The MFAP3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the human MFAP3 gene has been disrupted. This product provides a heterogeneous pool of Raji cells carrying diverse CRISPR-mediated modifications at the MFAP3 locus, enabling loss-of-function studies in a population context rather than a single clonal derivative. The knockout model is designed for researchers investigating microfibril-associated protein 3 and its roles in extracellular matrix biology, TGF-beta signaling, and B lymphocyte function.
The host cell line, Raji, is an EBV-positive B lymphocyte line derived from a Burkitt lymphoma patient. Widely used as an immortalized B cell model, Raji cells express characteristic surface markers and exhibit features of transformed B lymphocytes. Their robust growth in suspension culture and well-characterized signaling pathways make them a versatile platform for studying gene function in immune cell adhesion, migration, and lymphoma biology. The EBV-positive background further provides a context for examining viral?Chost interactions within the tumor microenvironment.
MFAP3 encodes a microfibril-associated glycoprotein integral to elastic fibers. Its expression is regulated by TGFB1 and TGFB2 via SMAD2/3 signaling, and the protein interacts with FBN1, FBN2, LTBP1, and LTBP2. MFAP3 facilitates elastic fiber assembly and ECM integrity. Downstream, its loss alters TGFB1 bioavailability, reduces ITGAV integrin expression, and dysregulates MMP2-dependent matrix remodeling. Key pathway components include FBN1, ELN, LOX, TGFB1, and ITGAV.
In Raji B lymphocytes, MFAP3 knockout impairs cell adhesion and TGF-beta signaling, modeling how ECM components influence lymphoma cell behavior. Disruption may alter integrin-mediated attachment and matrix deposition in the tumor microenvironment. This Burkitt lymphoma-derived system is ideal for studying microfibril contributions to B cell lymphomagenesis and drug resistance.
This polyclonal knockout pool supports protein and RNA validation (Western blot, RT-qPCR), adhesion/migration assays, flow cytometry for ITGAV, TGF-beta reporter assays, immunofluorescence, co-immunoprecipitation, RNA-seq, and drug sensitivity screens. These tools enable detailed exploration of ECM remodeling and TGF-beta signaling in lymphoma. For further information, please contact Ascent Research.
