Genome-edited Cells
Large intestine (colon)
The Casp8 Knockout MC-38 Cell Line is a CRISPR/Cas9-edited murine colon adenocarcinoma cell line with targeted disruption of the Casp8 gene. Caspase-8 is the initiator caspase of the extrinsic apoptosis pathway, activated by Fas and TRAIL receptors via FADD recruitment, and also regulates necroptosis by cleaving RIPK1. This knockout model enables investigation of apoptosis resistance, necroptosis signaling, and death receptor agonist responses in a syngeneic C57BL/6 background. Key applications include apoptosis and necroptosis assays, evaluation of TRAIL sensitivity, co-immunoprecipitation of DISC complexes, and syngeneic tumor studies. For more details, contact Ascent Research.
ATF6B Knockout Hela Polyclonal Cells
Cat. No. ARG37492
ELANE Knockout MCF7 Polyclonal Cells
Cat. No. ARG41113
OSBPL5 Knockout AGS Polyclonal Cells
Cat. No. ARG3214
FMNL2 Knockout Raji Polyclonal Cells
Cat. No. ARG1264
CPTP Knockout Raji Polyclonal Cells
Cat. No. ARG901
Nlrp3 Knockout HT22 Cell Line
Cat. No. ARG0433
The Casp8 Knockout MC-38 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring stable disruption of Casp8 in the MC-38 murine colon adenocarcinoma background. This loss-of-function model enables precise dissection of caspase-8?Cdependent signaling pathways in a syngeneic colorectal cancer context. By eliminating caspase-8 expression, researchers can investigate consequences of impaired death receptor signaling, altered apoptotic and necroptotic responses, and potential compensatory mechanisms in tumor cells.
MC-38 cells are a widely used C57BL/6-derived colon adenocarcinoma line that forms aggressive tumors in immunocompetent hosts. Their syngeneic nature and defined immunogenicity make them a standard model for immuno-oncology studies, including checkpoint blockade and adoptive T cell therapies. The C57BL/6 background facilitates integration with transgenic hosts for in vivo mechanistic investigations.
Caspase-8, the initiator caspase of the extrinsic apoptosis pathway, is activated upon death receptor ligation (Fas, TRAIL receptors, TNFR1) and FADD recruitment within the DISC. Active caspase-8 cleaves executioner caspases-3 and -7 and processes Bid, linking to mitochondrial apoptosis. Caspase-8 also suppresses necroptosis by cleaving RIPK1, thereby restraining RIPK1/RIPK3/MLKL necrosome formation. Additionally, caspase-8 interacts with FLIP and cIAP1/2 to modulate NF-??B signaling, underscoring its central role in cell fate decisions.
In MC-38 cells, caspase-8 knockout abolishes extrinsic apoptosis, conferring resistance to death receptor agonists such as TRAIL and potentially shifting cell death toward necroptosis. This model allows examination of how caspase-8 loss impacts tumor growth, immune cell infiltration, and response to immunotherapies, thereby illuminating mechanisms of immune evasion and therapeutic resistance in colorectal cancer. Moreover, caspase-8 deficiency may unlock necroptotic death in the presence of caspase inhibition, providing a platform to study RIPK1/RIPK3/MLKL pathway dynamics.
Key applications include screening for caspase-8 modulators, necroptosis signaling studies using phospho-RIPK3 and phospho-MLKL readouts, co-immunoprecipitation of DISC components, and apoptosis assays such as Annexin V/PI staining. The line is also suited for syngeneic tumor models to assess tumor progression and immunotherapy responses. Standard techniques like Western blotting for caspase-8 fragments and flow cytometry for death receptor expression are directly applicable. For further information or to request a quotation, please contact Ascent Research.
