The CASP7 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma line, targeting the CASP7 gene. This heterogeneous product captures a spectrum of CRISPR/Cas9-mediated gene disruptions, providing a robust loss-of-function model for studying executioner caspase biology without clonal selection bias. The polyclonal format is particularly suited for population-level functional assays and drug screening applications.
HeLa cells are an immortalized cervical adenocarcinoma epithelial line containing integrated human papillomavirus type 18 (HPV-18) sequences, which functionally inactivate the tumor suppressors p53 and Rb. This genetic background makes HeLa cells a well-established platform for investigating apoptosis regulation and cancer biology. Their robust proliferation, ease of genetic manipulation, and extensive literature support enable reproducible experimental systems for studying cell death pathways.
CASP7 is an executioner caspase activated by initiator caspases CASP8 and CASP9 upon engagement of the extrinsic and intrinsic apoptosis pathways, respectively. Once activated, CASP7 proteolytically cleaves critical substrates including PARP1, DFF45/ICAD, LMNA, GSN, and ROCK1 to execute apoptotic cell death. Upstream signals from death receptors such as FASLG/FAS and TNF/TNFR1, the mitochondrial pathway involving BAX, BID, CYCS, and APAF1, and the p53 tumor suppressor converge on CASP7 activation. The caspase is directly inhibited by XIAP, which is antagonized by the mitochondrial protein SMAC/DIABLO. Disruption of CASP7 in this knockout population impairs the apoptotic proteolytic cascade, allowing dissection of caspase-dependent signaling networks.
CASP7 knockout in the HeLa background generates a model of apoptosis resistance that is highly relevant to cancer research. The combined loss of CASP7 function and the inherent p53 and Rb inactivation in HeLa cells mirrors scenarios of chemoresistance often observed in malignancies. This model enables systematic investigation of how cancer cells evade programmed cell death induced by therapeutics and death receptor ligands, and facilitates identification of compensatory survival pathways that emerge upon executioner caspase deficiency. The system is also valuable for exploring synthetic lethal interactions in an apoptosis-compromised context.
Researchers can utilize this product in diverse assays including western blotting for cleaved CASP7 and PARP1, fluorogenic caspase activity assays, Annexin V staining with flow cytometry for apoptosis quantification, and RT-qPCR for CASP7 mRNA analysis. Applications span apoptosis mechanism studies, high-throughput screening for agents that overcome drug resistance, and proteomic identification of novel caspase substrates. The polyclonal knockout population is ideal for CRISPR-based synthetic lethality screens to uncover targets that selectively kill CASP7-null cells. For further information, including genotyping data and bulk pricing, please contact Ascent Research.
