The IAH1 Knockout HAP1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout population derived from the HAP1 cell line, featuring disruption of the IAH1 gene. This mixed population retains editing heterogeneity, providing a versatile loss-of-function model that circumvents clonal selection artifacts. It serves as a robust tool for probing IAH1-dependent cellular processes in a near-haploid genetic background.
The HAP1 host line is a near-haploid, adherent cell model originating from KBM-7 chronic myeloid leukemia cells. These cells display fibroblastic morphology and express the BCR-ABL fusion oncogene. Their haploid karyotype enables efficient gene disruption and clear genotype-phenotype correlations, making HAP1 a preferred system for functional genomics and knockout-based screening applications.
IAH1 encodes an esterase that hydrolyzes acetyl-CoA and short-chain acetate esters to acetate and CoA, directly regulating the acetyl-CoA pool. This metabolic node is modulated by upstream signals such as intracellular acetyl-CoA levels, acetate availability, and AMPK signaling. IAH1 activity influences global protein acetylation by affecting substrate supply for KATs and substrate clearance by HDACs and sirtuins. It is interconnected with acetyl-CoA biosynthetic enzymes like ACSS2 and ACLY, positioning IAH1 as a key regulator of acetate metabolism, energy homeostasis, and the acetylation landscape.
In the HAP1 context, IAH1 knockout enables dissection of acetyl-CoA dynamics in a genetically tractable, cancer-relevant system. The haploid background simplifies loss-of-function analysis and enhances the utility of this model for high-throughput genetic screens. Researchers can explore how IAH1-mediated control of acetyl-CoA availability impacts metabolic reprogramming and epigenetic regulation in a BCR-ABL-positive setting, potentially revealing cancer metabolic liabilities.
Applications include acetyl-CoA quantitation, acetyltransferase activity assays, western blotting for acetyl-lysine modifications, RT-qPCR profiling of metabolic gene expression, and metabolic tracing using labeled acetate. The cells are compatible with pooled CRISPR loss-of-function screens to map genetic interactions. This knockout model facilitates systematic study of IAH1??s role in metabolic and epigenetic processes. For additional information, please reach out to Ascent Research.
