The PARP3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population in the Raji B lymphocyte cell line, designed to disrupt the PARP3 gene and provide a loss-of-function model for studying DNA damage repair and mitosis-associated roles of PARP3.
The Raji cell line is a human B lymphocyte model derived from a Burkitt??s lymphoma patient and is characterized by Epstein-Barr virus (EBV) transformation. It serves as a widely used system for investigating B-cell malignancies, DNA repair mechanisms, and oncogenic signaling in a lymphoblastoid background.
PARP3 encodes a nuclear poly(ADP-ribose) polymerase that senses DNA strand breaks and catalyzes poly(ADP-ribose) (PAR) synthesis to scaffold DNA repair complexes. It functions downstream of DNA damage-activated kinases such as ATM, ATR, and DNA-PKcs, and is rapidly recruited to sites of oxidative stress and ionizing radiation-induced lesions. Through its PARylation activity, PARP3 facilitates the recruitment of key repair factors including XRCC1, DNA ligase III, and APLF to promote base excision repair (BER) and non-homologous end joining (NHEJ). Additionally, PARP3 interacts with NuMA and TRF2, contributing to mitotic spindle assembly and telomere length maintenance.
In the context of Burkitt??s lymphoma-derived Raji cells, disruption of PARP3 provides a powerful model to dissect the contributions of PAR-driven DNA repair and mitotic regulation to B-cell tumor biology. Given the reliance of lymphoid malignancies on DNA damage response pathways, this polyclonal knockout population enables the study of how PARP3 loss affects genomic stability, cell cycle progression, and sensitivity to DNA-damaging agents. The EBV-positive background further permits investigation of viral?Chost interactions in DNA repair pathway modulation.
Researchers can utilize the PARP3 knockout Raji polyclonal cells in diverse experimental workflows, including western blotting to confirm loss of PARP3 protein, ??H2AX immunofluorescence and comet assays to assess DNA damage accumulation, and PARP activity assays to quantify catalytic function. These cells are suitable for PARP inhibitor cytotoxicity and colony formation assays to probe synthetic lethality and drug response, as well as flow cytometry for cell cycle analysis to examine mitotic defects. Additionally, co-immunoprecipitation studies can map altered protein?Cprotein interactions in the absence of PARP3. For additional information or custom orders, please contact Ascent Research.
