The CCDC106 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from HEK293T cells, designed to disrupt the CCDC106 gene and provide a loss-of-function model for p53 pathway studies. As a polyclonal pool, these cells capture a range of editing events, minimizing clonal bias and offering a robust representation of CCDC106 deficiency. This product enables detailed dissection of CCDC106??s role in modulating p53 stability and activity.
HEK293T is a human embryonic kidney epithelial cell line originally derived from HEK293 cells, stably expressing adenovirus type 5 DNA and the SV40 large T antigen. This genetic background endows the cells with exceptional transfection efficiency and high-level recombinant protein expression, making them a standard host for functional genomics, viral production, and signaling studies. The SV40 large T antigen inactivates p53 and retinoblastoma proteins, which facilitates the investigation of p53 pathway components in a controlled context.
CCDC106 promotes p53 degradation by serving as a cofactor for the E3 ubiquitin ligase MDM2. CCDC106 physically interacts with p53 and MDM2, enhancing MDM2-mediated ubiquitination of p53 and directing it to proteasomal destruction. This activity suppresses p53-dependent transcription of downstream targets such as BAX and p21, thereby inhibiting apoptosis and promoting cell cycle progression. Upstream regulators, including DNA damage and oncogenic stress, impinge on this axis, positioning CCDC106 as a key modulator of the p53 tumor suppressor network in response to cellular insults.
In the HEK293T background, where p53 function is already partially attenuated by SV40 large T antigen, CCDC106 knockout further disinhibits p53, potentially restoring some tumor-suppressive signaling. This model allows for examination of CCDC106??s specific contribution to p53 regulation independent of other interfering factors. The polyclonal composition avoids clonal artifacts, ensuring that phenotypes reflect genuine CCDC106 loss rather than adaptational noise. Combined with HEK293T??s high transfectability, the model supports complementation and rescue experiments to confirm genotype?Cphenotype relationships.
These CCDC106 knockout cells are applicable to a broad range of cancer research and p53 signaling studies. Typical assays include western blotting and co-immunoprecipitation to monitor p53?CMDM2 interactions, ubiquitination assays to quantify p53 turnover, and apoptosis assays to measure cell death sensitivity. Cell proliferation assays enable evaluation of CCDC106??s growth-promoting functions, while drug screening efforts can identify compounds that modulate the p53?CMDM2 axis. For additional information, please contact Ascent Research.
