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.
FTO Knockout HT29 Polyclonal Cells
Cat. No. ARG14409
DDX19A Knockout Hela Polyclonal Cells
Cat. No. ARG7955
ARAF Knockout HT29 Polyclonal Cells
Cat. No. ARG33001
CCPG1 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG43327
DNAJC10 Knockout jurkat Polyclonal Cells
Cat. No. ARG39193
ANPEP Knockout AGS Polyclonal Cells
Cat. No. ARG26572
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.
