The CCS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, designed for loss-of-function studies of the CCS gene. This product consists of a mixed population of cells carrying targeted disruptions in the CCS locus, enabling interrogation of CCS-dependent pathways without clonal selection. The knockout model provides a physiologically relevant system to dissect the role of the copper chaperone for superoxide dismutase (CCS) in copper delivery and antioxidant defense.
Raji is an EBV-positive human Burkitt lymphoma-derived B lymphocyte model widely used in immunology, oncology, and signal transduction research. These suspension cells exhibit robust growth and are amenable to functional assays, including flow cytometry, immunoprecipitation, and biochemical analysis. Raji cells express B-cell markers and are commonly used to study B-cell receptor signaling, apoptosis, and oncogene function. The well-characterized EBV-transformed background and accessible multi-omics data offer a defined genetic context for investigating cellular stress responses, metal homeostasis, and lymphoma biology.
CCS encodes a metallochaperone that specifically delivers copper ions to cytosolic SOD1, an essential step for SOD1 enzymatic maturation. In the copper loading cycle, CCS interacts with SOD1 and copper ions, promoting formation of the active Cu,Zn-SOD1 homodimer. Once activated, SOD1 catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide, thereby mitigating oxidative stress. CCS expression and copper delivery are responsive to intracellular copper levels and oxidative conditions, influenced by metal-responsive transcription factors. Disruption of CCS therefore impairs SOD1 activation, leading to accumulation of superoxide and enhanced susceptibility to oxidative damage. This knockout model provides a clean background for examining the CCS-SOD1 axis in the absence of compensatory mechanisms.
Within the Raji B lymphocyte context, CCS knockout offers a unique opportunity to explore how copper chaperone deficiency modulates redox balance, cell survival, and signaling in a lymphoma-derived line. B lymphocytes rely on tight regulation of reactive oxygen species for proliferation, differentiation, and apoptosis, making them sensitive to perturbations in antioxidant defenses. The CCS knockout polyclonal population enables researchers to dissect the contribution of CCS-dependent SOD1 activity to overall cellular resistance to oxidative insults. This platform can also evaluate the interplay between copper homeostasis and lymphomagenesis, and the impact of impaired CCS function on B-cell signaling.
Typical applications include Western blotting and co-immunoprecipitation to assess CCS-SOD1 interaction, SOD1 enzymatic activity assays, and flow cytometric detection of reactive oxygen species. Cell viability assays under oxidative stress conditions (e.g., paraquat or hydrogen peroxide) quantify CCS-dependent cytoprotection. This model is suitable for studying ALS-linked SOD1 dysregulation, copper metabolism disorders, and chaperone-targeted therapies. For additional information or to inquire about custom services, please contact Ascent Research.
