The CLEC11A Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B-lymphocyte line, in which the CLEC11A gene is disrupted. This heterogeneous pool eliminates osteolectin (SCGF) expression, providing a loss-of-function model for population-level studies. The polyclonal nature avoids single-cell cloning bias, enabling robust functional assays in B-cell lymphoma research.
Raji is an EBV-positive Burkitt’s lymphoma B-cell line lacking surface immunoglobulin, extensively used to study B-cell biology, lymphomagenesis, and antibody responses. Its rapid proliferation and well-characterized signaling networks make it an ideal host for CRISPR/Cas9-mediated gene knockout. The EBV-transformed phenotype provides a relevant background to investigate growth factor signaling and oncogenic mechanisms in hematologic cancers.
CLEC11A encodes osteolectin, a secreted lectin that binds integrin ??v??3 to activate FAK and downstream PI3K/AKT and MAPK/ERK pathways. This signaling enhances hematopoietic stem/progenitor cell proliferation and osteoblast differentiation, involving phosphorylation of AKT, ERK1/2, and STAT3, and upregulation of Cyclin D1 and BCL2L1. Upstream regulators include RUNX2, Notch, and inflammatory cytokines IL-1?? and TNF-??; osteolectin also interacts with FGFR1 and heparan sulfate proteoglycans.
In Raji cells, CLEC11A may operate through autocrine/paracrine mechanisms to support survival and proliferation, potentially contributing to lymphomagenesis. Knockout of CLEC11A disrupts integrin ??v??3-mediated activation of PI3K/AKT/mTOR and RAS/RAF/MEK/ERK/ELK1 cascades, reducing expression of pro-survival factors like BCL2L1. This polyclonal model enables investigation of osteolectin??s role in B-cell survival independent of BCR signaling, and its crosstalk with bone marrow stromal components.
Applications include proliferation and apoptosis assays (CellTiter-Glo, Annexin V), phospho-protein analysis by flow cytometry or Western blotting, and drug sensitivity profiling with agents like doxorubicin and venetoclax. Co-culture with stromal cells allows study of hematopoietic niche interactions, while RT-qPCR and phospho-ERK/AKT flow cytometry monitor signaling activity. The polyclonal format minimizes clonal artifacts in population-based readouts. For further information, please contact Ascent Research.
