In Stock Cell Lines
Mus musculus (Mouse)
Brain
Adherent and suspension
The Nlrp3 Knockout BV-2 Cell Line is a CRISPR/Cas9-edited immortalized murine microglial cell line with targeted disruption of the Nlrp3 gene, encoding the NLRP3 inflammasome sensor protein. Derived from C57BL/6 mouse, BV-2 cells retain core microglial functions such as phagocytosis and inflammatory signaling, making this a robust model for neuroinflammation studies. NLRP3 interacts with ASC and NEK7 to activate caspase-1, which cleaves pro-IL-1?? and pro-IL-18 into active cytokines and gasdermin D to induce pyroptosis. This knockout line allows precise investigation of inflammasome-dependent cytokine release and pyroptosis, and is applicable to NLRP3 inhibitor screening, Alzheimer's disease research, and inflammasome characterization using western blotting, ELISA, and immunofluorescence.
CAMSAP1 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30610
MERTK Knockout HGC-27 Polyclonal Cells
Cat. No. ARG18213
CDKN1B Knockout jurkat Polyclonal Cells
Cat. No. ARG13522
ATXN2 Knockout Hela Polyclonal Cells
Cat. No. ARG37585
MPZL2 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17849
CSTF2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4333
The Nlrp3 Knockout BV-2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the immortalized murine microglial BV-2 line, engineered to disrupt the Nlrp3 gene. This loss-of-function model allows researchers to interrogate NLRP3-dependent signaling in a microglial context.
The BV-2 host cell line originates from C57BL/6 mouse brain and was immortalized through retroviral expression of v-raf and v-myc oncogenes. It maintains key microglial characteristics such as immune surveillance, phagocytosis, and responsiveness to inflammatory stimuli. As an adherent cell line, BV-2 facilitates consistent culture and is extensively employed in neuroinflammation studies.
The Nlrp3 gene encodes the sensor component of the NLRP3 inflammasome, a multiprotein complex that assembles following activation by stimuli such as TLR4 agonists (e.g., LPS), extracellular ATP acting on the P2X7 receptor, potassium efflux, reactive oxygen species (ROS), and lysosomal cathepsin B release. Upon activation, NLRP3 interacts with the adaptor ASC (PYCARD) and the kinase NEK7 to recruit procaspase-1, driving its autocatalytic cleavage into active caspase-1. Active caspase-1 then proteolytically processes the downstream targets pro-IL-1?? and pro-IL-18 into mature, secreted cytokines, and cleaves gasdermin D (GSDMD) to release its N-terminal domain, which oligomerizes to form membrane pores, executing pyroptotic cell death. This pathway is primed by NF-??B-dependent transcriptional upregulation of NLRP3 and pro-IL-1??, linking it to broader inflammatory signaling networks.
In the BV-2 microglial context, NLRP3 inflammasome activity is a critical mediator of neuroinflammatory processes implicated in Alzheimer’s disease, acute brain injury, and chronic neurodegenerative conditions. The Nlrp3 knockout cell line enables specific interrogation of NLRP3-dependent IL-1??/IL-18 release and pyroptosis separate from parallel pathways such as Toll-like receptor and NF-??B signaling. This model is invaluable for studying microglial contributions to neuroinflammation and for evaluating the efficacy and specificity of NLRP3-targeted pharmacological inhibitors.
Key research applications include mechanistic studies of inflammasome assembly, profiling cytokine secretion by ELISA, analyzing ASC speck formation via immunofluorescence, and measuring caspase-1 enzymatic activity. The line supports drug screening for NLRP3 inhibitors, pyroptosis quantification by flow cytometry (PI uptake) or LDH release, and gene expression analysis by real-time RT-qPCR. It is also widely used in Alzheimer’s disease research and microglial functional studies. For technical inquiries, please contact Ascent Research.
