The KIAA0319L Knockout HeLa Polyclonal Cells product is a CRISPR/Cas9-edited heterogeneous cell population derived from the HeLa cell line, designed to disrupt the KIAA0319L gene and create a robust loss-of-function model. This polyclonal knockout pool, generated via targeted gene disruption, enables researchers to interrogate the functional role of KIAA0319L in viral entry and cellular trafficking mechanisms without relying on single-cell clones.
HeLa cells are an immortalized epithelial cell line originally isolated from a cervical adenocarcinoma in 1951. These cells are positive for human papillomavirus type 18 (HPV-18) and exhibit an aneuploid karyotype with an adherent morphology. The HeLa cell line is a staple in biomedical research, particularly in cancer biology, virology, and gene expression studies, due to its robust growth, ease of transfection, and well-characterized signaling pathways.
KIAA0319L, also known as the adeno-associated virus receptor (AAVR), functions as the primary cellular receptor for AAV serotypes, mediating clathrin-dependent endocytosis of viral particles. The protein contains immunoglobulin-like and polycystic kidney disease domains, which are essential for viral capsid binding. Upon interaction with AAV capsid proteins, KIAA0319L recruits the AP-2 adaptor complex, clathrin heavy chain, and accessory endocytic proteins to facilitate viral internalization. Downstream, the pathway involves dynamin-mediated vesicle scission, early endosome formation marked by Rab5 and EEA1, and subsequent trafficking to the nuclear pore complex for viral genome delivery. Knockout of KIAA0319L disrupts this cascade, abolishing viral attachment and preventing productive transduction.
In the HeLa cell context, where endogenous AAV entry pathways are intact, the KIAA0319L knockout provides a critical tool for dissecting receptor-ligand interactions and host factor dependencies. Given HeLa cells’ widespread use in viral infection studies, this polyclonal knockout population enables direct assessment of how AAV infection efficiency is compromised when the primary receptor is missing, while still preserving the heterogeneous genetic background that mimics population-level variation.
This product is ideally suited for a range of advanced applications, including mechanistic studies of AAV transduction, gene therapy vector optimization, and host factor screening. Researchers can employ standard assays such as AAV reporter transduction assays, western blotting for KIAA0319L protein, immunofluorescence to visualize viral binding, flow cytometry for transduction efficiency, and RT-qPCR for viral genome internalization. Inhibitor-based studies with dynasore or chlorpromazine can further validate endocytic pathway involvement. For additional details, please contact Ascent Research.
