CPB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human Raji B lymphocyte line. This product is designed for researchers to study the functional consequences of CPB2 gene disruption. The polyclonal population contains a heterogeneous mix of edited alleles, enabling investigation of gene function without the selection bias of single-cell cloning. CRISPR/Cas9-mediated gene disruption introduces loss-of-function mutations at the target locus, providing a robust knockout model for analyzing CPB2??s role in cellular processes.
The host cell line, Raji, is an Epstein-Barr virus (EBV)-positive human Burkitt lymphoma B lymphocyte line that grows in suspension and exhibits a lymphoblastoid morphology. Raji cells are widely employed in biomedical research due to their B cell characteristics, including immunoglobulin production, antigen presentation, and responsiveness to immune signals. Their well-characterized genome and rapid proliferation make them an ideal platform for gene editing and functional studies, particularly in immunology, oncology, and hematology.
CPB2 encodes procarboxypeptidase B, also known as thrombin-activatable fibrinolysis inhibitor (TAFI). The zymogen is activated by the thrombin-thrombomodulin complex, and the active enzyme (CPB2a) cleaves C-terminal lysine and arginine residues from protein substrates. Its primary function is to dampen fibrinolysis: by removing C-terminal lysines from partially degraded fibrin, CPB2a reduces plasminogen binding and activation by tissue plasminogen activator (tPA) or urokinase (uPA), thereby stabilizing blood clots. Beyond hemostasis, CPB2 modulates inflammation by inactivating proinflammatory mediators such as complement C5a, bradykinin, and osteopontin. Upstream regulators include thrombin, plasmin, and the thrombin-thrombomodulin complex; key interacting partners encompass plasminogen, fibrin, thrombomodulin, and components of the plasminogen activation system.
In the Raji B lymphocyte background, CPB2 knockout provides a unique model to explore the interface between coagulation, inflammation, and adaptive immunity. While CPB2 is predominantly expressed in the liver and secreted into plasma, extrahepatic expression in immune cells may contribute to local regulation of inflammatory responses. Disrupting CPB2 in Raji cells may affect the processing of immunomodulatory peptides and influence B cell functions such as antibody production and antigen presentation. This model can be used to dissect how CPB2-mediated inactivation of inflammatory mediators impacts lymphocyte behavior in inflammatory microenvironments, potentially revealing new links between fibrinolysis and immune cell regulation.
Typical applications of this knockout model include investigating the molecular mechanisms of fibrinolysis regulation, exploring the crosstalk between coagulation and inflammation, and validating CPB2 as a therapeutic target for thrombotic and inflammatory disorders. Researchers can employ a variety of assays, such as Western blotting, RT-qPCR, carboxypeptidase activity measurements, clot lysis assays, flow cytometry, and RNA sequencing, to characterize CPB2 function. Additionally, the knockout cells can be used in drug screening to identify modulators of CPB2 activity or downstream pathways. For additional details and ordering information, please contact Ascent Research.
