EID1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EID1 gene. Derived from HAP1 cells, this heterogeneous loss-of-function model avoids single-cell cloning artifacts and provides a robust tool for functional genomics. The polyclonal cells are supplied live and ready for expansion.
The HAP1 cell line is a near-haploid, adherent human cell line originating from KBM-7 chronic myeloid leukemia. Its haploidy enables effective single-copy gene disruption, facilitating clear phenotypic readouts in genetic screens and drug sensitivity assays. HAP1 is widely used in cancer research due to its leukemic background and fibroblast-like morphology.
EID1 functions as a transcriptional corepressor and inhibitor of differentiation by negatively regulating EP300/CBP histone acetyltransferase activity. Direct interaction with EP300/CBP suppresses acetylation-dependent transcription, repressing differentiation and promoting proliferation. EID1 is activated by retinoic acid and TGF-??, interacts with nuclear receptors and p53, and modulates p53-dependent transcription, influencing cell cycle arrest and apoptosis. Key downstream targets include CDKN1A (p21) and CCND1 (cyclin D1). EID1 also associates with HDACs, forming repressor complexes. Thus, EID1 integrates signals from retinoic acid, TGF-??, p53, and Notch pathways to control gene expression programs governing cell fate.
Disrupting EID1 in the HAP1 near-haploid background provides a model to study proliferation, differentiation, and therapy resistance. Because HAP1 retains leukemic properties, EID1 loss may alter growth and apoptotic responses, relevant to chronic myeloid leukemia research. The polyclonal nature reflects diverse editing outcomes, enabling pooled genetic screens and assessment of gene essentiality, and facilitating discovery of synthetic lethal interactions.
Applications include differentiation blockade, cell cycle profiling, apoptosis assays, and haploid genetic screens. Assays such as Western blotting for EID1, p21, and cyclin D1; RT?qPCR of target genes; reporter assays for EP300/CBP activity; and co?immunoprecipitation of EID1?EP300 complexes are commonly employed. Viability, proliferation, and flow cytometric cell cycle analysis further support mechanistic studies. This model is suited for comparative analyses with wild-type HAP1 cells, enabling rigorous dissection of EID1?dependent pathways. For technical inquiries, contact Ascent Research.
