This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 near-haploid human cell line, in which the H1-2 gene has been disrupted to create a loss-of-function model. The H1-2 gene encodes a linker histone that plays critical roles in chromatin organization, apoptosis regulation, and the DNA damage response. The polyclonal format provides a heterogeneous pool of gene-edited cells, enabling flexible experimental design and robust representation of genetic diversity. This knockout model is ideal for investigating the mechanistic contributions of H1-2 to cellular processes without the constraints of single-cell clonal isolation.
The HAP1 host cell line is a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia cell line. HAP1 cells exhibit an adherent, fibroblast-like morphology and are widely employed in functional genomics and genetic knockout screens due to their haploid karyotype, which simplifies gene targeting and phenotypic analysis. This background provides a human cellular context for studying gene function, with particular relevance to cancer biology and hematopoietic lineage research. The parental KBM-7 origin also links HAP1 cells to leukemia-associated signaling pathways, offering a disease-relevant platform.
H1-2 (histone H1.2) is a member of the linker histone family that binds to nucleosomes and promotes higher-order chromatin compaction. Mechanistically, H1-2 is regulated by p53 and cyclin-dependent kinases in response to DNA damage signals. It interacts with nucleosomes, DNA, and chromatin remodeling complexes to globally influence gene expression. During apoptosis, H1-2 is released from mitochondria and contributes to p53-mediated transcriptional activation of pro-apoptotic factors such as BAK, thereby engaging caspase-dependent execution pathways. This positions H1-2 at the intersection of chromatin dynamics and programmed cell death signaling.
In the HAP1 cellular context, disruption of H1-2 enables precise dissection of linker histone functions in chromatin organization and apoptosis. This knockout model is particularly valuable for studying p53-dependent apoptosis mechanisms, DNA damage response pathways, and the role of linker histones in leukemia and other cancers. The near-haploid nature of HAP1 cells reduces genetic complexity, allowing clear attribution of phenotypic changes to H1-2 loss. Moreover, the model facilitates investigation into neurodevelopmental disorders linked to H1-2 dysfunction, supporting translational research efforts.
Researchers can apply this knockout cell population in a variety of assays, including ChIP-seq for genome-wide chromatin profiling, Western blot and immunofluorescence for protein analysis, caspase activity assays and flow cytometry for apoptosis quantification, RT-qPCR for gene expression studies, and colony formation assays to assess cellular fitness. This product is optimized for use in chromatin biology, apoptosis research, and cancer genetic screens. For further technical details or bespoke services, please contact Ascent Research.
