The KIAA0319L Knockout NCI-H1975 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1975 human lung adenocarcinoma cell line. This loss-of-function model disrupts the KIAA0319L gene, which encodes the adeno-associated virus receptor (AAVR). The polyclonal format provides a heterogeneous knockout population, enabling robust evaluation of gene function without clonal artifacts. The product is designed for gene-edited cell-based assays in virology, cancer biology, and cell adhesion research.
NCI-H1975 is a well-characterized human non-small cell lung cancer (NSCLC) cell line derived from a female never-smoker with lung adenocarcinoma. It harbors activating EGFR mutations L858R and T790M, the latter conferring resistance to first-generation EGFR tyrosine kinase inhibitors. This epithelial cell line serves as a clinically relevant model for studying EGFR-driven oncogenic signaling and therapeutic resistance. The NCI-H1975 background thus provides a unique genetic context for examining the non-viral functions of KIAA0319L in cancer cell adhesion and invasion.
KIAA0319L encodes a multi?pass transmembrane protein that acts as the primary cellular receptor for adeno?associated viruses (AAVs). AAV entry is mediated by direct binding of the viral capsid proteins VP1, VP2, and VP3 to AAVR, followed by recruitment of the GPR108 co?receptor and the clathrin?dependent endocytic machinery, including the AP2 adaptor complex and dynamin. Internalized virions traffic through Rab5? and Rab7?positive endosomes, ultimately releasing their genome. Beyond its viral receptor role, KIAA0319L participates in cell?ECM adhesion, potentially through ??1 integrin interactions, and has been implicated in modulating E?cadherin?mediated cell?Ccell adhesion and PI3K/AKT signaling.
Disruption of KIAA0319L in the NCI-H1975 knockout polyclonal cells abrogates AAV transduction, as the essential entry receptor is lost. This makes the model invaluable for investigating AAV host dependency factors, evaluating engineered AAV capsid variants, and dissecting the endocytic trafficking pathway. Moreover, the EGFR?mutant background enables studies of potential crosstalk between AAVR?mediated adhesion and oncogenic signaling. By eliminating AAVR, researchers can discriminate its viral entry functions from its roles in cell adhesion, migration, and signal transduction, particularly in the context of NSCLC metastasis.
These polyclonal knockout cells are suitable for a broad range of research applications, including AAV transduction assays with reporter?encoding vectors (e.g., GFP?AAV) quantified by flow cytometry, co?immunoprecipitation of AAV capsid components, immunofluorescence imaging of AAV internalization, and western blotting for KIAA0319L expression. Additionally, they enable cell migration and adhesion assays to uncover the non?viral functions of AAVR in cancer biology. This cell product supports functional genomics screens, gene therapy vector optimization, and antiviral target validation. For further technical specifications and availability, please contact Ascent Research.
