The ANTXR1 Knockout HT29 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of human HT29 colorectal adenocarcinoma cells with targeted disruption of the ANTXR1 gene. This heterogenous knockout pool serves as a loss-of-function model without clonal selection, enabling functional studies of ANTXR1 in an epithelial context. It is designed for investigations into cell adhesion, migration, and angiogenesis.
HT29 cells originate from a colorectal adenocarcinoma in a 44-year-old female and are a well-established model for intestinal epithelial research. These cells are capable of differentiation and polarization, forming tight junctions and exhibiting enterocyte-like features. They are widely employed to study barrier function, colorectal cancer biology, and drug absorption, providing a physiologically relevant background for CRISPR-mediated gene disruption.
ANTXR1, or tumor endothelial marker 8 (TEM8), is a transmembrane receptor that mediates adhesion to extracellular matrix proteins, particularly collagen IV and laminin. It regulates actin cytoskeleton dynamics and cell migration through integrin-associated signaling. Ligand-bound ANTXR1 activates FAK and Src kinases, which stimulate downstream pathways including ERK1/2, AKT, and the Rho GTPases Rac1 and RhoA, promoting actin polymerization and focal adhesion turnover. Additionally, ANTXR1 is the receptor for anthrax protective antigen, facilitating toxin endocytosis, a process disrupted by its knockout. The receptor??s function is modulated by upstream factors such as VEGF, HIF-1??, and WNT ligands, integrating microenvironmental cues.
In HT29 cells, deletion of ANTXR1 is expected to impair adhesion-dependent signaling and cytoskeletal organization. This model allows dissection of the receptor??s role in both undifferentiated and differentiated epithelial states. Researchers can assess how loss of ANTXR1 affects barrier integrity, collective migration, and response to angiogenic signals. The knockout also enables study of interactions between ANTXR1 and WNT pathway components, relevant to colorectal tumor progression where WNT signaling is often aberrantly activated.
This polyclonal knockout population is suitable for adhesion assays on collagen IV or laminin, Transwell migration, and wound healing assays. Western blotting can assess downstream effectors like phosphorylated FAK and ERK, while immunofluorescence visualizes F-actin reorganization. RT-qPCR can profile integrin and angiogenic gene expression changes. The model is valuable for anti-angiogenic drug screening and anthrax toxin mechanism studies. For further details or custom inquiries, contact Ascent Research.
