The CLEC3B Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, designed for targeted disruption of CLEC3B. This loss-of-function model facilitates investigation of Tetranectin biology in a human Burkitt lymphoma context. The polyclonal format offers a genetically mixed population with disrupted CLEC3B, enabling functional studies without clonal selection. These cells are a versatile tool for studying plasminogen activation, extracellular matrix remodeling, and associated pathways in lymphoid malignancy.
The Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphoblast line from a Burkitt lymphoma patient, retaining malignant B cell characteristics and serving as a model for B cell biology, lymphomagenesis, and humoral immunity. Its EBV positivity permits exploration of viral-host interactions, including potential crosstalk with the plasminogen system, making it relevant for CLEC3B functional studies. Raji cells are widely used due to rapid proliferation, B cell marker expression, and susceptibility to manipulation.
CLEC3B encodes Tetranectin, a C-type lectin that binds plasminogen via its kringle 4 domain and facilitates plasmin generation by tPA and uPA. This action promotes fibrinolysis and MMP activation, contributing to ECM degradation. Tetranectin interacts with fibrin, heparin, calcium, and fibronectin, influencing cell adhesion, migration, and tissue mineralization. Its expression is induced by TGF-beta and regulated by vitamin D receptor, estrogen receptor, and promoter methylation. Downstream, Tetranectin enhances plasmin formation, MMP activity, and cell migration, linking it to the fibrinolysis and ECM organization pathways. Representative pathway components include plasminogen, tPA, uPA, PAI-1, plasmin, MMPs, and fibrin.
In Raji B lymphoma cells, CLEC3B disruption allows dissection of Tetranectin??s role in lymphoma cell adhesion, invasion, and interaction with the tumor microenvironment. The EBV-positive background may reveal virus-specific modulation of plasminogen activation. This model can elucidate Tetranectin??s contribution to proliferation, survival, and migration of malignant B cells, shedding light on its function in hematological malignancies. It also aids in evaluating Tetranectin as a biomarker or target in lymphoma and related cancers like multiple myeloma, breast, and ovarian carcinomas.
These polyclonal knockout cells support diverse assays: Western blotting and qRT-PCR for gene disruption verification, plasminogen activation assays, fibrin zymography, and migration/invasion assays. Flow cytometry measures surface plasminogen binding; co-immunoprecipitation probes protein interactions. Proliferation, apoptosis, and xenograft studies enable comprehensive phenotyping. Applications include studying CLEC3B in EBV-driven lymphomagenesis and biomarker validation. For inquiries, contact Ascent Research.
