The KDM4B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the KDM4B gene in the HAP1 cell line. This heterogeneous pool of cells carries loss-of-function mutations introduced by CRISPR/Cas9-mediated gene disruption, enabling efficient loss-of-function studies without clonal isolation. The knockout model provides a valuable tool for probing KDM4B deficiency in a near-haploid human background.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells, displaying an adherent fibroblast-like morphology. Its near-haploid karyotype simplifies genetic analysis, as disruption of a single allele often yields complete loss of function, making it ideal for knockout studies. Widely adopted for functional genomics, HAP1??s robust growth and compatibility with CRISPR editing support mechanistic investigations.
KDM4B (JMJD2B) is a histone lysine demethylase that removes di- and trimethylation from H3K9, serving as an epigenetic eraser that relieves repressive chromatin marks to promote transcriptional activation. Regulated by HIF-1??, androgens, and growth factors, KDM4B interacts with the androgen receptor and NuRD complex components, linking hormone signaling to chromatin remodeling. Downstream targets include cell cycle regulators and oncogenes, mediating effects on DNA repair, proliferation, and differentiation.
In HAP1 cells, KDM4B knockout enables dissection of epigenetic regulation in a leukemic context. The near-haploid background enhances phenotype penetrance, facilitating attribution of effects to KDM4B loss. This model is particularly relevant to cancer research, where KDM4B overexpression alters H3K9 methylation to drive oncogenesis. It supports studies on chromatin state alterations, gene expression changes, and cellular responses to DNA damage or targeted agents.
Applications include epigenetic studies using ChIP-qPCR for H3K9me3 profiling, western blotting for histone marks, and RT-qPCR for target gene expression. Cell proliferation and drug sensitivity assays assess the functional impact of KDM4B loss on cancer cell fitness and treatment response. This knockout tool is also suited for functional genomics screens aiming to decipher epigenetic pathways in disease. For further details, contact Ascent Research.
