The KRT19 Knockout 786-O Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the KRT19 gene in the 786-O human renal cell adenocarcinoma line. This polyclonal knockout model provides a genetically heterogeneous loss-of-function system, suitable for studying the collective impact of KRT19 ablation on epithelial cell biology. Through CRISPR/Cas9-mediated gene disruption, the population exhibits abrogation of keratin 19 expression, allowing researchers to probe functional consequences without clonal selection biases. The cells are validated for knockout efficiency and are ready for downstream applications in cancer biology and intermediate filament research.
The host cell line, 786-O, originates from a renal clear cell carcinoma and harbors a well-characterized VHL deficiency, making it a principal model for hypoxia-driven renal tumorigenesis. 786-O cells maintain a basal epithelial phenotype and express key intermediate filament components, including keratin 8 (KRT8), which partners with KRT19. This background renders the cell line particularly relevant for investigating cytoskeletal dynamics and adhesion properties in the context of renal cell carcinoma progression.
Keratin 19, encoded by KRT19, is a type I intermediate filament protein that assembles obligate heterodimers with its type II partner KRT8, forming stable 10 nm filaments that provide structural integrity to epithelial cells. Expression of KRT19 is regulated by transcription factors such as HNF4A and GATA6, and by retinoic acid signaling, positioning it as a responsive element in epithelial differentiation. KRT19 interacts directly with desmoplakin, plectin, and epiplakin, linking intermediate filaments to desmosomal and hemidesmosomal complexes. Downstream, KRT19 influences cytoskeletal reorganization, cell adhesion, and mechanosensitive gene expression, thereby modulating cell shape and mechanical resilience.
In the 786-O renal carcinoma context, KRT19 knockout is anticipated to disrupt intermediate filament network organization, potentially impairing cell?Ccell adhesion and altering mechanotransduction pathways. Loss of KRT19 may lead to rearrangements of the cytoskeleton, affecting migration and invasion properties that are critical in carcinoma progression. This model enables dissection of how intermediate filament integrity contributes to the aggressive behavior of VHL-deficient renal cancer cells and provides a platform to study epithelial-to-mesenchymal transition and metastatic potential.
This knockout product supports a wide range of research applications, including epithelial-to-mesenchymal transition (EMT) studies, cancer cell migration and invasion assays (e.g., wound healing and Transwell assays), intermediate filament biology, renal cell carcinoma pathogenesis, and investigation of drug resistance mechanisms. Representative experimental techniques include western blotting for KRT19 and KRT8, immunofluorescence staining of intermediate filament networks, RNA-seq transcriptomic profiling, cell stiffness measurements, and viability or apoptosis assays. For additional details or technical support, please contact Ascent Research.
