COPRS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line, designed for loss-of-function studies of the COPRS scaffold protein. This product provides a genetically heterogeneous pool of cells with targeted disruption of the COPRS gene, enabling robust functional genomics investigations in a lymphoid context without requiring single-cell clonal isolation. The polyclonal format captures a range of editing events, making it well suited for pooled screening approaches and studies where population-level responses to COPRS loss are assessed. Researchers can employ this model to interrogate COPRS-dependent signaling networks and cellular phenotypes directly in B lymphocytes, a cell type central to humoral immunity and lymphomagenesis.
The Raji cell line, established from a human Burkitt lymphoma, is a widely utilized B lymphocyte model that retains features of antibody production, antigen presentation, and immune responsiveness. These suspension cells grow rapidly and express characteristic B cell surface markers, facilitating their use in immunological and oncological assays. As a lymphoma-derived line, Raji cells harbor dysregulated proliferative signaling, yet they maintain dependency on key tumor suppressor pathways, providing a relevant background for examining how COPRS modulates p53 function and cell fate. The knockout population therefore allows dissection of COPRS activities within the context of endogenous B cell regulatory networks.
COPRS encodes a scaffold protein that bridges the PRMT5 methyltransferase complex to p53, facilitating PRMT5-mediated arginine methylation of p53 and thereby modulating p53 transcriptional output. This interaction enhances p53-dependent expression of target genes such as CDKN1A (p21) and BAX, which govern cell cycle arrest and apoptosis. COPRS functions downstream of p53 activation by DNA damage response pathways and upstream of PRMT5 methylation targets, with its activity requiring the PRMT5 cofactor MEP50. By coordinating the PRMT5?Cp53 signaling axis, COPRS integrates post-translational modification signals to fine-tune cellular stress responses, making it a critical node in p53-mediated tumor suppression and cell cycle regulation.
In Raji B lymphocytes, disruption of COPRS is expected to attenuate PRMT5-dependent p53 methylation, potentially altering the expression of p53 target genes and impairing cell cycle checkpoints or apoptotic responses. Given the role of B cells in humoral immunity and the prevalence of p53 pathway alterations in lymphoproliferative disorders, this knockout model offers a physiologically pertinent system to study how COPRS contributes to B cell homeostasis and malignant transformation. The Raji background additionally permits investigation of COPRS function in the context of antigen presentation and antibody production, linking p53 pathway regulation to immune cell function.
Typical applications include mechanistic studies of p53 signaling and PRMT5 methyltransferase activity in B cells, functional genomics screenings in lymphoma models, and evaluation of PRMT5 inhibitors as potential cancer therapeutics. Commonly employed downstream assays encompass Western blot analysis of p53, p21, and BAX protein levels; PRMT5 methyltransferase activity measurements; flow cytometry-based cell cycle and apoptosis profiling; RNA-seq transcriptomic analysis; and immunofluorescence to monitor p53 subcellular localization. These approaches enable comprehensive phenotypic and molecular characterization of COPRS loss. For additional details or inquiries regarding this product, please contact Ascent Research.
