The KDM3B Knockout HAP1 Polyclonal Cells constitute a polyclonal population of HAP1 cells in which the KDM3B gene has been disrupted by CRISPR/Cas9-mediated genome editing. This loss-of-function model enables systematic investigation of KDM3B-dependent epigenetic regulation without the confounding effects of clonal variation. As a polyclonal knockout product, it provides a heterogeneous yet genetically defined pool of cells carrying various KDM3B-disrupting alleles, making it well-suited for pooled functional genomics screens and robust population-level assays.
The HAP1 host cell line is a near-haploid human cell line derived from a male patient with chronic myeloid leukemia. It is BCR-ABL1 positive and exhibits an adherent, fibroblast-like morphology. HAP1??s haploid karyotype facilitates straightforward gene-function analysis because a single gene copy is targeted, and phenotypic consequences can be directly attributed to the introduced mutation. This feature has established HAP1 as a powerful platform for genetic screens and mechanistic studies in a myeloid lineage background.
KDM3B (lysine demethylase 3B) is a histone demethylase that specifically removes mono- and dimethyl marks from lysine 9 of histone H3 (H3K9me1/me2). By demethylating H3K9 at target gene promoters, KDM3B functions as a transcriptional coactivator for nuclear receptors such as androgen receptor (AR) and retinoic acid receptor alpha (RARA). It is activated by androgen receptor ligands, all?trans retinoic acid, and hypoxia?inducible factors, and orchestrates expression of downstream targets including PSA, CD11b, and CD14. KDM3B forms complexes with AR and RARA, and its activity is central to chromatin remodeling events that control myeloid differentiation and hormone?responsive gene programs.
In the HAP1 myeloid leukemia background, disruption of KDM3B offers a defined genetic model to dissect the epigenetic underpinnings of myeloid differentiation and leukemogenesis. Because HAP1 cells retain BCR-ABL1 signaling and a near?haploid genome, the knockout population allows unambiguous linkage of KDM3B activity to changes in histone methylation patterns and transcriptional outputs. This system is particularly valuable for exploring how KDM3B?dependent chromatin remodeling contributes to the pathology of acute myeloid leukemia and myelodysplastic syndromes, and for evaluating therapeutic strategies targeting epigenetic modifiers in these diseases.
Researchers have applied this knockout model in a range of experimental workflows, including ChIP?qPCR to map H3K9me2 dynamics, RT?qPCR and RNA?seq to profile transcriptional changes, and flow cytometry using CD11b and CD14 to assess myeloid differentiation status. It is also used in drug sensitivity assays to test compounds that modulate epigenetic enzymes or nuclear receptor signaling. The polyclonal format enhances assay reproducibility in population-based readouts and is compatible with high?throughput screening approaches. Together, these applications make the KDM3B Knockout HAP1 Polyclonal Cells a versatile tool for functional genomics, cancer epigenetics, and nuclear receptor biology. For technical support or further information, please contact Ascent Research.
