IRF2BPL Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population engineered to disrupt the IRF2BPL gene within the HT29 human colorectal adenocarcinoma epithelial cell line. This polyclonal knockout pool provides a heterogeneous loss-of-function model, enabling investigation of IRF2BPL-dependent cellular processes without the selection bottlenecks of clonal isolation. The product is intended for advanced functional studies in cancer biology, transcriptional regulation, and signal transduction, supporting comparative analyses between wild-type HT29 cells and a genetically disrupted population.
The HT29 cell line is a well?characterized model of colorectal adenocarcinoma, originally derived from a primary tumor of the intestinal epithelium. These cells harbor homozygous mutations in APC and TP53, along with the BRAF V600E mutation, and exhibit microsatellite stability (MSS). HT29 cells are widely used to study colorectal cancer biology, including oncogenic signaling, tumor suppressor inactivation, and epithelial differentiation. Their adherent epithelial morphology and retention of certain intestinal features make them suitable for modeling the intestinal epithelium and for assaying drug responses in a clinically relevant genetic background.
IRF2BPL functions as a transcriptional corepressor, interacting with IRF2 to repress interferon-stimulated gene (ISG) expression. It also possesses putative E3 ubiquitin ligase activity, targeting substrates for proteasomal degradation. This dual role links innate immune signaling via interferon-alpha/beta and STAT1/STAT2 to ubiquitin-dependent control of apoptosis regulators and proliferation. Interacting partners include E2 ubiquitin-conjugating enzymes and corepressor complexes, positioning IRF2BPL as a node between transcriptional repression and proteostasis.
In the HT29 colorectal adenocarcinoma cell line, which carries mutations in APC, TP53, and BRAF, IRF2BPL loss-of-function may alter interferon-stimulated gene expression and ubiquitin-mediated protein degradation, impacting key cellular processes such as proliferation and apoptosis. This model enables the investigation of IRF2BPL??s role in colorectal cancer biology and provides insights into the interaction between oncogenic pathways and innate immune signaling. Given its role in neuroendocrine regulation, the model may also inform studies of neurodevelopmental disorders.
IRF2BPL Knockout HT29 Polyclonal Cells are suitable for functional assays including western blotting, RT-qPCR, cell proliferation and apoptosis assays, ISG expression analysis, ubiquitination assays, and colony formation assays. These applications support research into IRF2BPL??s functions in transcriptional repression and ubiquitin ligase activity within colorectal cancer models, as well as drug target validation and functional genomic screening. For additional information, please contact Ascent Research.
