The F11 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population from the Raji B lymphocyte line, disrupting the F11 gene encoding coagulation factor XI (FXI). This heterogeneous gene-edited pool serves as a loss-of-function model for studying FXI in intrinsic coagulation and related pathways, without monoclonal isolation. The polyclonal format preserves population-level heterogeneity, reflecting natural variation in gene disruption responses.
Raji cells, derived from Burkitt lymphoma, are EBV-positive lymphoblastoid B cells maintaining antibody production, antigen presentation, and immune surveillance. Widely used in immunology and oncology, they provide a reproducible background for studying B cell biology, signaling, and transformation. Their robust growth and well-characterized transcriptional profile support consistent gene knockout studies in a lymphocytic setting.
FXI, a serine protease zymogen encoded by F11, is activated by factor XIIa or thrombin in the intrinsic coagulation cascade. Upon activation, it cleaves factor IX to amplify factor Xa generation, culminating in thrombin burst and fibrin clot. FXI also interacts with high molecular weight kininogen and glycoprotein Ib-IX-V on platelets, bridging contact activation and platelet signaling. Upstream regulators include the contact activation complex, while downstream targets involve factor IX and possibly factor X and XII, placing FXI at a critical intersection of hemostasis, inflammation, and thrombosis.
Disrupting F11 in Raji cells allows dissection of non-canonical FXI roles in B lymphocytes, including cell survival, proliferation, and immune signaling. EBV transformation may intersect with the coagulation network, and this model permits exploration of viral latency effects. Additionally, FXI loss in an antigen-presenting cell line enables study of how coagulation proteases modulate adaptive immunity, revealing hemostasis-immune crosstalk.
This polyclonal knockout model supports various applications: western blotting and RT-qPCR to confirm FXI depletion, aPTT coagulation assays to assess functional impact, and factor IX activation assays to evaluate enzymatic activity. Flow cytometry profiles FXI expression, and thrombin generation assays probe downstream clot formation. In drug discovery, the cells enable screening of FXI-targeted anticoagulants; in basic research, they facilitate studies on FXI??s role in B cell proliferation, apoptosis, and inflammation. Contact Ascent Research for further support.
