PCYOX1L Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in the Raji B lymphocyte background, designed for functional study of prenylcysteine oxidase 1-like (PCYOX1L). This product is a loss-of-function model generated via CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with targeted disruption of the PCYOX1L locus. The polyclonal format reflects the inherent diversity of editing outcomes and is suitable for population-level analyses of PCYOX1L-dependent processes.
Raji cells are an established human B lymphocyte line derived from an EBV-positive Burkitt lymphoma, characterized by the diagnostic t(8;14) c-MYC translocation and suspension growth properties. These cells express hallmark B cell surface markers CD19 and CD20, making them a widely used model for investigating B cell receptor signaling, lymphomagenesis mechanisms, and Epstein-Barr virus biology. The EBV-positive status further renders them relevant for studying viral latency and transformation programs in B cell contexts.
PCYOX1L encodes a FAD-dependent prenylcysteine oxidase that catalyzes oxidative cleavage of prenylcysteine to cysteine and prenal, a key step in prenylated protein catabolism. This enzymatic activity links PCYOX1L to turnover of prenylated small GTPases (RAS, RAC1), thereby modulating RAS GTPase activity and MAPK signaling. Under oxidative stress, PCYOX1L expression is regulated by NFE2L2/NRF2 and HIF1A, placing it within cellular redox and hypoxia pathways. Additionally, PCYOX1L interacts with p62/SQSTM1 and influences LC3-II conversion, implicating autophagy in prenylated protein clearance. Thus, PCYOX1L knockout likely impairs prenylcysteine degradation, causing accumulation of prenylated proteins, altered AKT phosphorylation, and dysregulated autophagy.
In the Raji Burkitt lymphoma background, PCYOX1L knockout serves as a critical tool to dissect how prenylated protein metabolism intersects with oncogenic signaling driven by c-MYC translocation and EBV latency. By eliminating PCYOX1L function, researchers can examine the dependency of B lymphoma cells on prenylation-dependent RAS/MAPK and PI3K/AKT pathways, as well as the impact on oxidative stress responses and autophagic flux. This model enables the study of how dysregulated prenylation contributes to B cell lymphomagenesis and identifies potential vulnerabilities in prenylation-dependent signaling networks.
The PCYOX1L Knockout Raji Polyclonal Cells enable diverse assays, including Western blot (RAS, p-AKT, LC3), flow cytometry (ROS, apoptosis), RT-qPCR (PCYOX1L), proliferation, and drug sensitivity testing with statins or FTIs. These support target validation for prenylation-related therapies and mechanistic studies of PCYOX1L in oxidative stress and autophagy within B cell lymphoma. For additional information or technical inquiries, please contact Ascent Research.
