The EFNB1 Knockout 786-O Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human renal cell adenocarcinoma line. This loss-of-function model targets the EFNB1 gene, which encodes ephrin-B1, providing a heterogeneous pool of edited cells that robustly represent the knockout phenotype while minimizing clonal selection effects inherent to monoclonal lines.
The 786-O cell line is a canonical model for clear cell renal cell carcinoma (ccRCC), originating from a primary tumor and carrying a naturally occurring VHL mutation that results in constitutive stabilization of hypoxia-inducible factors (HIFs). This genetic backdrop mimics the pseudohypoxic state typical of ccRCC, making these cells ideal for investigating signaling pathways that drive renal malignancy, including cell migration, invasion, and angiogenic programs.
EFNB1 encodes ephrin-B1, a transmembrane ligand that engages Eph receptor tyrosine kinases, notably EphB2 and EphB4, to initiate bidirectional signaling. Reverse signaling through ephrin-B1 recruits Src and focal adhesion kinase (FAK), triggering cytoskeletal reorganization and enhanced motility, whereas forward signaling modulates adhesion and cell segregation. Upstream regulators including TCF/LEF, NF-??B, EGF, and FGF control ephrin-B1 expression, with downstream effectors like RhoA, Rac1, and MAPK/ERK. Ephrin-B1 also interacts with PDZ-domain proteins and adaptor Grb4 to assemble signaling complexes.
In 786-O renal carcinoma cells, ephrin-B1 reverse signaling has been associated with increased invasive capacity, and its interplay with VHL loss may accentuate malignant behavior. Accordingly, this knockout model serves as a powerful tool to dissect the contribution of ephrin-B1 to ccRCC progression. Beyond renal cancer, EFNB1 mutations cause craniofrontonasal syndrome, and aberrant ephrin-B1 expression is documented in breast and prostate cancers, broadening the research utility of this cell population.
These polyclonal knockout cells are suited for transwell migration and invasion assays to evaluate motility, co-immunoprecipitation to probe ephrin-B1 interactomes, and phospho-signaling analysis of Src and FAK pathways. Coupled with transcriptomic profiling by RNA-seq and immunofluorescence imaging, the model enables comprehensive functional genomics studies. It is ideal for drug target validation and high-content screening. For further specifics, contact Ascent Research.
