In Stock Cell Lines
Mus musculus (Mouse)
Brain
Adherent and suspension
The Gba Knockout BV-2 Cell Line is a CRISPR/Cas9-edited knockout cell line based on the C57BL/6-derived BV-2 microglial line, providing a loss-of-function model for lysosomal glucocerebrosidase. Disruption of Gba impairs glucosylceramide hydrolysis, disrupts autophagy, and alters signaling through TFEB-TFE3-MITF networks and interacting partners such as saposin C and LIMP-2/SCARB2. This microglial knockout model facilitates research into neuroinflammation, Gaucher disease, and Parkinson's disease, including studies of ??-synuclein clearance, cytokine profiling (e.g., IL-1??, TNF), and drug screening with assays for lipid accumulation, autophagy flux, and lysosomal health.
CA3 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22204
Cdc7 Knockout RAW 264.7 Polyclonal Cells
Cat. No. ARG12477
ADRM1 Knockout HCT116 Polyclonal Cells
Cat. No. ARG23196
HMBOX1 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30720
CA13 Knockout Hela Polyclonal Cells
Cat. No. ARG41629
EIF2AK2 Knockout HT29 Polyclonal Cells
Cat. No. ARG40942
The Gba Knockout BV-2 Cell Line is a CRISPR/Cas9-edited knockout cell line designed for the study of lysosomal glucocerebrosidase function and neuroinflammatory processes. This product features targeted disruption of the murine Gba gene in BV-2 microglial cells, resulting in a loss-of-function model for investigating sphingolipid metabolism and autophagy-lysosomal pathway dysregulation.
The BV-2 host cell line is an immortalized murine neonatal microglial cell line derived from C57BL/6 mice, widely employed as a model for central nervous system immune surveillance and inflammatory mediator production. BV-2 cells retain key characteristics of primary microglia, including responsiveness to immune stimuli and phagocytic capacity, making them a robust system for neuroinflammation research.
GBA encodes lysosomal glucocerebrosidase, which hydrolyzes glucosylceramide to ceramide and glucose, a critical step in sphingolipid metabolism. The enzyme is regulated by the CLEAR network transcription factors TFEB, TFE3, and MITF, and its activity is facilitated by interacting partners such as saposin C and the lysosomal receptor LIMP-2/SCARB2. Downstream, GBA influences ceramide generation, autophagy flux, and ??-synuclein clearance. Knockout of Gba disrupts these processes, leading to accumulation of glucosylceramide and sphingolipid intermediates, impaired autophagic turnover marked by altered LC3B-I/II conversion and p62/SQSTM1 levels, and lysosomal dysfunction evident through changes in LAMP1, LAMP2, and cathepsin D processing.
In microglial cells, loss of GBA function mirrors key pathological features of Gaucher and Parkinson’s diseases, where lysosomal dysfunction and chronic neuroinflammation are central. The BV-2 knockout model recapitulates glucosylceramide accumulation, autophagy blockade, and heightened production of pro-inflammatory cytokines such as IL-1?? and TNF, providing a physiologically relevant platform for studying microglia-mediated neurodegeneration and lipid storage disorders.
Typical applications include neuroinflammation modeling, investigation of glucocerebrosidase-related pathologies such as Gaucher disease and Parkinson’s disease, and functional studies of autophagy-lysosomal dysfunction. The line is well-suited for drug screening of GBA modulators and anti-inflammatory compounds, with readouts including glucocerebrosidase enzymatic assays, lipidomic quantification of glucosylceramide, western blotting for LC3B and p62, and cytokine profiling by RT-qPCR or ELISA. Additional assays such as phagocytosis, LysoTracker-based lysosomal pH measurement, and apoptosis detection further expand its utility for characterizing microglial immune responses and lysosomal health. For further details, please contact Ascent Research.
