The ANXA13 Knockout A-549 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ANXA13 gene in the A-549 lung adenocarcinoma line. This pooled product contains cells with CRISPR/Cas9-mediated gene disruptions, creating a loss-of-function model without overexpression artifacts. The polyclonal nature captures diverse editing events, providing a robust tool for functional genomics studies. Leveraging the well-characterized A-549 background, these cells enable authentic investigation of ANXA13??s endogenous roles.
The A-549 host cell line is a widely used human lung adenocarcinoma epithelial line derived from a male patient. It retains features of alveolar type II pneumocytes and is extensively employed in cancer biology, EMT, drug response, and metastasis research. A-549 cells are easily manipulated and serve as an ideal platform for genetic knockout studies, facilitating the creation of isogenic models to explore gene function in lung adenocarcinoma.
ANXA13 is a calcium-dependent phospholipid-binding annexin that governs membrane organization, epithelial polarity, exocytosis, and cell adhesion. Its expression is activated by CDX2 transcription factor and modulated by calcium ions and Wnt signaling. ANXA13 interacts with phospholipids and other annexins upon calcium binding, localizing to membrane domains and orchestrating cell adhesion complex assembly. Functioning downstream of CDX2, ANXA13 links calcium-mediated signaling to membrane trafficking and adhesion molecule dynamics, with disruption expected to impair these processes.
In lung adenocarcinoma, ANXA13 knockout disrupts calcium-dependent membrane organization and epithelial polarity, altering cell adhesion and potentially tumor cell behavior. This model allows dissection of ANXA13??s role in migration, invasion, and colony formation, and its impact on membrane-associated signaling pathways. Direct comparison of isogenic knockout and wild-type A-549 cells enables attribution of phenotypic changes to ANXA13 loss, advancing understanding of its contribution to lung cancer pathophysiology.
The polyclonal knockout cells are suitable for western blotting, RT-qPCR, immunofluorescence, cell adhesion, migration, and calcium flux assays. They provide a valuable resource for studying ANXA13-dependent signaling, epithelial polarity, and cancer cell motility, and can be used in colony formation and drug screening applications. Researchers examining calcium-mediated signaling in epithelial cancers will find this model ideal. For information, contact Ascent Research.
