The CPXM1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the human Burkitt’s lymphoma-derived Raji B lymphocyte line. This suspension cell product features targeted disruption of the CPXM1 locus, encoding a zinc-dependent metallocarboxypeptidase, generating a loss-of-function model. The polyclonal pool incorporates a spectrum of edits, ensuring robust protein depletion without clonal selection bias. Provided as a living culture, the cells are ready for immediate expansion and functional assays in immunology and oncology research.
The Raji parental line was established from an 11-year-old male with Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma. These suspension cells retain antigen-independent B cell receptor signaling, EBV latency gene expression, and resistance to apoptosis, serving as a workhorse model for lymphomagenesis and virology. Widely used to study NF-??B, PI3K/AKT, and apoptotic pathways, Raji cells offer a clinically relevant malignant B-cell context for exploring novel genetic dependencies.
CPXM1 belongs to the M14 metallocarboxypeptidase family and requires a zinc ion cofactor for its exopeptidase activity, which removes C-terminal amino acids from target substrates. Although its upstream regulators and downstream effectors remain undefined, CPXM1 is hypothesized to process extracellular matrix (ECM) proteins and peptide hormones, thereby influencing ECM organization and protein digestion/absorption. By cleaving C-terminal residues, CPXM1 may modulate the bioactivity, stability, or receptor interactions of its substrates. The knockout therefore eliminates this post-translational processing, potentially disrupting cell-cell and cell-matrix communication in lymphocytes.
Loss of CPXM1 in Raji cells provides a model to examine the carboxypeptidase’s contribution to B-cell malignancy. In the tumor microenvironment, CPXM1-mediated ECM remodeling or peptide maturation could affect proliferation, survival, and migration. The polyclonal nature avoids artifacts from single-cell cloning while reflecting heterogeneous knockout effects. This system enables investigation of whether CPXM1 influences lymphoma cell behavior through autocrine/paracrine loops or by altering integrin-mediated adhesion. The model may also reveal unanticipated roles of metallocarboxypeptidases in EBV-driven B-cell biology.
Applications encompass knockout validation via Sanger sequencing (indel detection), Western blotting, and RT-qPCR, alongside functional assays such as flow cytometry for B-cell markers, proliferation (CellTiter-Glo), apoptosis (Annexin V), and migration/invasion transwell assays. The cells are suitable for substrate-screening approaches like terminal amine isotopic labeling of substrates (TAILS) to identify CPXM1 targets. Coculture experiments with stromal cells or ECM substrates can explore the peptidase’s role in the tumor microenvironment. For further details or custom requests, please contact Ascent Research.
