The MIA3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from Raji B lymphocytes, in which the MIA3 (TANGO1) gene has been disrupted. This heterogeneous pool of knockout cells eliminates MIA3 protein function without clonal selection, offering a robust loss-of-function model. The cells maintain typical lymphoblastoid morphology and proliferation, providing a versatile platform for studying collagen secretion and extracellular matrix biology.
Raji cells are an EBV-positive human B lymphocyte line from a Burkitt’s lymphoma patient, extensively used in immunological and cancer research. Their active secretory pathway and well-characterized signaling make them suitable for investigating ER-to-Golgi transport, despite not being professional collagen secretors. The Raji background enables dissection of COPII-dependent sorting mechanisms in a hematopoietic context.
MIA3/TANGO1 acts as a cargo receptor at ER exit sites, essential for packaging large procollagens into COPII vesicles. It directly binds procollagens (COL1A1, COL1A2, COL7A1) and recruits SEC23A/SEC24C via cTAGE5 to form enlarged carriers. MIA3 expression is regulated by TGFB1, CREB3L2, and ER stress sensors (ATF6), while chaperones like HSPA5/BiP assist loading. Knockout disrupts collagen secretion, causing ER accumulation, ER stress, and ECM defects.
In Raji cells, MIA3 knockout allows study of collagen secretion defects in a non-fibroblastic lineage, highlighting universal ER cargo receptor mechanisms. It provides a model for ER stress induction by procollagen retention and potential B-cell roles in ECM remodeling relevant to lymphoma progression. The cells?? amenability to high-throughput screening suits drug discovery for secretory pathway modulators.
Applications include mechanistic analyses of collagen trafficking, modeling osteogenesis imperfecta, and cancer metastasis research. Assays such as Western blotting, immunofluorescence, pulse-chase, RT-qPCR, and ER stress marker assessment are recommended. Functional studies of cell migration and invasion explore ECM-dependent phenotypes, while electron microscopy examines ER exit site changes. For further details, please contact Ascent Research.
