The FBXO7 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the FBXO7 gene has been disrupted, generating a loss-of-function model in the human Raji B lymphocyte line. This polyclonal format maintains diverse editing events introduced via CRISPR/Cas9-mediated gene disruption, offering a robust system for studying FBXO7-dependent processes without relying on single-cell clonal isolates.
Raji cells are a suspension-adapted human B lymphocyte line originally derived from a Burkitt??s lymphoma patient. These lymphoma-derived B cells retain key immunological functions including antibody production, antigen presentation, and immune memory capabilities, making them a versatile host for investigating signaling networks. Their rapid proliferation and ease of culture have established Raji cells as a standard model for lymphomas and general cellular biology.
FBXO7 encodes an F-box protein that functions as a substrate recognition component of the SCF (SKP1-CUL1-F-box protein) E3 ubiquitin ligase complex. Within this complex, FBXO7 interacts directly with SKP1 and CUL1, targeting substrates such as TRAF2 for ubiquitin-dependent proteasomal degradation. In parallel, FBXO7 cooperates with PINK1 and Parkin (PRKN) in the regulation of mitophagy. It acts downstream of oxidative stress and PINK1 kinase activity, promoting Parkin mitochondrial translocation and subsequent autophagosome formation with LC3. Through these dual roles, FBXO7 coordinates protein quality control and mitochondrial turnover.
In the Raji B lymphocyte context, disruption of FBXO7 provides a unique model to dissect how the ubiquitin-proteasome system and mitophagy intersect with immune cell homeostasis. Because FBXO7 is genetically linked to PARK15 Parkinson’s disease, this Raji knockout population allows researchers to explore non-neuronal aspects of FBXO7-related neurodegeneration, particularly proteasomal stress and mitochondrial dysfunction. While Raji cells are not neuronal, they offer a tractable system to study the core biochemical functions of FBXO7 in a human cell background.
This knockout cell population is suited for a wide range of experimental applications, including targeted investigation of Parkinson??s disease mechanisms, mitophagy flux assays using LC3 turnover measurement, mitochondrial membrane potential assessment with JC-1, co-immunoprecipitation studies to probe FBXO7 interactions with SKP1, CUL1, PINK1, and Parkin, and Western blotting or RT-qPCR for validation. Flow cytometry-based apoptosis assays can further assess the cellular consequences of FBXO7 loss. The product is also valuable for drug screening campaigns aimed at neurodegenerative disorders. For further information and support, please contact Ascent Research.
