The PARP16 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population generated through targeted disruption of the PARP16 gene in the Raji B lymphoblastoid cell line. This loss-of-function model eliminates PARP16 protein expression across a heterogeneous pool of knockout cells, providing a powerful tool for investigating mono-ADP-ribosylation signaling, endoplasmic reticulum (ER) stress responses, and autophagy regulation within a human Burkitt lymphoma context. The product is supplied as a ready-to-use polyclonal knockout cell population, optimized for downstream functional assays and molecular pathway analyses without requiring clonal isolation.
Raji cells are a suspension-growing, Epstein?CBarr virus-positive B lymphoblastoid line derived from a male patient with Burkitt lymphoma. This cell line retains hallmark features of mature B lymphocytes, including the ability to produce antibodies and mediate immune responses, while also serving as a well-characterized model for B-cell malignancies. The Raji background enables robust proliferation in culture and is widely employed in cancer research, immunology, and drug screening studies focusing on B-cell-derived tumors. Its EBV-positive status further recapitulates a common oncogenic context relevant to lymphomagenesis.
PARP16 encodes a mono-ADP-ribosyltransferase that dynamically modifies target proteins with single ADP-ribose units, thereby fine-tuning signaling cascades. In the unfolded protein response (UPR), PARP16 is activated by ER stress inducers such as tunicamycin and thapsigargin, and it functionally interacts with central UPR kinases PERK (EIF2AK3) and IRE1?? (ERN1). PARP16-mediated ADP-ribosylation modulates the activity states of PERK and IRE1??, which in turn regulate downstream transcriptional programs driven by XBP1s, ATF4, and CHOP (DDIT3). Additionally, PARP16 interfaces with the autophagy machinery through interactions with p62/SQSTM1 and LC3B, bridging stress signaling with autophagic degradation. Consequently, PARP16 deletion disrupts the coordinated control of ER stress responses and autophagic flux, as these processes become uncoupled from key regulatory modifications.
In the Raji Burkitt lymphoma model, PARP16 knockout introduces a deficiency in stress-adaptive pathways that are frequently exploited by cancer cells to survive proteotoxic challenges. The loss of PARP16-dependent regulation of PERK and IRE1?? sensitizes cells to ER stress-induced apoptosis and impairs autophagy-mediated clearance of damaged organelles and protein aggregates. This heightened vulnerability offers a unique experimental window into the determinants of lymphoma cell survival and may identify synthetic lethal interactions exploitable for therapeutic intervention. The polyclonal nature of the knockout population also captures the heterogeneity of gene disruption, making it suitable for bulk profiling studies that require population-level analysis without clonal bias.
Researchers can apply the PARP16 Knockout Raji Polyclonal Cells in a diverse array of experimental workflows. Typical applications include dissecting UPR signaling dynamics in B-cell malignancies using Western blotting for phosphorylated PERK, IRE1??, CHOP, and BiP; monitoring autophagy flux via LC3-I/II conversion and p62 turnover; assessing apoptosis through annexin V/propidium iodide staining; and measuring cell viability with MTS assays under ER stress challenge. Immunofluorescence detection of LC3 puncta and quantitative RT-PCR of XBP1 splicing further resolve mechanistic details. These cells are particularly valuable for drug sensitivity screens targeting ADP-ribosylation pathways or ER stress modulators. For additional technical information, researchers may contact Ascent Research.
