ANTXR2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, with targeted disruption of the ANTXR2 gene. This diverse pool of gene-edited cells provides a loss-of-function model for studying ANTXR2-mediated signaling, extracellular matrix (ECM) interactions, and anthrax toxin susceptibility. The polyclonal format captures a range of knockout alleles, enabling robust functional studies.
The parental A-549 cell line, established from a 58-year-old Caucasian male, displays epithelial morphology and expresses E-cadherin, serving as a model of alveolar type II-like epithelial cells. Widely used in cancer biology and drug metabolism research, A-549 cells retain key signaling pathways. Their adhesion and migration properties, influenced by integrin-ECM interactions, make them a relevant host for investigating ANTXR2 functions in cell-matrix dynamics.
ANTXR2 encodes a type I transmembrane protein that acts as a receptor for anthrax toxin protective antigen (PA), mediating toxin internalization. Additionally, ANTXR2 binds collagen IV (COL4A1) and laminin (LAMC1), interacting with actin and fibronectin (FN1) to regulate cell adhesion, spreading, and migration. Its activity is modulated by upstream factors including hypoxia (HIF1A), TGF-??1 (TGFB1), and ECM stiffness, and it signals through downstream effectors such as FAK, paxillin (PXN), MAPK/ERK (MAPK1), and Rho GTPases. ANTXR2 may coordinate with integrin heterodimers like ITGAV/ITGB3 and downstream mediators SRC and ??-catenin (CTNNB1) to control cytoskeletal organization and focal adhesion turnover.
In A-549 cells, ANTXR2 knockout allows dissection of its putative tumor suppressor role and its impact on ECM signaling. Given the epithelial origin and integrin expression of A-549 cells, loss of ANTXR2 perturbs adhesion, spreading, and migration, enabling modeling of hyaline fibromatosis syndrome, anthrax toxin cytotoxicity, and lung adenocarcinoma. This model interrogates ANTXR2-dependent crosstalk between integrin pathways and ECM organization in a disease-relevant context.
This knockout population is suitable for diverse functional assays, including anthrax toxin internalization studies, adhesion assays to collagen IV/laminin, migration and invasion transwell assays, and phospho-FAK analysis. It enables investigation of transcription factor regulation (e.g., HIF1A, TGFB1) and validation of protein interactions with ECM components. Researchers can perform rescue experiments with wild-type or mutant ANTXR2 constructs to map functional domains. For additional technical information, please contact Ascent Research.
