ERMP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human Raji B lymphocytes, with targeted disruption of the ERMP1 gene. This heterogeneous loss-of-function model enables investigation of endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways without clonal selection artifacts.
Raji is an EBV-positive Burkitt lymphoma cell line, growing in suspension as lymphoblasts, and widely used to study EBV-driven lymphomagenesis and B-cell signaling. Its latency III program drives proliferation and apoptosis resistance, providing a stringent background to dissect ER stress regulators like ERMP1 in lymphoid cancers.
ERMP1 encodes an ER-resident zinc metalloprotease that attenuates ER stress-induced apoptosis by modulating the UPR. Upstream regulators include ATF4, ATF6, and XBP1, and ERMP1 interacts with GRP78/BiP and ERAD machinery. Knockout sensitizes cells to thapsigargin and tunicamycin, enhancing UPR signaling through PERK, IRE1, and ATF6, leading to CHOP-mediated upregulation of BAX and downregulation of BCL2, with caspase activation. ERMP1 loss also impairs AKT-mediated survival and disrupts mitochondria-associated membrane contacts via MFN2 and VDAC1, while miR-148a provides regulatory control.
In Raji cells, ERMP1 knockout creates a relevant model to study how ER stress dysregulation contributes to lymphoma. EBV latent proteins may synergize with ERMP1 loss to shift the UPR toward apoptosis, making this polyclonal pool ideal for investigating viral oncogenesis, ER stress tolerance, and survival pathways in B-cell malignancies.
This model supports functional studies of ERMP1, drug screening for ER stress modulators, and apoptosis research. Assays include Western blotting for UPR markers (GRP78, CHOP), RT-qPCR, flow cytometry for Annexin V, viability under tunicamycin, co-immunoprecipitation with GRP78, and ER immunofluorescence. Researchers can also explore PI3K/AKT signaling and mitochondrial cross-talk. For further details, contact Ascent Research.
