The ANTXR1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte line, featuring targeted gene disruption of ANTXR1 to create a loss-of-function model. This heterogeneous cell pool enables robust investigation of ANTXR1-dependent mechanisms without clonal isolation, providing a versatile tool for studying receptor-mediated signaling, adhesion, and toxin entry in a T-cell context.
Jurkat cells are an immortalized T lymphocyte line originally derived from a patient with acute T cell leukemia. As a suspension cell model, they are extensively characterized for studies of T cell receptor signaling, apoptosis, and leukemogenesis, making them a reliable platform for dissecting pathways relevant to immune function and cancer biology. Their genetic manipulability and well-documented signaling networks facilitate mechanistic studies using knockout approaches.
ANTXR1 (Anthrax Toxin Receptor 1/TEM8) is a transmembrane protein that functions as a receptor for the protective antigen of anthrax toxin and for collagen VI, mediating cell-extracellular matrix adhesion and migration. At the signaling level, ligand engagement by collagen VI or Wnt ligands leads to activation of SRC family kinases, ERK1/2, and AKT, as well as ??-catenin stabilization through interaction with the Wnt co-receptor LRP6. This results in TCF/LEF-mediated transcription of target genes. Upstream regulators include VEGF signaling, hypoxia-inducible factor HIF1A, and inflammatory cytokines such as IL-1?? and TNF??, while downstream effects involve modulation of Rho GTPases, integrin expression, and cytoskeletal remodeling. ANTXR1 also interacts with ??1 integrin and actin-associated proteins, integrating adhesive and growth factor signals.
In the Jurkat T lymphocyte context, loss of ANTXR1 provides a physiologically relevant model to interrogate its functions in immune cell adhesion, migration, and leukemia pathophysiology. ANTXR1 knockout may impair both collagen-dependent attachment and Wnt-driven transcriptional programs, potentially altering T cell interactions with the tumor microenvironment and affecting processes such as metastasis and angiogenesis. This model is particularly valuable for studying how integrin-mediated and Wnt/??-catenin pathways converge in leukemic cells, and for exploring GAPO syndrome-related mechanisms where ANTXR1 mutations cause fibroblastic and vascular defects.
This polyclonal knockout product is suited for a broad array of experimental applications, including anthrax toxin protection assays to study toxin internalization; collagen I and VI adhesion and migration assays to evaluate cell-matrix interactions; TOPFlash luciferase reporter assays for Wnt/??-catenin transcriptional activity; and phospho-ERK/AKT analyses by Western blotting or intracellular flow cytometry. Additional uses encompass co-culture models to examine immune-tumor cell crosstalk, pharmacological inhibition studies targeting SRC or AKT, and CRISPR-based rescue experiments. It serves as a valuable resource for cancer biology, angiogenesis research, and rare disease modeling. For technical support or order inquiries, please contact Ascent Research.
