The IQGAP2 Knockout Jurkat Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphoblasts with targeted disruption of the human IQGAP2 gene, providing a versatile loss-of-function model for investigating scaffold protein-mediated signaling networks. This polyclonal knockout pool preserves the heterogeneity inherent to the parental cell line while eliminating IQGAP2 expression across the population, enabling robust studies of its roles in cell adhesion, migration, and signal transduction. The cells are suitable for a broad range of functional and biochemical assays without the clonal artifacts that may arise from single-cell-derived lines.
Derived from the peripheral blood of a 14-year-old male with acute T cell leukemia, Jurkat cells are an immortalized human T lymphocyte line widely employed as a model system for T cell receptor (TCR) signaling, apoptosis, and leukemogenesis. Their well-characterized signaling pathways and rapid proliferation make them an ideal host for gene-editing approaches aimed at dissecting molecular mechanisms in immune cell biology and cancer.
IQGAP2 functions as a scaffolding protein that orchestrates cross-talk between cell adhesion receptors and growth factor receptor pathways, thereby modulating actin cytoskeletal dynamics, cell polarity, and gene expression. It interacts with key regulators including Rac1, Cdc42, calmodulin, ??-catenin, and E-cadherin, and is positioned downstream of integrin receptors and receptor tyrosine kinases such as EGFR and FGFR. IQGAP2 influences MAPK/ERK signaling by linking focal adhesion kinase (FAK) and Src to ERK1/2 activation, and participates in Wnt/??-catenin and Rho GTPase pathways that govern cellular migration and adhesion.
In the Jurkat T lymphoblast context, disruption of IQGAP2 enables dissection of its contributions to immune cell adhesion, migration, and TCR-proximal signaling events. The knockout model provides a platform to examine how scaffold-protein dysfunction may contribute to immune dysregulation and leukemic cell behavior, particularly given IQGAP2’s established roles in hepatocellular, gastric, and colorectal cancers and its association with metastasis.
This polyclonal IQGAP2 knockout Jurkat cell population is optimized for applications in cancer cell signaling, tumor progression and metastasis research, immune cell adhesion and migration studies, and cytoskeletal dynamics analyses. Representative experimental approaches include Western blotting to assess IQGAP2 and downstream targets such as ERK1/2 and ??-catenin, flow cytometry for apoptosis and surface receptor profiling, transwell migration and invasion assays, adhesion assays, phospho-ERK analysis, and co-immunoprecipitation of IQGAP2-containing signaling complexes. For additional information or technical support, please contact Ascent Research.
