The ADPGK Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human near-haploid HAP1 cell line, designed to disrupt expression of the ADPGK gene. This product provides a genetically defined loss-of-function model for investigating the role of ADP-dependent glucokinase (ADPGK) in cellular metabolism and stress response. The pooled knockout cells enable robust and scalable experimental setups while preserving the inherent advantages of the HAP1 background for genetic screens and functional genomics studies.
The HAP1 cell line originates from a chronic myeloid leukemia (CML) patient and features a near-haploid karyotype, which significantly minimizes functional redundancy arising from diploid genomes. This characteristic makes HAP1 cells an optimal host for CRISPR-based genetic modifications by reducing the likelihood of residual wild-type alleles. The cell line is widely adopted in biomedical research for its suitability in high-throughput genetic screens, targeted gene editing, and phenotypic profiling, particularly in the context of cancer biology and metabolic research.
ADPGK encodes an ADP-dependent glucokinase that catalyzes the phosphorylation of glucose to glucose-6-phosphate (G6P) using ADP rather than ATP as a phosphate donor. This alternative glycolytic step is particularly important under hypoxia, where ATP is scarce. ADPGK expression is regulated by hypoxia-inducible factor 1-alpha (HIF1A), linking its activity to oxygen availability. The generated G6P serves as a substrate for glycolysis and the pentose phosphate pathway, thereby sustaining glycolytic flux and nucleotide biosynthesis. Thus, ADPGK acts upstream of key metabolic nodes to maintain energy homeostasis and anabolic processes during metabolic stress.
In HAP1 cells with a near-haploid genome, ADPGK knockout eliminates the ADP-dependent route of glucose phosphorylation, forcing reliance on ATP-dependent hexokinases. This makes the model ideal for studying metabolic rewiring and hypoxia tolerance without confounding gene redundancy. The polyclonal population preserves cellular heterogeneity, offering a more realistic representation of tumor cell behavior than clonal isolates. Consequently, this model supports investigations into how cancer cells adapt their metabolism to survive adverse microenvironments.
This ADPGK polyclonal knockout cell model is highly applicable to diverse research areas including cancer metabolism, glycolysis, hypoxia response, and metabolic drug target validation. Representative experimental applications include glucose uptake assays, lactate production measurements, Seahorse metabolic flux analysis, Western blotting, RT-qPCR, enzyme activity assays, and hypoxia survival assays. By providing a versatile tool for functional interrogation of ADPGK-dependent pathways, these cells facilitate mechanistic studies and therapeutic screening in oncology and metabolic disease contexts. For further information, technical support, or customized cell services, please contact Ascent Research.
