The CASP7 Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population targeting CASP7 in HAP1 cells. This loss-of-function model uses CRISPR/Cas9-mediated gene disruption to generate a heterogeneous pool of cells with CASP7 disruption, providing a robust system for apoptosis studies without clonal selection artifacts. It is a research-grade reagent for advanced molecular and cellular biology investigations.
HAP1 cells are derived from KBM-7 chronic myeloid leukemia, exhibiting a near-haploid karyotype and adherent, fibroblast-like morphology. This near-haploid background simplifies genetic manipulation and facilitates efficient CRISPR-based knockout generation and phenotypic screening. Their leukemic origin provides a disease-relevant context for studying apoptosis dysregulation in hematological malignancies.
CASP7 is an executioner caspase activated by initiator caspases CASP8 and CASP9 downstream of death receptors (FAS, TNFRSF10A/B) and the mitochondrial apoptosome (APAF1/cytochrome c), respectively. Once activated, it cleaves substrates such as PARP1, DFFA, LMNA, GSN, and ACTB, mediating cellular disassembly. Its activity is inhibited by XIAP and BIRC2, which are antagonized by DIABLO and HTRA2, and can be directly processed by GZMB. Thus, CASP7 integrates signals from extrinsic, intrinsic, and immune cytotoxic pathways.
In HAP1 cells, the near-haploid genome ensures that CRISPR-mediated disruption likely results in functional knockout, creating a highly penetrant loss-of-function model. This model allows dissection of CASP7-dependent apoptosis in a leukemic context, enabling studies of drug sensitivity, compensatory signaling, and the role of executioner caspases in CML biology. The polyclonal nature averts clonal adaptation, better mimicking heterogeneous tumor populations.
Applications include mechanistic apoptosis research, cancer drug target validation, and high-throughput screens for apoptosis regulators. It supports synthetic lethality profiling, drug sensitivity assays, and resistance studies. Compatible assays: caspase-7 activity assays, Annexin V staining, western blotting for cleaved CASP7 and PARP1, TUNEL, cell viability assays (MTT, CellTiter-Glo), clonogenic survival, and RNA-sequencing. For ordering or technical support, contact Ascent Research.
