The DLG1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population engineered to disrupt the human DLG1 gene in the Raji B lymphoblastoid cell line. This loss-of-function model enables systematic investigation of DLG1-dependent molecular mechanisms without the need for small-molecule inhibitors or RNA interference approaches. The polyclonal format offers a heterogeneous pool of gene-edited cells, facilitating population-level studies of signaling dynamics and functional redundancy within the B cell receptor pathway.
Raji cells are an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. They serve as a well-established model for studying B cell receptor (BCR) signaling, EBV latency and transformation, and lymphoma biology. The cells retain key features of antigen-experienced B cells and are widely used for drug screening and immunological synapse research. Their rapid proliferation and ease of genetic manipulation make Raji cells an ideal host for CRISPR-based gene editing.
DLG1 encodes a scaffold protein of the membrane-associated guanylate kinase (MAGUK) family that coordinates receptor clustering, tight junction assembly, and cell polarity. In B lymphocytes, DLG1 interacts with key signaling mediators downstream of the BCR, including SYK kinase and BLNK adaptor, and is regulated by LYN kinase and BCR crosslinking. Mechanistically, DLG1 nucleates signaling complexes at the immunological synapse to couple BCR activation to NF-??B and JNK cascades, while also modulating Wnt/??-catenin and Hippo pathway outputs. Additional interactions with APC, PTEN, CASK, and the actin-binding ERM proteins reinforce DLG1??s role in linking membrane receptors to the cytoskeleton and transcriptional responses.
Disruption of DLG1 in the Raji background directly perturbs BCR signal transduction, as evidenced by impaired phosphorylation of proximal effectors such as SYK and BLNK. This deficiency compromises immunological synapse formation and downstream activation of NF-??B and JNK, resulting in attenuated B cell activation and proliferation. Consequently, DLG1 knockout Raji polyclonal cells provide a physiologically relevant system for dissecting BCR-dependent growth signals and for evaluating therapeutic sensitivities, particularly to BTK inhibitors and other agents targeting B cell malignancies.
This knockout model is suited for a broad range of experimental applications, including quantitative phospho-flow cytometry and Western blotting to measure SYK and BLNK activation, immunofluorescence imaging of immunological synapse architecture, and co-immunoprecipitation studies of DLG1 interactomes. Researchers may also employ cell viability and apoptosis assays to profile drug responses in the context of disrupted BCR signaling. The polyclonal population enables robust protein interaction mapping and high-throughput screening campaigns. For additional product details or custom inquiries, please contact Ascent Research.
