The NINJ1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line. This product features targeted disruption of the NINJ1 gene, eliminating its expression across a heterogeneous cell pool. As a polyclonal knockout model, the cells preserve genetic diversity while abolishing NINJ1 function, making them suitable for bulk assays where population-level responses are monitored. The knockout is achieved via CRISPR/Cas9-mediated genome editing, introducing loss-of-function modifications at the NINJ1 locus without clonal isolation or single-cell expansion, thus avoiding potential clonal artifacts. These cells serve as a powerful tool for investigating NINJ1-dependent mechanisms of plasma membrane rupture and lytic cell death pathways.
The host Raji cell line originates from an EBV-positive Burkitt??s lymphoma patient and provides an immortalized B lymphocyte model widely used in lymphoma biology and immunological research. Raji cells exhibit high proliferative capacity and express key B-cell markers, making them a robust in vitro system for studying lymphocyte signaling, viral oncogenesis, and tumor immunology. As a suspension cell line, Raji is particularly amenable to high-throughput screening and flow cytometry-based applications. The EBV-driven transformation renders Raji cells susceptible to various death stimuli, including pyroptotic and necroptotic triggers, which are directly relevant to NINJ1??s function. This background offers a physiologically pertinent context for dissecting NINJ1-dependent cell death in B-cell malignancies.
NINJ1 is a key executor of plasma membrane rupture in pyroptosis and necroptosis, acting downstream of pore-forming GSDMD and MLKL. Activated by TNF-??, IL-1??, or LPS via NF-??B, NINJ1 oligomerizes to form lytic pores, causing release of DAMPs like HMGB1 and cytokines IL-1?? and IL-18. This process requires NLRP3 inflammasome, caspase-1/11, and RIPK1/RIPK3 signaling. NINJ1 also interacts with integrins and cytoskeleton regulators, linking cell adhesion to inflammatory lysis. Thus, NINJ1 sits at a critical node controlling inflammatory cell death. The knockout in Raji cells blocks membrane rupture, enabling study of pore events without lysis.
In the Raji Burkitt??s lymphoma context, NINJ1 knockout enables exploration of lytic cell death and DAMP release regulation in B lymphocytes under inflammatory and oncogenic stress. B-cell lymphoma studies can uncover how NINJ1 influences tumor microenvironment via cytokine release and assess pyroptotic/necroptotic lysis dependency, revealing therapeutic vulnerabilities. Additionally, the EBV-positive background permits investigation of viral latency interactions with NINJ1-mediated cell death, and the model is valuable for studying immunogenic DAMP release that shapes anti-tumor immunity.
These cells support diverse assays: Western blotting and qRT-PCR for NINJ1 disruption, propidium iodide uptake and LDH release to assess lysis, time-lapse microscopy of membrane dynamics, co-immunoprecipitation for oligomerization, and ELISA for HMGB1 and IL-1??/IL-18 release. Flow cytometry enables high-throughput viability analysis. Applications include inhibitor screening for lytic cell death in B lymphoma, inflammatory disease modeling, and DAMP-driven immune response studies. For further information, contact Ascent Research.
