The ERGIC1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, designed to disrupt endogenous human ERGIC1 expression. This loss-of-function model allows investigation of ERGIC1 function in the early secretory pathway without introducing clonal genotypes. As a pooled polyclonal population, it preserves genetic heterogeneity and provides a robust platform for functional genomics and phenotypic screening in a B-cell lymphoma background.
The parental Raji cell line is an Epstein-Barr virus (EBV)-positive B-lymphoblastoid line from a Burkitt lymphoma patient. Raji cells grow in suspension and are widely used as a model for B-cell biology and lymphomagenesis, retaining characteristics like constitutive NF-??B and MYC activation. Their malignant B-cell phenotype makes them suitable for studying oncogenic mechanisms and therapeutic interventions in lymphoid cancers.
ERGIC1 encodes a transmembrane protein of the ER-Golgi intermediate compartment (ERGIC), hypothesized to act as a cargo receptor in COPII- and COPI-mediated trafficking. It is predicted to interact with COPII components SAR1, SEC23, SEC24, and the COPI coatomer with ARF1, and may associate with ERGIC-53 (LMAN1). Upstream regulation potentially involves ER stress-responsive transcription factors XBP1 and ATF6, linking ERGIC1 to the unfolded protein response (UPR). Its disruption is expected to perturb anterograde and retrograde transport, affecting surface delivery of secretory and membrane proteins.
In Raji B cells, ERGIC1 knockout provides a tool to study ER-Golgi trafficking in lymphoma. B cells have high secretory demand for immunoglobulins, so disrupting ERGIC1 may impair antibody secretion and alter receptor expression, potentially impacting proliferation and survival. This model enables exploration of how early secretory pathway defects contribute to ER stress and UPR activation in cancer, with implications for drug resistance. Additionally, the EBV-positive background allows investigation of viral manipulation of host secretory machinery.
Researchers can use these cells in Western blotting and RT-qPCR to confirm ERGIC1 loss and monitor UPR markers, and immunofluorescence to assess ERGIC compartment integrity with markers like ERGIC-53. Flow cytometry quantifies surface receptor changes, and ELISA measures secreted immunoglobulin. MTT and apoptosis assays link trafficking defects to viability. The polyclonal knockout population is ideal for screening modulators of ER-Golgi transport or evaluating ERGIC1 as a target in B-cell malignancies. For further information, please contact Ascent Research.
