The IQSEC1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphoblast cell line. This product introduces targeted gene disruption of IQSEC1 (also known as BRAG2 or GEP100), generating a loss-of-function model for studying the functional roles of this guanine nucleotide exchange factor in T cell biology and beyond. The polyclonal format provides a heterogeneous population of edited cells, suitable for diverse functional assays without requiring clonal isolation.
Jurkat cells are an immortalized suspension cell line originally isolated from a patient with acute T cell leukemia. Widely used as a model for T cell signaling, activation, and apoptosis, they recapitulate key aspects of T lymphoblast physiology, including rapid proliferation and responsiveness to external stimuli. Their genetic tractability and well-characterized signaling pathways make them an ideal host for CRISPR-mediated gene editing studies.
IQSEC1 encodes a PIP3-dependent GEF for ARF6, connecting integrin ligation and growth factor receptor signaling (e.g., EGFR, PDGFR) to ARF6-mediated membrane trafficking. PI3K-generated PIP3 recruits IQSEC1 to the membrane, where it activates ARF6. ARF6-GTP then promotes Rac1 activation, actin polymerization, and integrin recycling to the plasma membrane. IQSEC1 forms complexes with ARF1, the AP-2 adaptor, ??-arrestin, and integrin cytoplasmic tails, thereby coordinating endosomal sorting with adhesion dynamics. Together, these interactions position IQSEC1 as a critical mediator linking phosphoinositide signals to cytoskeletal and adhesive outputs.
In Jurkat T cells, IQSEC1-dependent integrin trafficking underpins adhesion, migration, and immunological synapse assembly. Disruption of IQSEC1 in this polyclonal population permits dissection of PIP3/ARF6-mediated control of T cell polarity, motility, and LFA-1 surface expression. The model is particularly suited for analyzing T cell?Cextracellular matrix interactions and for investigating the molecular basis of IQSEC1 involvement in cancer metastasis and neurodevelopmental disorders.
Applications include adhesion assays on fibronectin or ICAM-1, chemotaxis and migration chambers, flow cytometric quantitation of integrin surface levels, co-immunoprecipitation of IQSEC1?CARF6 complexes, and Western blot analysis of ARF6-GTP and phospho-AKT. Confocal microscopy can reveal actin and integrin localization defects. The knockout cells are amenable to high-throughput screening for modulators of the PI3K/ARF6 axis and rescue experiments with IQSEC1 variants. In oncology, they support invasion assays to probe the contribution of IQSEC1-driven integrin recycling to metastasis. For additional technical details, please contact Ascent Research.
