CPPED1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the Raji B lymphocyte lineage, wherein the gene encoding CPPED1 has been disrupted to establish a loss-of-function model. This polyclonal knockout cell pool provides a heterogeneous yet gene-targeted system for investigating the functional impact of CPPED1 ablation on cellular signaling networks, proliferation, and survival, without relying on single-cell clonal selection. The product is supplied as a ready-to-use population of genomically edited cells, enabling versatile experimental designs in cancer biology and signal transduction research.
The host Raji cell line is an EBV-positive Burkitt lymphoma model originally established from a male patient. These B lymphocytes express characteristic B-cell surface markers and maintain an activated B-cell phenotype, recapitulating key features of aggressive lymphomas. As a well-characterized immune cell line, Raji cells are extensively used to dissect pathways governing lymphomagenesis, B-cell receptor signaling, and oncogenic transformation, providing a robust cellular context for dissecting the roles of tumor suppressors and oncogenes in haematological malignancies.
CPPED1 encodes a serine/threonine phosphatase that directly dephosphorylates and inactivates critical signaling effectors, including AKT1, MAPK1 (ERK2), MAPK3 (ERK1), and STAT3. By deactivating these kinases, CPPED1 functions as a negative regulator of the PI3K?CAKT?CmTOR, RAS?CRAF?CMEK?CERK, and JAK?CSTAT3 pathways, thereby restraining cell cycle progression, proliferation, and anti-apoptotic programs. Upstream, TP53 and cellular stress signals modulate CPPED1 expression, while downstream signaling outputs converge on transcriptional programs that govern cell growth and survival. In its native form, CPPED1 serves as a molecular brake on oncogenic cascades frequently hyperactivated in lymphomas.
Disruption of CPPED1 in Raji cells is anticipated to relieve this negative regulation, resulting in sustained hyperactivation of AKT, ERK, and STAT3 signaling. This mimics the pathological signaling landscape observed in many aggressive B-cell lymphomas, where constitutive kinase activity drives uncontrolled proliferation and enhanced survival. The polyclonal knockout population thus represents a powerful model to examine tumor suppressor function in a lymphoma-relevant setting and to investigate how loss of phosphatase-mediated control reshapes the phospho-signaling network in malignant B cells.
These knockout cells are ideally suited for a broad range of functional and phenotypic assays. Researchers can monitor pathway activity via Western blotting for phospho-AKT (Ser473), phospho-ERK1/2 (Thr202/Tyr204), and phospho-STAT3 (Tyr705), and assess cellular responses using CCK-8 or MTT proliferation assays, Annexin V-based apoptosis detection by flow cytometry, cell cycle profiling, and colony formation in soft agar. In vivo tumorigenicity studies can further validate the oncogenic potential of CPPED1 loss, while RNA-seq and phospho-signaling analyses provide comprehensive molecular insights. For further technical information and support, please contact Ascent Research.
