DDR2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphoblastoid line, with targeted disruption of the DDR2 gene. This product provides a heterogeneous loss-of-function model ideal for studying collagen receptor signaling in a human Burkitt lymphoma background. The polyclonal format minimizes clonal selection bias and is well-suited for functional genomics, signaling analyses, and drug screening applications.
The Raji cell line is an EBV-positive B lymphoblastoid model established from a Burkitt lymphoma patient. These suspension cells recapitulate key features of lymphomagenesis and are widely employed to investigate B-cell malignancies, viral oncology, and microenvironmental interactions.
DDR2 is a receptor tyrosine kinase activated by fibrillar collagens (types I and III). Upon binding, DDR2 autophosphorylates and triggers the Src/FAK cascade leading to ERK1/2, the JAK/STAT3 pathway, and PI3K/Akt signaling. It also modulates NF-??B and upregulates MMP-2 and MMP-9, facilitating matrix remodeling and invasion. Downstream targets include STAT3, NF-??B, Src, FAK, ERK1/2, Akt, and matrix metalloproteinases. Interacting partners include integrin ??2??1 and adaptors such as Shc and Grb2. In Raji cells, DDR2 disruption is expected to impair collagen-driven adhesion, migration, and survival signaling.
Collagen receptor signaling is increasingly implicated in B-cell lymphoma progression, particularly in tumor-stroma crosstalk and drug resistance. DDR2 may influence lymphoma cell interaction with the extracellular matrix and contribute to EBV-driven oncogenesis. This Raji DDR2 knockout model allows dissection of collagen-dependent signaling pathways in lymphoblastoid cells, enabling studies on adhesion, invasion, and survival mechanisms.
Applications include Western blotting and RT-qPCR for DDR2 validation, flow cytometry for surface expression, and collagen adhesion or migration assays. The cells support phospho-kinase arrays, proliferation and apoptosis assays, and drug sensitivity tests with agents such as doxorubicin and rituximab. This polyclonal knockout model is particularly suited for investigating tumor microenvironment interactions and mechanisms of drug resistance in lymphoma. For further details and ordering information, please contact Ascent Research.
