The ANTXR2 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ANTXR2 gene in the HAP1 cell line. This product provides a heterogeneous mix of edited cells with disrupted ANTXR2 expression, enabling loss-of-function studies without clonal selection. The polyclonal format preserves genetic diversity while eliminating the target protein, making it suitable for pooled functional genomics screens and bulk assays.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia line and exhibit a near-haploid karyotype, which simplifies gene editing and genetic analysis. These cells grow as adherent fibroblast-like cultures and are widely used as a screening platform due to their single-copy genome. The near-haploid background facilitates unambiguous interpretation of knockout phenotypes by reducing gene dosage effects and minimizing the need for complementation, offering a robust model for studying gene function.
ANTXR2 encodes a transmembrane receptor for anthrax protective antigen and extracellular matrix components collagen IV and laminin. It mediates cellular adhesion, ECM remodeling, and anthrax toxin internalization. ANTXR2 interacts with LRP6 to modulate Wnt signaling, while its activation is regulated by TGFB1, VEGFA, and TNF. Downstream, it influences RhoA, RAC1, FAK, and MMP2, linking integrin signaling and cytoskeletal dynamics. Through these interactions, ANTXR2 participates in angiogenesis and developmental pathways.
Disruption of ANTXR2 in the near-haploid HAP1 background provides a simplified system to interrogate its role in ECM-receptor interaction and Wnt/??-catenin signaling. The polyclonal knockout population enables assessment of heterogeneous cellular responses and avoids artefacts from clonal selection. This model is particularly suited for studying angiogenesis-related processes and anthrax toxin sensitivity, as the haploid state may accentuate loss-of-function effects on cell adhesion and signaling.
Researchers can employ these cells to investigate anthrax toxin mechanism, ECM biology, and Wnt pathway regulation using assays such as anthrax toxin protection assays, cell adhesion and tube formation assays, and TOPFlash reporter assays. They also serve as a tool for Hyaline Fibromatosis Syndrome modeling and cancer angiogenesis studies. For additional details or to inquire about custom applications, please contact Ascent Research.
