The EXD2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji human Burkitt??s lymphoma B cell line, designed to disrupt the gene encoding the 3??-5?? exonuclease EXD2. This loss-of-function model enables dissection of EXD2??s dual roles in nuclear DNA repair and mitochondrial maintenance, providing a heterogeneous system for functional genomics studies.
The Raji cell line, an EBV-positive B lymphocyte model, is characterized by constitutive c-MYC overexpression and inherent genomic instability, making it highly relevant for investigating DNA damage response pathways. As a suspension culture, Raji cells facilitate high-throughput assays and are extensively used to study B-cell malignancies.
EXD2 functions in both the nucleus and mitochondria. In the nucleus, it is recruited to DNA double-strand breaks via the MRN complex (MRE11-RAD50-NBS1) and promotes DNA end resection for homologous recombination, a process involving BRCA1 and RAD51 and regulated by ATM/ATR kinases. In mitochondria, EXD2 processes RNA primers during mtDNA replication by interacting with mtSSB, and associates with the mitochondrial ribosome to modulate translation, impacting mtDNA copy number and mitochondrial protein synthesis.
In Raji lymphoma cells, EXD2 disruption impairs DNA end resection, leading to defective homologous recombination and heightened sensitivity to genotoxic stress. Concurrently, mitochondrial EXD2 loss may disrupt mtDNA maintenance and oxidative metabolism, highlighting the model??s value for studying nuclear-mitochondrial crosstalk in oncogenic survival and drug resistance.
Applications include mechanistic studies of DNA repair in B-cell malignancies, functional analysis of mitochondrial genome stability, and drug sensitivity screening with PARP inhibitors. Representative assays encompass Western blotting, ??H2AX immunofluorescence, comet assay, mtDNA copy number qPCR, Seahorse metabolic analysis, and homologous recombination reporter assays. For further information, please contact Ascent Research.
