoprecipitation of ITGAV/ITGB8, RT-qPCR of target genes, cytokine profiling, and apoptosis assays further characterize the knockout phenotype. For further information, please contact Ascent Research.
