The ASRGL1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid human HAP1 cell line, targeting the ASRGL1 gene for loss-of-function studies. This product enables investigation of ASRGL1??s role in amino acid metabolism and related signaling pathways without the constraints of clonal selection.
HAP1 cells, originating from the KBM-7 chronic myeloid leukemia line, are a widely adopted model for functional genomics and drug screening due to their near-haploid karyotype and stable growth properties. This host cell line reduces genetic complexity, facilitating clear genotype-phenotype correlations in CRISPR-based screens.
ASRGL1 encodes an enzyme that deamidates L-asparagine to L-aspartate and ammonia, and also possesses isoaspartyl peptidase activity for protein repair. Transcriptionally activated by ATF4 and MYC under amino acid deprivation, ASRGL1 regulates intracellular asparagine availability, which in turn controls mTORC1 signaling and protein synthesis. The enzyme functionally interacts with L-asparagine and beta-aspartyl peptides, and its activity is integrated with asparagine synthetase (ASNS) and transaminases GOT1 and GOT2 to balance amino acid homeostasis and metabolic flux.
Disruption of ASRGL1 in HAP1 cells perturbs asparagine equilibrium, leading to mTORC1 signaling dysregulation and potential metabolic vulnerabilities. This model is valuable for studying acute lymphoblastic leukemia, where asparagine dependence determines response to asparaginase, and retinal dystrophy linked to impaired protein repair. The polyclonal knockout population is suitable for high-throughput drug sensitivity profiling to explore metabolic drug targets.
Applications include cancer metabolism research, functional genomics screens, and amino acid deprivation assays. Standard techniques such as L-asparaginase activity assays, LC-MS amino acid profiling, cell viability under starvation, Western blotting, RT-qPCR, and flow cytometry are compatible with this model. For more information, contact Ascent Research.
