The ALCAM Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ALCAM gene in the human Jurkat T lymphocyte line. This polyclonal model disrupts ALCAM expression across the population without clonal selection, eliminating the activated leukocyte cell adhesion molecule (ALCAM/CD166), a key mediator of T cell adhesion and immune synapse formation. The resulting loss of function provides a tool for studying adhesion-dependent signaling in lymphocytes.
The Jurkat cell line, a widely used human T lymphocyte model derived from T cell leukemia, is instrumental for studying T cell receptor (TCR) signaling. These cells constitutively express CD3 and CD28 and recapitulate early activation events, including the recruitment of ZAP70 and LAT. Their robust proliferation and susceptibility to genetic modification enable efficient generation of gene-edited derivatives like the ALCAM knockout population for functional studies.
ALCAM (CD166) is a transmembrane glycoprotein mediating homophilic adhesion and heterophilic binding to CD6, linking the extracellular space to the actin cytoskeleton. In T cells, ALCAM facilitates immune synapse formation and stabilization. Its expression is regulated by TCR activation, CD3/CD28 costimulation, and TNF-alpha. Downstream, ALCAM signals through ERK, NF-kB, and AKT, which govern T cell activation and survival. ALCAM knockout in Jurkat cells abrogates these interactions, impairing immune synapse architecture and attenuating TCR-proximal signaling through ZAP70, LAT, and SLP-76.
In Jurkat cells, ALCAM deficiency provides a model to dissect the role of cell adhesion in T cell function and pathology. ALCAM is implicated in cancer metastasis, multiple sclerosis, and leukocyte transendothelial migration, making this knockout valuable for disease research. This model enables investigation of how adhesion molecules modulate signaling thresholds, migration, and tumor microenvironment interactions, offering insights into adhesion-dependent regulatory networks in immune activation and autoimmune disorders.
Applications include T cell activation studies, immune synapse research, and cell adhesion assays. Methods such as Western blotting, flow cytometry, adhesion assays, and T cell activation assays provide functional validation, while co-immunoprecipitation and phospho-signaling analysis reveal altered signaling complexes. These polyclonal cells support research in cancer immunology, drug discovery, and autoimmune diseases. For more information, contact Ascent Research.
