The ITGB6 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte cell line, featuring targeted disruption of the ITGB6 gene. This loss-of-function model eliminates integrin beta-6 expression, thereby preventing formation of the alphaVbeta6 heterodimer. The polyclonal format avoids clonal selection bias and provides a heterogeneous knockout background suitable for a range of pooled functional studies.
Jurkat cells are an immortalized human T-cell line from acute T-cell leukemia, widely used to study T-cell signaling, apoptosis, and oncogenesis. They retain key T-cell receptor pathways and are readily amenable to genetic modification, making them an ideal host for CRISPR-mediated gene editing to dissect lymphocyte biology.
ITGB6 encodes integrin beta-6, which partners exclusively with ITGAV to form alphaVbeta6 integrin. This receptor binds fibronectin and LAP-TGF-beta, activating latent TGF-beta via mechanical force. Downstream, this triggers TGFBR1/2-mediated phosphorylation of SMAD2/3 and activates PI3K/AKT and FAK/Src signaling. Expression is regulated by EGF, TGF-beta, and transcription factors ETS1 and AP-1, while integrin activation requires talin and kindlin. Thus, ITGB6 links extracellular matrix adhesion to TGF-beta and growth factor pathways.
In Jurkat T cells, ITGB6 knockout allows dissection of alphaVbeta6-dependent functions in a leukemia background. Although typically an epithelial integrin, alphaVbeta6 may contribute to T-cell adhesion, migration, and TGF-beta activation in the tumor microenvironment. This model enables investigation of integrin-mediated signaling in leukemic cell invasion and survival, as well as its role in immune cell?Cmatrix interactions relevant to fibrosis and cancer.
Research applications include adhesion assays on fibronectin, transwell migration, and TGF-beta bioassays with phospho-SMAD2/3 detection and downstream transcriptional analysis. The cells support drug discovery targeting alphaVbeta6?CTGF-beta pathways, with knockout controls for integrin-specific effects. Assays such as flow cytometry, Western blotting for FAK/AKT/ERK, and RT-qPCR can validate outcomes. For further details and protocol support, please contact Ascent Research.
