The AXL Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the AXL gene in the HAP1 background. This product offers a heterogeneous pool of cells with targeted disruption of AXL, enabling loss-of-function studies without the selection of a single clonal isolate. The polyclonal format captures diverse editing events, providing a robust model system for interrogating AXL-dependent phenotypes across a population of cells.
The HAP1 cell line is a human near-haploid line derived from the KBM-7 chronic myeloid leukemia (CML) cell line. Its near-haploid karyotype reduces genetic redundancy, making it an ideal host for functional genomics and CRISPR-based screening applications. HAP1 cells retain key signaling pathways relevant to cancer biology, and their use in knockout models facilitates unambiguous genotype-phenotype correlations, particularly for genes involved in tumorigenesis and drug response.
AXL is a receptor tyrosine kinase that, upon binding to its ligand Gas6 (or Protein S), triggers downstream signaling cascades including the PI3K/AKT and MAPK/ERK pathways, which govern cell survival, proliferation, and migration. AXL also activates NF-??B signaling and promotes epithelial-mesenchymal transition (EMT) through transcription factors such as Snail and Slug. It interacts with other receptor tyrosine kinases like EGFR, HER2, Tyro3, and Mer, and signals to effectors including STAT3 and Bcl-2. Upstream regulators of AXL expression include MZF1 and HIF-1??, integrating hypoxic and transcriptional control.
In the HAP1 context, disruption of AXL abrogates Gas6-induced activation of PI3K/AKT and MAPK/ERK, thereby attenuating signals that drive proliferation and survival. This polyclonal knockout population allows researchers to study AXL??s role in modulating these pathways without clonal bias. The loss of AXL function in a CML-derived background is particularly relevant for dissecting mechanisms of drug resistance and immune evasion, as AXL is frequently overexpressed in hematological malignancies and solid tumors.
This knockout model supports a wide range of experimental applications, including functional genomics screens, drug sensitivity profiling with AXL inhibitors such as bemcentinib, cell migration and invasion assays, and quantitative signaling analyses via Western blotting for phospho-AKT and phospho-ERK ELISA. It is also suitable for studying crosstalk between AXL and other RTKs. By using these polyclonal knockout cells, researchers can dissect AXL-dependent signaling networks in a controlled genetic background. For additional information or custom inquiries, please contact Ascent Research.
