The EID2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the EID2 gene in HeLa cervical adenocarcinoma cells. This heterogeneous loss-of-function model avoids clonal selection artifacts, providing a genetically diverse background for studying EID2-mediated transcriptional repression, cell cycle regulation, and differentiation. The product is ideal for functional genomics, pathway analysis, and drug screening applications.
HeLa cells, derived from an HPV18-positive cervical adenocarcinoma of a 31-year-old patient, are a classic model in cancer biology and virology. Their epithelial origin and HPV status make them especially relevant for investigating oncogenic mechanisms linked to HPV and transcriptional corepressors. HeLa cells are well-suited for CRISPR/Cas9 editing and are routinely used in cell cycle, apoptosis, and gene expression studies, offering a robust platform for knockout experiments.
EID2 acts as a transcriptional corepressor by binding and inhibiting the histone acetyltransferases EP300 and CREBBP, leading to chromatin condensation and repression of cell cycle genes like cyclin D1 and MYC. It interacts with HDAC complexes and is regulated by retinoic acid and E2F transcription factors. EID2 functions downstream of RB1/E2F and upstream of EP300/CREBBP target genes, integrating signals from TGF-beta and retinoic acid pathways. This corepressor is a key modulator of proliferation and differentiation programs, making its disruption informative for dissecting these networks.
In the HeLa model, EID2 knockout is particularly significant due to the HPV18-driven disruption of RB1 and p53, which converges on E2F-dependent transcription. EID2 loss may reshape EP300/CREBBP-driven gene expression and affect cell cycle and differentiation responses in this HPV-positive background. This polyclonal knockout population enables investigation of EID2’s role in cervical cancer cell behavior, including retinoic acid sensitivity and colony formation ability.
Applications include western blot and RT-qPCR for knockout confirmation, flow cytometry for cell cycle analysis, colony formation assays, and retinoic acid-induced differentiation studies. RNA-seq and ChIP-qPCR can profile transcriptomic and epigenetic changes, while co-immunoprecipitation confirms disrupted EID2-EP300 interactions. This model supports functional genomics and cancer research. For inquiries, contact Ascent Research.
