This product is a CRISPR/Cas9-edited polyclonal knockout cell population lacking human DAB2 expression in the Raji B-cell background. The knockout is achieved through targeted gene disruption, generating a heterogeneous collection of cells with loss-of-function edits. This polyclonal format minimizes artifacts from clonal selection while providing a robust loss-of-function model. The matched parental Raji cell line is recommended as a control for all experiments.
Raji cells are suspension-adapted human B lymphocytes derived from a Burkitt’s lymphoma patient and are positive for Epstein-Barr virus. These lymphoblastoid cells retain features such as surface immunoglobulin expression, antigen presentation capability, and rapid proliferation, making them a versatile host for immunology and cancer research. Raji??s transformed phenotype and well-characterized signaling networks allow precise examination of oncogenic and tumor-suppressive mechanisms.
DAB2 is a multidomain adaptor that coordinates clathrin-mediated endocytosis and signal attenuation. It directly binds clathrin heavy chain (CLTC) and the AP2 complex (AP2A1/AP2B1) to promote internalization of TGF-beta receptors, integrins (ITGB3), and LRP co-receptors. Activated by TGFB1, EGF, and SRC kinase, DAB2 scaffolds receptor cargo and recruits MYO6 and OCRL for endosomal sorting. This interplay controls downstream events: DAB2 enhances SMAD2/3 phosphorylation downstream of TGFBR while inhibiting Ras-MAPK signaling. In Wnt pathways, DAB2 interacts with DVL2 and AXIN to modulate FZD-mediated signaling. Overall, DAB2 acts as a tumor suppressor by limiting mitogenic signals.
In the Raji background, DAB2 knockout enables dissection of endocytic control over B-cell signaling. Burkitt??s lymphoma is characterized by MYC overexpression; loss of DAB2 may amplify proliferative cues or impair TGF-beta-induced growth arrest. This model permits analysis of receptor trafficking in antigen presentation and immune surveillance, as DAB2-dependent internalization of integrins and TGFBRs influences lymphocyte adhesion and survival. Researchers can thus probe how endocytic adaptors tune lymphoma cell behavior and therapeutic responses.
Applications span cancer cell biology, signal transduction, and drug discovery. The knockout cells are suited for apoptosis, migration, and proliferation assays, as well as phospho-SMAD2/3 analysis and transferrin uptake studies to monitor endocytosis. Co-immunoprecipitation of adaptor complexes and RT-qPCR profiling of Wnt targets can reveal altered signaling networks. These tools support B-cell lymphoma modeling, tumor suppressor screening, and validation of therapeutic targets. For additional information or custom projects, please contact Ascent Research.
