The LARP1 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line. The editing process generates a heterogeneous mix of cells with disruptions in the LARP1 gene, providing a loss-of-function model that avoids clonal selection artifacts. This polyclonal format is suitable for studying collective effects of gene ablation in a lymphoma background.
Raji is an Epstein-Barr virus (EBV)-positive human Burkitt’s lymphoma-derived lymphoblastoid B cell line, originally isolated from a male patient. This myc-translocation-harboring line proliferates robustly in culture and features constitutive activation of NF-??B and PI3K/AKT pathways, surface immunoglobulin expression, and antigen presentation capacity. Widely used for B-cell malignancy, immune signaling, and viral oncogenesis research, Raji cells provide a physiologically relevant host for studying gene function in lymphoma.
LARP1 is an RNA-binding protein that functions as a key mTORC1 effector. Upon growth signal stimulation, mTORC1 directly phosphorylates LARP1 in a RAPTOR-dependent manner, relieving its translational repression on 5?? terminal oligopyrimidine (TOP) motif-containing mRNAs. These TOP transcripts encode components of the translational apparatus, including ribosomal proteins such as RPS6 and RPLP0, and translation elongation factors like EEF1A1. LARP1 physically interacts with the mTORC1 complex, PABP, and the TOP motif itself. Its activity is coordinated with 4E-BP1 and S6K1 downstream of PI3K/AKT and mTOR, integrating nutrient and growth factor signals to control ribosome biogenesis and protein synthesis.
In Raji cells, where mTOR signaling is frequently hyperactivated to sustain rapid proliferation, LARP1 knockout disrupts mTORC1-mediated translational control of ribosome biogenesis and protein synthesis, leading to growth impairment. This model consequently helps dissect how oncogenic signals rewire the protein synthesis machinery in B-cell lymphoma and allows evaluation of therapeutics targeting the mTORC1-LARP1-ribosome axis. The polyclonal knockout population captures a range of disruption severities, providing a versatile system to study dose-dependent effects and mechanisms of resistance to mTOR inhibitors.
For functional studies, these cells are compatible with western blotting to monitor LARP1, phospho-S6, and ribosomal protein levels; RT-qPCR for TOP mRNA quantification; polysome profiling for global translation changes; and cell proliferation assays (MTT, BrdU). RNA-immunoprecipitation can probe LARP1-RNA interactions, while drug sensitivity screens with rapamycin or mTOR kinase inhibitors test functional consequences of LARP1 loss. Thus, this polyclonal knockout cell population serves as a versatile tool for mTOR signaling, translational control, and lymphoma drug response research. For further details, technical support, or custom inquiries, please contact Ascent Research.
