The JAM3 Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout pool of Jurkat T lymphoblasts with targeted disruption of the JAM3 gene. This heterogeneous cell population provides a loss-of-function model without clonal isolation, preserving genetic diversity and enabling robust, population-level functional analyses. The polyclonal format minimizes clonal artifacts and is well suited for pooled screening and assays where averaged phenotypic responses are desired.
Jurkat cells are a widely used immortalized human T lymphoblast line derived from a T-cell leukemia patient. These suspension-adapted cells serve as a fundamental model for T-cell receptor signaling, apoptosis, and immune activation. Their well-characterized biology and ease of genetic manipulation make them an ideal host for investigating lymphocyte adhesion, migration, and signaling dynamics in a reproducible in vitro system.
JAM3 encodes junctional adhesion molecule C (JAM-C), a tight junction protein that mediates homophilic and heterophilic adhesion, critically regulating endothelial and epithelial barrier integrity. JAM3 forms complexes with JAM2, integrin ??V??3, and the scaffolding proteins ZO-1 and ZO-2 to anchor junctional structures to the actin cytoskeleton. Upstream, JAM3 expression is transcriptionally controlled by ZEB1 and Snail and is induced by pro-inflammatory cytokines TNF-??, IL-1??, and TGF-??. Downstream, JAM3 engagement activates AKT phosphorylation and ERK signaling, linking adhesion to survival and migratory pathways. Disruption of JAM3 dismantles tight junction architecture and enhances leukocyte transendothelial migration.
In the Jurkat T-cell context, JAM3 knockout offers a powerful tool to dissect how junctional adhesion governs lymphocyte trafficking. Loss of JAM3 impairs homophilic interactions and promotes paracellular diapedesis, directly impacting integrin ??V??3-mediated signaling and T-cell motility. Because Jurkat cells originate from a leukemic malignancy, this model is particularly relevant for studying adhesion-dependent mechanisms of hematologic cancer dissemination and immune cell extravasation across inflamed endothelia.
Typical applications include immunofluorescence labeling of tight junction components, Transwell migration assays to quantify altered leukocyte transmigration, and adhesion assays on endothelial monolayers. Western blotting confirms JAM3 ablation and monitors phospho-AKT, while flow cytometry assesses surface integrin ??V??3 expression. The polyclonal knockout format supports high-throughput functional genomics and dose-response studies in inflammatory and metastatic disease models. For additional technical information and customized support, please contact Ascent Research.
