The CD2AP Knockout A-549 Polyclonal Cells product provides a population of CRISPR/Cas9-edited human A-549 epithelial cells with targeted disruption of the CD2AP gene. As a polyclonal knockout pool, this product comprises a heterogeneous mixture of gene-edited variants, enabling functional loss-of-function studies without single-cell clonal expansion. This CRISPR/Cas9-mediated gene disruption model is designed for investigating CD2AP-dependent cellular processes in a well-characterized lung carcinoma cell background.
The A-549 cell line is derived from human lung adenocarcinoma and exhibits characteristics of alveolar type II epithelial cells. Widely utilized in oncology, respiratory biology, and drug discovery, A-549 cells provide a robust platform for examining epithelial cell adhesion, migration, and signaling. Their epithelial morphology and expression of key receptors such as EGFR make them particularly suitable for studying endocytic trafficking and cytoskeletal dynamics.
CD2AP encodes a scaffold adaptor protein that bridges membrane receptors to the actin cytoskeleton. It functions downstream of nephrin and the epidermal growth factor receptor (EGFR), and is activated by T-cell receptor/CD3 complex signaling. CD2AP interacts with cortactin, podocin, Cbl, and other partners to coordinate receptor-mediated endocytosis, actin filament assembly, and focal adhesion turnover. Through these interactions, CD2AP orchestrates cytoskeletal reorganization critical for cell adhesion and migration.
In the A-549 adenocarcinoma context, disruption of CD2AP alters EGFR internalization and downstream signaling, impacting actin dynamics and cell motility. The polyclonal knockout pool enables dissection of CD2AP’s role in cancer cell migration and adhesion, as well as modeling defects observed in focal segmental glomerulosclerosis where nephrin-CD2AP-podocin interactions are compromised. Loss of CD2AP may perturb cortactin-mediated actin polymerization and Cbl-mediated receptor ubiquitination, offering insight into mechanisms of metastasis and podocyte dysfunction.
This knockout cell pool is suited for applications in kidney disease modeling, cancer metastasis research, and membrane trafficking studies. Representative assays include transwell migration to assess invasiveness, EGFR internalization kinetics via immunofluorescence, Western blotting for downstream targets like cortactin and Cbl, and RT-qPCR for validating CD2AP disruption. The polyclonal nature allows population-level phenotypic screening. For further details and ordering information, please contact Ascent Research.
