The KDM5A Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population for loss-of-function studies of the KDM5A gene. Derived from the human HAP1 cell line, this product features heterogeneous knockout alleles generated by targeted gene disruption, avoiding clonal bias and enabling population-level analysis of chromatin dynamics, epigenetic mechanisms, and cancer biology.
HAP1 cells originate from the KBM-7 CML cell line, possessing a stable near-haploid karyotype and male genetic background. This haploid nature streamlines CRISPR-based knockouts by eliminating allelic redundancy, making HAP1 a preferred platform for functional genomics and genetic screens. The line retains myeloid progenitor features, including BCR-ABL1 expression, while providing clean phenotypes for mechanistic studies. The haploid genome simplifies genetic manipulation and phenotype interpretation, making it an ideal chassis for knockout studies.
KDM5A encodes a histone demethylase that removes di- and tri-methylation from H3K4, acting as a transcriptional co-repressor. Activated by E2F transcription factors, MYC, and retinoic acid receptor signaling, KDM5A represses targets such as CDKN1A (p21) and HOX genes, thereby regulating cell cycle progression and differentiation. KDM5A functions within repressive complexes including RB1, PRC2, NuRD, SIN3A, and KDM5B, coupling H3K4 demethylation to chromatin remodeling, Notch signaling, and RB pathway control. Its dysregulation is implicated in acute myeloid leukemia, lung cancer, breast cancer, and intellectual disability.
In the HAP1 haploid setting, KDM5A knockout permits unambiguous assessment of epigenetic effects, free from wild-type allele compensation. Given its CML origin, this model is particularly informative for hematologic cancer studies, where KDM5A alterations are common. ChIP-seq and ChIP-qPCR resolve histone mark changes with high clarity, and downstream target derepression can be directly monitored.
Applications include Western blot and RT-qPCR for knockout validation, ChIP-based assays for H3K4 methylation profiling, cell proliferation and colony formation analyses, and flow cytometry for cell cycle distribution. The polyclonal knockout population is suitable for drug target validation and functional genomics screens investigating KDM5A-dependent epigenetic reprogramming. For further information, please contact Ascent Research.
