The CSGALNACT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population generated from the human Burkitt lymphoma Raji B-cell line, featuring targeted disruption of the CSGALNACT2 gene to abolish its glycosyltransferase activity. This polyclonal pool, produced via CRISPR/Cas9-mediated gene disruption, offers a heterogeneous knockout model that avoids single-cell cloning artifacts, enabling robust functional interrogation of chondroitin sulfate biosynthesis in B lymphocytes.
Raji is an EBV-positive Burkitt lymphoma-derived B-cell line harboring a t(8;14) translocation that drives c-MYC overexpression. As a mature B-lymphocyte model, Raji cells maintain immunoglobulin production and antigen-presenting functions, and their well-characterized growth and genetic tractability make them a standard system for studying B-cell malignancies, signal transduction, and adaptive immunity.
CSGALNACT2 encodes a Golgi glycosyltransferase that initiates chondroitin sulfate chain synthesis by transferring GalNAc from UDP-GalNAc onto the proteoglycan linkage tetrasaccharide. This essential step enables subsequent polymerization by the chondroitin sulfate synthase complex (CHSY1, CHPF, CHPF2) and sulfation by enzymes such as CHST3 and CHST7, ultimately modifying core proteins like versican, decorin, and CD44. The enzyme is regulated upstream by TGF-??1, WNT signaling, BMP2, and SOX9, and interacts with CSGALNACT1 to orchestrate chondroitin sulfate-dependent processes including cell adhesion, migration, and extracellular matrix organization.
In Raji B lymphoma cells, CSGALNACT2 knockout abrogates chondroitin sulfate chain initiation, yielding proteoglycans with deficient or truncated chondroitin sulfate modifications. Because chondroitin sulfate on cell-surface receptors such as CD44 and syndecans modulates lymphocyte adhesion, homing, and cytokine binding, loss of CSGALNACT2 is predicted to impair these functions. This model thus enables dissection of how altered glycosylation contributes to B-cell lymphoma behavior, including tumor cell dissemination and interaction with the microenvironment, and parallels glycosylation defects seen in skeletal dysplasias and certain carcinomas.
Typical applications include flow cytometric and immunofluorescence detection of chondroitin sulfate loss using antibodies like CS-56, Western blot confirmation of CSGALNACT2 depletion, and genotyping PCR to validate gene disruption. Functional assays such as adhesion, migration, and invasion studies, combined with RNA-seq transcriptomics and proteoglycan chromatography, can delineate downstream molecular consequences. These polyclonal knockout cells are suited for drug target validation, glycosylation research in lymphomas, and modeling chondroitin sulfate-related disorders. For further details, please contact Ascent Research.
