EDIL3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte cell line, designed for loss-of-function studies of the EDIL3 gene. This polyclonal population harbors CRISPR/Cas9-mediated gene disruption, eliminating EDIL3 protein expression to enable investigation of its biological functions without clonal selection artifacts.
The parental Jurkat cell line (clone E6-1) is an immortalized T-lymphocyte model originally isolated from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Jurkat cells are widely employed for studying T-cell signaling, activation, and apoptosis, and serve as a robust platform for dissecting leukemia-relevant pathways.
EDIL3 encodes a secreted extracellular matrix protein that functions as a ligand for integrin ??V??3 (ITGAV/ITGB3). Upon binding, EDIL3 activates focal adhesion kinase (FAK) and SRC, leading to phosphorylation of AKT and ERK1/2 (MAPK1/3) and promoting cell adhesion, migration, and survival. EDIL3 expression is regulated by inflammatory and hypoxic stimuli, including TNF-??, IL-1??, NF-??B, HIF-1??, and TGF-??. Downstream, EDIL3-mediated signaling enhances integrin activation and FAK phosphorylation, coupling to PI3K/AKT and ERK/MAPK cascades that sustain prosurvival and migratory phenotypes.
In Jurkat T-cells, EDIL3 likely contributes to adhesion-dependent signaling and leukemic cell survival. By disrupting EDIL3, these polyclonal knockout cells allow researchers to dissect the role of EDIL3 in T-cell adhesion dynamics, integrin-mediated signal transduction, and apoptosis resistance. Given EDIL3’s involvement in inflammatory responses and angiogenesis, this model also facilitates studies on how leukemic cells interact with the microenvironment.
This knockout product is suited for a range of experimental applications, including investigation of T-cell adhesion and migration mechanisms, functional analysis of integrin signaling in leukemia, and screening of therapeutic inhibitors targeting the EDIL3?Cintegrin ??V??3 interaction. Representative assays include Western blotting for EDIL3 and phospho-AKT/ERK, adhesion assays to vitronectin or fibrinogen, flow cytometry for integrin ??V??3 surface expression, transwell migration assays, co-immunoprecipitation of EDIL3 with integrin partners, RT-qPCR for EDIL3 mRNA levels, and apoptosis evaluation. For further information or to discuss your specific research needs, please contact Ascent Research.
