The CASP7 Knockout Raji Polyclonal Cells represent a pooled population of human B lymphoblastoid Raji cells engineered via CRISPR/Cas9-mediated gene disruption of the CASP7 locus. This product provides a loss-of-function model for caspase-7, an executioner caspase central to the execution phase of apoptosis. As a polyclonal cell pool, this model contains a heterogeneous mixture of targeted alleles, enabling functional analysis at the population level without clonal selection biases. The knockout model facilitates the study of caspase-7-dependent signaling in a lymphoma-relevant context.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblastoid line widely used to model B-cell malignancies and immune cell biology. As mature B lymphocytes, Raji cells retain features of antigen-presenting cells and exhibit robust proliferation due to MYC translocation and EBV-driven immortalization. This background provides a physiologically relevant system for interrogating apoptosis pathways in lymphomagenesis, where dysregulation of programmed cell death contributes to tumor survival and chemoresistance.
Caspase-7 is a critical executioner caspase activated downstream of both extrinsic and intrinsic apoptotic signals. Through proteolytic cleavage by initiator caspases such as caspase-8 and caspase-9, caspase-7 becomes activated and subsequently processes key substrates including PARP, lamin A/C, ICAD/DFF45, and ROCK1, leading to characteristic apoptotic hallmarks. Its activity is tightly regulated by inhibitor of apoptosis proteins (IAPs) like XIAP, c-IAP1, and c-IAP2, counteracted by Smac/DIABLO release from mitochondria. The caspase-7 pathway integrates signals from death receptor ligands (FasL, TRAIL) and the cytochrome c/Apaf-1 apoptosome, placing it at the convergence of apoptosis cascades.
In the Raji background, CASP7 knockout disrupts the terminal effector phase of apoptosis, potentially conferring resistance to death-receptor- and mitochondrial-mediated cell death stimuli. This model recapitulates aspects of apoptosis evasion observed in Burkitt lymphoma and other B-cell malignancies, where caspase-7 downregulation is linked to tumor progression and drug resistance. By abrogating caspase-7 function, these cells enable systematic dissection of caspase-7-dependent versus -independent death pathways, and they provide a platform to evaluate therapeutic strategies aimed at restoring apoptosis in lymphoma.
Researchers can employ the CASP7 knockout Raji polyclonal cells in diverse experimental workflows, including apoptosis mechanism studies using Annexin V/PI flow cytometry, caspase-7 enzymatic activity assays, and PARP cleavage western blots. The model is well-suited for drug sensitivity profiling against chemotherapeutics or targeted agents, screening for caspase-7 modulators, and functional genomics approaches. Additional applications include RT-qPCR analysis of downstream targets and investigation of upstream regulators such as caspase-8 or XIAP. For further information, contact Ascent Research.
