The EID2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population in which the EID2 gene (encoding EP300-interacting inhibitor of differentiation 2) has been disrupted. This heterogeneous pool of HAP1 cells carries diverse loss-of-function alleles, providing a robust model for studying EID2-dependent transcriptional regulation without clonal selection. The polyclonal format is immediately suitable for population-based assays and pooled genetic screens, reflecting the editing outcomes of CRISPR-mediated gene targeting.
HAP1 cells are a near-haploid human cell line derived from the chronic myeloid leukemia (CML)-derived KBM-7 line. They display fibroblast-like adherent growth and retain haploidy in a majority of cells, with some spontaneous diploidization. The haploid genome simplifies genetic analyses by ensuring single-allele disruptions yield clear phenotypes, making HAP1 a favored platform for functional genomics, drug sensitivity testing, and signaling pathway dissection in cancer research.
EID2 functions as a transcriptional corepressor that binds EP300/p300 and RB1 to inhibit histone acetyltransferase activity and repress E2F-dependent transcription. It interacts with HDAC1 and E2F1, forming repressive complexes on promoters of target genes such as CCND1, MYC, and CDKN1A. EID2 is regulated by differentiation signals, MYC, and EP300, positioning it within pathways controlling cell cycle progression and differentiation. Loss of EID2 disrupts the p300/CBP?CE2F/RB axis and may alter Notch signaling outputs.
In HAP1 cells, EID2 knockout removes a repressive constraint on E2F activity, potentially upregulating proliferation-associated genes and perturbing cell cycle control. Given the CML background, this model is relevant for investigating leukemogenesis and tumor-suppressive roles of EID2. The near-haploid state enhances phenotype penetrance, enabling clear readouts of EID2??s impact on chromatin modification and transcriptional networks. Researchers can study how EID2 loss influences drug sensitivity and uncover synthetic lethal relationships in cancer cells.
These polyclonal knockout cells are compatible with multiple assays, including western blotting for protein knockdown, RT-qPCR for target gene expression, co-immunoprecipitation to probe EID2?CEP300/RB1 complexes, and luciferase reporters for E2F activity. ChIP-qPCR can map epigenetic changes at E2F targets, while flow cytometry assesses cell cycle alterations. Drug sensitivity assays further explore therapeutic responses. For inquiries, contact Ascent Research.
