The PARP1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the PARP1 gene has been disrupted in the Raji B lymphoblastoid cell line. This product provides a loss-of-function model for studying PARP1-dependent processes in a human B-cell lymphoma background. As a polyclonal knockout pool, it maintains genetic heterogeneity while enabling robust functional assessment of PARP1 deficiency without single-cell cloning artifacts. The knockout model is suitable for experiments requiring bulk populations where gene disruption is achieved across a diverse cell pool.
Raji cells are an EBV-positive lymphoblastoid B-cell line derived from a Burkitt lymphoma. They serve as a well-established model for B-cell malignancies, exhibiting characteristics such as rapid proliferation and expression of B-cell surface markers. The EBV-driven immortalization confers distinct signaling and survival pathways, making Raji cells particularly relevant for studies on lymphoma biology, viral oncogenesis, and immune cell function. Their suspension growth and ease of culture further facilitate high-throughput screening and pharmacological interventions.
PARP1 encodes a nuclear protein that acts as a DNA damage sensor and signal transducer. Upon binding to single-strand breaks induced by ionizing radiation, alkylating agents, or oxidative stress, PARP1 catalyzes poly(ADP-ribosyl)ation (PARylation) of itself and target proteins, including XRCC1, histone H1, and DNA ligase III. This modification recruits base excision repair (BER) factors such as DNA polymerase ?? and APE1. PARP1 also regulates transcription factors NF-??B and p53, and its hyperactivation triggers parthanatos via AIF and MIF translocation. ERK1/2-mediated phosphorylation further modulates PARP1 activity, linking DNA repair to cellular stress signaling.
In the Raji B-cell lymphoma context, PARP1 knockout enables dissection of DNA repair dependencies and synthetic lethal interactions. Lymphomas often exhibit high replication stress and altered DNA damage responses, making them susceptible to PARP inhibition. This polyclonal knockout model allows investigation of PARP1’s role in maintaining genomic stability and resistance to genotoxic agents. It is particularly relevant for exploring mechanisms underlying sensitivity or resistance to PARP inhibitors, which are of therapeutic interest in B-cell malignancies and cancers with homologous recombination deficiencies. Moreover, the EBV-positive background provides a unique opportunity to examine interplay between viral oncoproteins and host DNA repair pathways.
Researchers can employ the PARP1 knockout polyclonal Raji cells in diverse assays, including Western blotting to confirm PARP1 loss and PARylation, immunofluorescence for ??H2AX foci and AIF translocation, and comet assays for DNA strand breaks. Cell viability assays (MTT, CellTiter-Glo) and drug sensitivity profiling with PARP inhibitors provide functional readouts. RT-qPCR can quantify NF-??B targets, and flow cytometry assesses apoptosis markers. These applications support DNA damage response, lymphoma biology, target validation, and synthetic lethality screens. For further information, contact Ascent Research.
