The ENDOD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population from the Raji B-lymphocyte line, designed for loss-of-function studies of the ENDOD1 gene encoding a putative endonuclease. This polyclonal knockout pool provides robust population-level analysis, avoiding clonal selection biases. The gene disruption was achieved using CRISPR/Cas9 technology, generating a heterogeneous mixture with targeted ablation of ENDOD1, enabling functional investigation without mechanistic editing details.
The Raji cell line is a suspension-growing human Burkitt lymphoma model established from an EBV-positive patient. Raji cells exhibit an activated B-cell phenotype and are widely employed to study B-cell lymphomagenesis, oncogenic signaling, and virus-driven transformation. Their EBV-positive status permits exploration of viral contributions to apoptosis dysregulation and DNA repair. This line has been extensively used in DNA damage response and apoptosis research, providing a relevant background for endonuclease studies.
ENDOD1 encodes a nuclear-localized protein with predicted endonuclease activity, participating in nucleic acid metabolism, DNA repair, and apoptotic execution. It is regulated upstream by p53 in response to DNA damage and apoptotic stimuli, and it interacts with nuclear proteins and DNA repair factors to maintain genomic integrity. During apoptosis, ENDOD1 is thought to mediate DNA fragmentation through cooperation with caspase-3, leading to PARP cleavage and ??H2AX focus formation. Its involvement in ATM-mediated checkpoint signaling further links endonuclease function to both repair and cell death. Knockout of ENDOD1 disrupts these processes, potentially impairing DNA repair and apoptotic DNA cleavage, thereby altering survival and genomic stability in B-lymphoma cells.
In Raji cells, ENDOD1 knockout enables dissection of endonuclease functions in the context of lymphoma biology. Loss of ENDOD1 may sensitize cells to DNA-damaging agents or promote genomic instability, offering insight into therapeutic targets. The model facilitates investigation of how endonuclease deficiency impacts EBV-driven lymphomagenesis and maintains the malignant phenotype, combining the unique properties of this line with targeted gene disruption.
Applications include Western blotting for apoptosis markers (cleaved caspase-3, PARP), ??H2AX immunofluorescence for DNA damage foci, and cell viability assays under genotoxic stress. Subcellular fractionation and nuclease activity assays assess endonuclease function directly, while RNA-seq reveals transcriptomic consequences. These cells are ideal for studying endonuclease roles in apoptosis, DNA repair, and RNA metabolism in B-cell lymphoma. For further details or specific experimental inquiries, please contact Ascent Research.
