The CD2AP Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered from the HT29 human colorectal adenocarcinoma cell line. This product provides researchers with a stable loss-of-function model for investigating CD2AP biology through targeted disruption of the CD2AP gene. The polyclonal format offers a heterogeneous gene-edited population, enabling robust experimental designs without clonal artifacts, and is suitable for a wide range of functional and mechanistic studies.
The HT29 parental cell line was originally derived from a 44-year-old female with colorectal adenocarcinoma and is widely adopted for studying intestinal epithelial biology, drug transport, and cancer. These cells form polarized monolayers under appropriate culture conditions, making them particularly valuable for analyzing epithelial barrier function, apicobasal transport, and tumor cell behavior. As an established colorectal cancer model, HT29 cells exhibit typical adenocarcinoma characteristics and are frequently used in investigations of cancer cell signaling and therapeutic responses.
CD2AP functions as a multifunctional adaptor protein that bridges transmembrane receptors to the actin cytoskeleton, playing pivotal roles in endocytosis, cell adhesion, and signal transduction. Mechanistically, CD2AP is activated by T-cell receptor (TCR) engagement and nephrin signaling, and it interacts with partners such as CD2, podocin, c-Cbl, cortactin, and CIN85. Through these interactions, CD2AP orchestrates actin cytoskeleton remodeling, c-Cbl ubiquitination, cortactin activation, and endocytic trafficking, thereby integrating signals from the cell membrane to the cytoskeleton. Its involvement in pathways such as slit diaphragm signaling, TCR signaling, and mTOR signaling underscores its broad regulatory capacity across multiple cell types.
In the context of HT29 colorectal adenocarcinoma cells, disruption of CD2AP provides a powerful tool to dissect its contributions to cancer cell adhesion, migration, invasion, and epithelial barrier integrity. Given the cell line??s capacity to form polarized monolayers, this knockout model is ideally suited for investigating how CD2AP-dependent actin remodeling influences tight junction stability, transendothelial electrical resistance (TEER), and drug penetration. Moreover, because CD2AP interfaces with mitogenic and stress pathways, the knockout cells can help elucidate its role in colorectal cancer progression and therapeutic resistance.
Typical research applications include Western blotting, RT-qPCR, immunofluorescence, and flow cytometry to validate CD2AP loss and examine downstream signaling. Functional studies may employ cell migration and invasion assays, TEER-based barrier integrity measurements, apoptosis and metabolic assays, and drug sensitivity testing. These assays enable the dissection of CD2AP-mediated mechanisms in colorectal cancer biology and intestinal epithelial homeostasis, providing actionable insights for drug discovery and cancer research. For further information on this product, please contact Ascent Research.
