The E2F7 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population generated by targeted disruption of the E2F7 gene in HAP1 cells. This product offers a pooled loss-of-function model ideal for investigating E2F7-dependent transcriptional regulation in cell cycle control, DNA damage responses, and apoptosis, without the need for clonal isolation, thereby facilitating high-throughput screening.
HAP1 cells are haploid human fibroblast-like cells derived from the KBM-7 chronic myelogenous leukemia line. Their near-haploid genome enables clean gene disruption phenotypes without confounding allelic effects, making them a powerful platform for genetic screens, drug target validation, cancer biology research, and functional genomics studies.
E2F7 is a transcriptional repressor that antagonizes activator E2Fs such as E2F1 and E2F2, driving cell cycle exit and apoptosis in response to DNA damage. Its expression is induced by TP53 and MYC, and it represses a broad set of E2F target genes, including CCNE1, E2F1 itself, DHFR, and MCM family members. E2F7 forms repressive complexes with E2F8, TFDP1, and corepressors HDAC1, SIN3A, and NCOR1 to silence these loci. Functioning within the TP53-E2F7-E2F1-CCNE1-CDK2-RB1 pathway, E2F7 links genotoxic stress signaling to inhibition of cell cycle progression and activation of apoptotic programs, thereby enforcing the DNA damage checkpoint.
In the haploid HAP1 context, E2F7 gene disruption eliminates the compensatory buffering often present in diploid cells, providing a clear readout of its tumor-suppressive functions. This model is particularly valuable for dissecting how loss of E2F7-mediated repression contributes to uncontrolled proliferation in hepatocellular carcinoma, breast cancer, colorectal cancer, and acute myeloid leukemia, and for testing therapeutic agents that target the DNA damage response and cell cycle checkpoints.
These polyclonal knockout cells are amenable to a variety of assays, including cell cycle profiling via flow cytometry, apoptosis detection, and proliferation measurements. They enable analysis of DNA damage by comet assay and can be used for RNA-seq or ChIP-qPCR to delineate transcriptional and epigenetic consequences of E2F7 loss. Furthermore, they serve as a platform for genetic interaction screens to identify modulators of E2F7-dependent pathways. For additional technical information, please contact Ascent Research.
