ATAD2B Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the ATAD2B gene has been disrupted to create a loss-of-function model. This product delivers a heterogeneous pool of HAP1 cells harboring targeted gene disruption, enabling functional interrogation of ATAD2B in a near-haploid human background. The polyclonal format avoids single-cell clone isolation and is well suited for pooled phenotypic screens and bulk biochemical analyses where population-level responses are informative. Researchers can utilize these cells to dissect ATAD2B-dependent processes without the selective pressure of clonal expansion, providing a physiologically relevant window into gene function.
HAP1 is a human male near-haploid chronic myeloid leukemia cell line originally derived from the KBM-7 line, with a largely haploid karyotype except for a disomic region of chromosome 15. This genetic simplicity makes HAP1 an exceptional host for CRISPR-mediated knockout studies, as a single guide RNA can achieve functional gene disruption without the complication of multiple alleles. The near-haploid state reduces the need for homozygous targeting and facilitates straightforward interpretation of loss-of-function phenotypes. HAP1 cells retain key signaling networks and DNA damage response pathways inherent to myeloid cells, making them a versatile platform for studying chromatin biology and oncogenic mechanisms relevant to hematologic malignancies and solid tumors.
ATAD2B encodes an AAA+ ATPase and bromodomain-containing chromatin regulator that binds acetylated histones H3 and H4 to modulate chromatin architecture. As part of its molecular function, ATAD2B facilitates DNA replication fork progression and DNA repair by interacting with replication protein A and the FACT complex, and it contributes to homologous recombination through connections with RAD51 and the MCM complex. ATAD2B is activated by upstream E2F transcription factors and MYC, and can be regulated by nuclear receptors, positioning it at the nexus of cell cycle control and oncogenic transcription. Downstream, ATAD2B promotes the expression or activity of cell cycle regulators and chromatin remodeling complexes, while pathway components such as ATM, ATR, CHK1, and CDC45 further coordinate the DNA damage response.
In the HAP1 background, disruption of ATAD2B offers a powerful system to examine the interplay between chromatin dynamics, replication stress, and genomic instability. The polyclonal knockout population provides a broad representation of editing events, enabling the study of ATAD2B-dependent phenotypes in a context that mirrors the heterogeneity of tumor cell populations. This model is particularly valuable for investigating oncogenic coactivation, as ATAD2B has been implicated in breast cancer, hepatocellular carcinoma, acute myeloid leukemia, and other solid tumors. By combining near-haploid genetics with a loss-of-function approach, researchers can efficiently map ATAD2B-dependent vulnerabilities and identify synthetic lethal interactions relevant to targeted therapy development.
Typical applications include drug target validation, functional genomics, and DNA damage repair studies, where ATAD2B??s role in replication stress response can be probed using assays such as immunoblotting, RT-qPCR, ChIP-qPCR, and cell cycle analysis. The knockout cells are also suitable for drug sensitivity assays to test compounds that exploit chromatin regulatory defects, and for flow cytometry-based apoptosis and proliferation analyses. These cells support immunofluorescence microscopy to assess chromatin changes and repair foci formation. For further information or technical support, please contact Ascent Research.
