The DRG1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DRG1 gene in the Raji B lymphoblastoid cell line. This product is supplied as a heterogeneous pool of cells carrying diverse loss-of-function mutations introduced by CRISPR/Cas9-mediated gene targeting, enabling robust functional ablation of DRG1 without prior clonal selection. The polyclonal format preserves genetic diversity within the knockout population, allowing researchers to study DRG1-dependent phenotypes while mitigating clonal artifacts. This model is optimized for immediate use in downstream analyses, including biochemical, molecular, and cell-based assays, and provides a versatile tool for investigating DRG1 in ribosome biogenesis and translation regulation.
Raji cells are an EBV-immortalized B lymphoblastoid line derived from a patient with Burkitt’s lymphoma, a highly aggressive B-cell malignancy. These suspension-adapted cells retain key features of mature B lymphocytes, including surface immunoglobulin expression and active immune signaling, making them a widely employed model in immunology and oncology research. The Raji line is particularly valued for studies of B-cell biology, lymphomagenesis, and antibody production, as well as for drug screening and translational investigations. Their robust growth in culture and well-characterized molecular landscape facilitate reproducible experimental outcomes and comparative analyses across published datasets.
The DRG1 gene encodes a highly conserved GTPase that functions as an essential regulator of ribosome biogenesis and global protein synthesis. DRG1 forms a stable heterodimeric complex with the interactor DFRP1 (C7orf50), which together facilitate ribosomal subunit assembly and translation initiation. DRG1 activity is governed by upstream regulatory inputs from the mTORC1 signaling hub and cell cycle regulators, while it directly promotes ribosome production and controls the expression of critical downstream effectors such as cyclin D1. Within the translational control network, DRG1 interacts with ribosomal subunits and translation initiation factors, including eIF4E, and operates in concert with mTOR and ribosomal proteins to modulate cellular growth and metabolic output.
In the Raji B-cell context, CRISPR/Cas9-mediated disruption of DRG1 provides a physiologically relevant system to dissect the gene’s contribution to ribosome biology and oncogenic growth programs. Loss of DRG1 is predicted to impair ribosomal assembly and markedly reduce global protein synthesis, potentially attenuating the proliferative capacity and malignant behavior of these lymphoma cells. This knockout model therefore offers a unique opportunity to explore the interplay between translational dysregulation, mTOR signaling, and B-cell lymphomagenesis. Moreover, given DRG1’s emerging links to neurodevelopmental disorders, the Raji knockout population may serve as a surrogate platform for investigating conserved cellular mechanisms underlying microcephaly and epilepsy, despite the non-neuronal origin of the host line.
This DRG1 knockout product enables a broad spectrum of detailed functional investigations tailored to professional researchers in cell biology, cancer biology, and translational medicine. Representative applications include polysome profiling and ribosome footprinting to monitor ribosome biogenesis dynamics, Western blotting and RNA-seq to quantify changes in protein and transcript levels, and cell proliferation assays coupled with flow cytometric cell cycle analysis to assess growth phenotypes. Co-immunoprecipitation experiments can characterize DRG1-DFRP1 complex formation and interactions with ribosomal subunits, while migration and invasion assays may reveal roles in cancer metastasis. These polyclonal knockout cells constitute a robust loss-of-function model for drug target validation studies and mechanistic dissection of the mTOR-DRG1-ribosome axis. For further technical specifications and custom inquiries, please contact Ascent Research.