The BRD2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, in which the BRD2 gene has been disrupted. This product provides a heterogeneous pool of knockout cells suitable for pooled functional genomics studies and drug sensitivity assays, allowing researchers to assess the functional consequences of BRD2 loss without clonal selection bias. The polyclonal format circumvents clonal artifacts and is ideal for screens requiring diverse knockout populations.
HAP1 is a near-haploid human cell line originally derived from the KBM-7 chronic myelogenous leukemia line. It is adherent, male, and retains a single copy of most chromosomes, making it an ideal model for haploid genetic studies. Its hematopoietic origin provides a physiologically relevant background for investigating blood cancers and hematopoiesis-related signaling pathways.
BRD2 is a BET family bromodomain protein that functions as an epigenetic reader of acetylated histones, facilitating the recruitment of transcriptional machinery including TBP, TFIID, Mediator, and SWI/SNF complexes. It is activated by CDK9/P-TEFb-mediated phosphorylation and functions downstream of NF-??B and JAK-STAT pathways. BRD2 transcriptionally activates critical proliferation and survival genes such as c-MYC, CCND1, BCL2, and CDK6, thereby promoting cell cycle progression and E2F target gene expression. Through these interactions, BRD2 integrates signaling to drive chromatin remodeling and transcription elongation.
In the HAP1 haploid model, BRD2 knockout eliminates a central activator of proliferative gene programs. The absence of a second allele ensures the full manifestation of loss-of-function phenotypes, enabling clear genotype-phenotype correlations. Disruption of BRD2 impairs the expression of downstream targets, leading to cell cycle arrest and altered sensitivity to pharmacological BET inhibition. This cellular system is therefore particularly useful for dissecting BRD2-dependent transcriptional control in hematopoietic cells and for evaluating the functional consequences of BET bromodomain inhibition.
Key applications include functional genomics, cancer biology research, BET inhibitor resistance studies, and drug target validation. The polyclonal knockout cells are compatible with Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, cell proliferation assays, flow cytometry, and BET inhibitor sensitivity assays. These cells can be used to investigate BRD2??s role in chromatin remodeling and transcription elongation, and to identify genetic interactions with other BET family members or compensatory pathways. For additional technical information or product inquiries, please contact Ascent Research.
