The CCDC91 Knockout 786-O Polyclonal Cells consist of a heterogeneous population of 786-O renal carcinoma cells in which the CCDC91 gene has been disrupted using CRISPR/Cas9 genome editing. As a polyclonal knockout pool, this product retains genetic diversity typical of mixed edited populations, avoiding artifacts that can arise from clonal selection. The population-level gene disruption enables consistent and reproducible assessment of CCDC91 function across experiments. Each lot is validated for target-gene knockout efficiency, providing a reliable loss-of-function model for downstream applications.
The 786-O cell line is a well-characterized epithelial model of clear cell renal cell carcinoma (ccRCC), isolated from a primary tumor. It harbors mutations typical of ccRCC, such as VHL inactivation, and is widely utilized to study renal cancer biology, including signaling, metabolism, and drug response. Its adherent growth and ease of handling make it suitable for standard cell-based assays, ensuring robust experimental outcomes. The renal epithelial origin of 786-O provides a biologically relevant context for investigating genes implicated in membrane trafficking and receptor regulation in carcinoma cells.
CCDC91 is a coiled-coil domain-containing protein that functions as a cargo adaptor at the trans-Golgi network (TGN) and endosomes. It directly interacts with GGA1 and GGA2 adaptors, the AP-1 complex, and clathrin to mediate vesicular transport of proteins. Upstream regulators include ARF GTPases, which recruit CCDC91 to membranes, while downstream targets encompass lysosomal enzymes and cell surface receptors. By facilitating sorting of glycoproteins and signaling receptors, CCDC91 occupies a central node that couples biosynthetic trafficking to endocytic recycling pathways. Its disruption can lead to mislocalization of these cargoes and downstream signaling defects.
In the 786-O renal carcinoma background, knockout of CCDC91 may significantly impact tumor cell phenotypes. Proper Golgi-to-endosome trafficking is essential for the surface presentation of growth factor receptors and adhesion molecules; loss of CCDC91 could impair receptor tyrosine kinase signaling and cell?Cextracellular matrix interactions. Consequently, this polyclonal knockout model is a valuable tool for dissecting how altered endomembrane dynamics contribute to ccRCC progression. It allows investigation of processes such as proliferation, migration, and apoptosis that are often deregulated in kidney cancer through aberrant trafficking.
Research applications for this knockout cell pool include co-immunoprecipitation and western blotting to verify interactions among CCDC91, GGA proteins, and clathrin. Immunofluorescence microscopy can visualize Golgi dispersal or cargo accumulation, while flow cytometry quantifies receptor surface levels. Functional assays??such as wound healing and transwell invasion??assess metastatic behavior, and drug sensitivity tests evaluate chemotherapeutic responses. These cells are therefore suited for mechanistic studies of endosomal sorting and for preclinical cancer research. For detailed product information or technical support, please contact Ascent Research.
