The ANGPTL4 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population of HAP1 cells harboring a targeted disruption of the human ANGPTL4 gene. This loss-of-function model enables systematic dissection of ANGPTL4-dependent molecular mechanisms without the confounding influence of residual wild-type alleles in the polyclonal pool. The knockout population is produced using CRISPR/Cas9-mediated gene disruption, providing a robust and flexible platform for gene-function studies across diverse experimental contexts.
The HAP1 host cell line is a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia (CML) cell line. HAP1 cells are of male origin, exhibit fibroblast-like morphology, and grow in suspension. Their near-haploid karyotype simplifies genetic analysis and reduces complexity associated with diploid genomes, making them particularly well-suited for knockout and functional genomics applications in a malignant myeloid progenitor background.
ANGPTL4 encodes a secreted glycoprotein that functionally inhibits lipoprotein lipase (LPL), thereby regulating triglyceride clearance and lipid metabolism. Beyond its lipolytic role, ANGPTL4 promotes angiogenesis, vascular permeability, inflammation, and tumor metastasis through integrin-mediated signaling. Upstream regulators include PPAR??/?? agonists, HIF-1?? under hypoxia, TGF-??, TNF-??, insulin, and free fatty acids. Upon binding integrins ??5??1 and ??5 and interacting with extracellular matrix proteins, ANGPTL4 activates focal adhesion kinase (FAK) and Src, leading to ERK1/2 phosphorylation and subsequent expression of matrix metalloproteinases such as MMP-9. This signaling axis modulates endothelial permeability and facilitates invasive cell behavior. ANGPTL4 is also processed by proprotein convertases like furin and PACE4, influencing its activity and localization.
In the HAP1 context, ablation of ANGPTL4 allows direct investigation of its dual functions in a CML-derived, near-haploid myeloid progenitor cell line. Because HAP1 cells retain relevant integrin and signaling pathways, this knockout model is particularly valuable for dissecting ANGPTL4??s contributions to leukemic cell adhesion, migration, and invasion. Moreover, the simplified genetic background facilitates studies on how ANGPTL4 integrates metabolic signals and microenvironmental cues to modulate malignant phenotypes.
This polyclonal knockout population is ideally suited for a range of research applications, including analysis of LPL regulation and triglyceride metabolism, screening for modulators of metabolic pathways, and mechanistic studies of tumor cell migration and metastasis. Typical assays include LPL activity measurements, fatty acid uptake assays, transwell migration and invasion assays, tube formation assays to evaluate angiogenesis, western blotting for phosphorylated FAK and ERK, and xenograft models to assess metastatic potential. The cells also support transcriptomic approaches such as RNA-seq. For detailed specifications and ordering information, please contact Ascent Research.
