The CPEB4 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the Raji B lymphocyte cell line. This product provides a loss-of-function model for studying the RNA-binding protein CPEB4, enabling investigation of its roles in post-transcriptional regulation. The polyclonal nature captures the heterogeneity of editing outcomes, making it suitable for population-level functional assays without clonal isolation biases.
The Raji cell line is a suspension-adapted human B lymphocyte line originally isolated from a Burkitt lymphoma patient. It is Epstein-Barr virus (EBV)-positive and widely employed in immunology and cancer research, particularly as a model for B cell malignancies. Raji cells exhibit robust growth and are amenable to a variety of genetic manipulations and functional assays, providing a physiologically relevant context for studying B cell biology and oncogenic mechanisms.
CPEB4 is an RNA-binding protein that specifically recognizes cytoplasmic polyadenylation elements (CPEs) in the 3′ UTR of dormant mRNAs. Upon phosphorylation by kinases such as Aurora A kinase, downstream of calcium signaling and the MAPK/ERK pathway, CPEB4 recruits poly(A) polymerase through interactions with symplekin, CPSF, eIF4E, and PABP, leading to poly(A) tail elongation and translational activation. Its key targets include cyclin B1 and c-myc mRNAs, as well as transcripts encoding pro-apoptotic factors. By controlling the translation of these regulators, CPEB4 orchestrates cell cycle progression and apoptosis. In the knockout cells, disruption of CPEB4 impairs this mechanism, causing dysregulation of cell division and survival pathways.
In the context of Raji cells, CPEB4 knockout provides a powerful tool to dissect the role of translational control in B cell malignancies. Dysregulation of mRNA translation is a hallmark of many cancers, and CPEB4 has been implicated in promoting proliferation and inhibiting apoptosis in B cell lymphomas. This model allows researchers to examine how loss of CPEB4-mediated regulation affects the stability and translation of oncogenic transcripts, such as c-myc, and how it alters the cellular response to apoptotic stimuli. It is especially relevant for studying EBV-driven lymphomagenesis and for validating CPEB4 as a potential therapeutic target.
This polyclonal knockout cell population is well-suited for a range of applications, including: investigating translational control mechanisms by luciferase reporter assays and RT-qPCR; profiling global mRNA translation changes via RNA-seq; assessing cell cycle and apoptosis using flow cytometry and proliferation assays; and validating drug targets with western blotting. Researchers can employ this model to explore the interplay between CPEB4 and its interacting partners in B cell signaling networks. For further details or to order this product, please contact Ascent Research.
