The ERGIC3 Knockout Raji Polyclonal Cells product provides a polyclonal population of human Raji B lymphoblasts in which the ERGIC3 gene has been disrupted using CRISPR/Cas9-mediated gene editing. This loss-of-function model enables investigation of ERGIC3-dependent processes in a physiologically relevant B-cell context. The polyclonal format preserves genetic heterogeneity, allowing assessment of gene disruption effects across a diverse cell pool and minimizing clone-specific artifacts.
Raji cells are a suspension B lymphoblast cell line derived from a Burkitt lymphoma patient and are latently infected with Epstein-Barr virus (EBV). They serve as a well-established model for studying humoral immunity and B-cell biology, constitutively expressing surface immunoglobulin and capable of antibody secretion. Raji cells exhibit rapid proliferation and are widely used in immunological and cancer research, particularly for investigating B-cell receptor signaling, antigen presentation, and lymphomagenesis.
ERGIC3 encodes a cargo receptor residing in the ER-Golgi intermediate compartment (ERGIC) that facilitates the transport of membrane and secretory proteins from the endoplasmic reticulum to the Golgi apparatus. It functions as a central component of the COPII vesicle-mediated trafficking pathway, acting downstream of the ER stress sensors PERK, ATF6, and the transcription factor XBP1, which regulate its expression during the unfolded protein response. ERGIC3 interacts with the coatomer complex, ERGIC2, and the COPII coat proteins SEC23 and SEC24 to select client glycoproteins, cell surface receptors, and secreted cytokines for anterograde transport. The pathway also involves SAR1, SEC13, ARF1, and Golgi SNAREs for vesicle formation, targeting, and fusion. Disruption of ERGIC3 impairs ER-to-Golgi trafficking, leading to retention of cargo proteins in the ER and altered processing and secretion of their downstream targets.
In the Raji B-cell line, loss of ERGIC3 is expected to disrupt the trafficking and surface expression of immunologically relevant proteins, including cytokine receptors and secreted antibodies, thereby modulating humoral immune responses and potentially influencing lymphoma cell growth. The EBV-positive background adds further complexity, as viral latency and oncogenic programs rely on host secretory pathways. This knockout model thus provides a valuable tool to examine the intersection of protein secretion, oncogenic signaling, and immune cell function in a cancer-relevant context.
The ERGIC3 Knockout Raji Polyclonal Cells are suitable for a range of experimental applications, including investigation of ER-to-Golgi transport mechanisms, analysis of cancer cell secretome changes, and exploration of therapeutic strategies targeting protein trafficking. Representative assays include western blotting to assess cargo protein levels, immunofluorescence and flow cytometry for surface receptor expression, secretion ELISA to quantify released cytokines, cell proliferation assays to evaluate growth dependency, and RNA-seq for global transcriptomic profiling. For further details or customized support, please contact Ascent Research.
