The AXL Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the AXL gene has been disrupted to create a loss-of-function model for studying receptor tyrosine kinase signaling. Jurkat cells, an acute T-cell leukemia-derived T lymphocyte line, were engineered using CRISPR/Cas9 to introduce target-gene disruption, resulting in a heterogeneous pool of edited cells. This polyclonal format preserves genetic diversity within the knockout population, enabling robust functional studies without clonal bias. The cells serve as a versatile research tool for dissecting AXL-mediated pathways in a T-cell context.
The host Jurkat cell line is a well-established model for T lymphocyte biology, extensively characterized for T-cell signaling, immune response, and leukemia pathogenesis. Derived from an acute T-cell leukemia patient, Jurkat cells exhibit constitutive activation of many T-cell signaling cascades, providing a sensitive background for investigating receptor tyrosine kinases such as AXL. Their rapid proliferation and ease of manipulation make them ideal for high-throughput screening and detailed mechanistic analyses of signal transduction networks involved in cell survival, proliferation, and migration.
AXL is a receptor tyrosine kinase that, upon binding its ligand Gas6, initiates intracellular signaling cascades critical for cellular homeostasis. Mechanistically, Gas6-activated AXL recruits the adaptor protein GRB2 and the p85 regulatory subunit of PI3K (PIK3R1), leading to downstream phosphorylation of AKT1 and ERK1/2. These kinases in turn regulate effectors including mTOR, RPS6, NF-??B, and cyclin D1, thereby promoting cell survival, proliferation, and migration. AXL signaling is also modulated by interacting factors such as SOCS1, which provides negative feedback. The disruption of AXL in these knockout cells abrogates Gas6-dependent activation of the PI3K/AKT and MAPK/ERK pathways, impairing downstream signal propagation.
In the Jurkat T-cell context, AXL knockout is particularly significant for understanding immune homeostasis and oncogenic signaling. Loss of AXL function is expected to sensitize cells to apoptosis by attenuating pro-survival signals normally transduced through AKT and ERK. This model enables precise investigation of how AXL contributes to T-cell leukemia cell survival and resistance to chemotherapeutics. Moreover, because AXL expression is often upregulated in various cancers and associated with immune evasion, these polyclonal knockout cells provide a platform to validate AXL as a therapeutic target in immuno-oncology and to explore its role in T-cell-mediated immune responses.
Typical research applications include functional studies of AXL in T-cell signaling, cancer drug resistance mechanisms, and immunotherapy target validation. The polyclonal knockout cells are suitable for apoptosis and survival assays, such as Annexin V-based flow cytometry detection and MTS/CCK-8 proliferation measurements, following Gas6 stimulation. Western blotting for AXL and phospho-AKT or phospho-ERK, RT-qPCR for AXL expression, and migration assays further enable dissection of downstream signaling events. These applications support drug discovery and academic research aimed at understanding AXL biology. For further technical information, please contact Ascent Research.
