HDAC5 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human HAP1 cells, generated for loss-of-function studies of the HDAC5 gene. This product comprises a genetically diverse pool of cells carrying disruptive mutations at the HDAC5 locus, providing a robust model to investigate HDAC5-dependent biology without clonal selection bias. The knockout format supports population-level assays and is suitable for a broad range of functional genomics and drug discovery applications.
The host HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. Its near-haploid karyotype permits efficient single-allele knockout and unambiguous phenotype assignment, making it a widely used system for CRISPR-based genetic screens. HAP1 cells retain myeloid signaling characteristics and are amenable to high-throughput transfection, imaging, and biochemical analyses.
HDAC5 is a Class IIa histone deacetylase that represses transcription by deacetylating histone H3 and H4 and recruiting corepressor complexes including NCoR and SMRT. Its activity is controlled by phosphorylation from upstream kinases such as CaMKII, CaMKIV, PKD1, AMPK, and PKA, leading to 14-3-3 protein binding and nuclear export. In the nucleus, HDAC5 directly interacts with MEF2 transcription factors (MEF2A, MEF2C, MEF2D), RUNX2, FOXO factors, NFAT, and p53, thereby regulating gene programs in cell growth, cardiac hypertrophy, neuronal differentiation, and metabolic signaling. This positions HDAC5 as an integrator of MAPK, cAMP, calcium, and AMPK pathway inputs.
In the HAP1 context, HDAC5 disruption enables precise dissection of its role in CML-derived cells and epigenetic regulation. The near-haploid background minimizes genetic redundancy, facilitating clear genotype-phenotype correlations. The polyclonal nature of the product mirrors cellular heterogeneity, making it valuable for drug response studies and resistance profiling. Loss of HDAC5 in this model allows investigation of altered histone acetylation patterns, MEF2 target gene derepression, and cross-talk with other chromatin modifiers.
Researchers can utilize these cells for HDAC inhibitor screening, epigenetic mechanistic studies, and functional analyses of MEF2-dependent transcription. Typical assays include western blotting and immunofluorescence for HDAC5 expression and localization, ChIP-qPCR for promoter histone acetylation, co-immunoprecipitation with 14-3-3 or MEF2, and flow cytometry for cell cycle and apoptosis. Transcriptomic profiling via RNA-seq can reveal global changes upon HDAC5 loss. For further information or to inquire about custom knockout cell solutions, please contact Ascent Research.
