The ING5 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function analyses of the ING5 tumor suppressor gene. This product provides a heterogeneous pool of cells carrying diverse gene-disrupting edits introduced by CRISPR/Cas9, enabling robust assessment of ING5-dependent phenotypes without clonal selection artifacts. The polyclonal format is particularly suited for pooled functional genomics screens, high-throughput phenotyping, and studies where population-level responses are desired.
The host HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) isolate, which has been adapted for adherent culture. Its near-haploid karyotype (except for a disomic chromosome 8) simplifies mutational analysis and reduces genetic redundancy, making it an exemplary platform for CRISPR-based knockout screens and functional investigation of tumor suppressors. HAP1 cells retain key signaling pathways, allowing dissection of cancer-relevant mechanisms in a genetically tractable system.
ING5 functions as a core subunit of the HBO1 (KAT7) and MOZ/MORF (KAT6A/KAT6B) histone acetyltransferase complexes, where it directs acetylation of histone H3 and H4 tails to promote an open chromatin state. Critically, ING5 also facilitates acetylation of the tumor suppressor TP53 at lysine residues, enhancing its transcriptional activity. This results in upregulation of cell cycle inhibitor CDKN1A (p21) and pro-apoptotic effector BAX, thereby coupling histone modification to TP53-dependent cell cycle arrest and apoptosis. The protein interacts with complex members EPC1 and MEAF6 and is regulated by DNA damage response kinases ATM/ATR and by transcription factor E2F1, establishing a stress-responsive signaling axis.
Disruption of ING5 in the HAP1 near-haploid background creates a valuable model for probing the interplay between histone acetylation and tumor suppression. Because HAP1 cells possess a simplified genome, phenotypic consequences of ING5 loss are more directly attributable to the gene disruption, facilitating identification of synthetic lethal relationships and downstream effectors. This cell model enables investigation of altered histone modification landscapes, impaired DNA damage signaling through ATM-TP53, and deregulated cell cycle progression, providing insights into oncogenic processes where ING5 is often downregulated, such as colorectal, gastric, and head and neck cancers.
Research applications encompass broad functional studies: chromatin immunoprecipitation (ChIP-qPCR) to measure changes in histone H3/H4 acetylation at target promoters, transcriptional profiling via RNA-seq or RT-qPCR to assess downstream effectors like CDKN1A and BAX, and functional assays for cell cycle arrest and apoptosis. The polyclonal population is also suited for colony formation, migration/invasion assays, and drug sensitivity testing with HDAC inhibitors or genotoxic agents. This ING5 knockout model thus supports cancer biology, epigenetics, and drug discovery research. For further information, please contact Ascent Research.
