The PAIP2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid line, providing a loss-of-function model for the translational repressor PAIP2. This heterogeneous pool avoids clonal artifacts and enables robust studies of PAIP2-dependent translation control. PAIP2 inhibits cap-dependent translation by disrupting initiation complex assembly, making this model valuable for post-transcriptional gene regulation research in B cells.
The Raji cell line, isolated from a Burkitt??s lymphoma patient, is EBV-positive and expresses B cell markers, serving as a key model for B cell malignancies. Its active proliferation and oncogenic signaling pathways make it relevant for studying translational dysregulation in lymphomagenesis. The polyclonal knockout format retains population-level diversity, better reflecting physiological conditions and allowing assessment of PAIP2 function across a varied cellular background.
PAIP2 represses cap-dependent translation by binding PABPC1 and blocking its interaction with eIF4G, thereby preventing mRNA circularization. This repression is regulated by mTORC1, oxidative stress, and eIF2?? kinases, which modify PAIP2 or PABPC1 interactions to relieve inhibition. Downstream, PAIP2 suppresses global cap-dependent translation and proliferation-related mRNAs. It directly interacts with PABPC1 and indirectly with eIF4G and eIF4A within the translation initiation complex, involving eIF4E, the m7G cap, and the 40S subunit, positioning PAIP2 at a critical intersection of mTOR signaling and the integrated stress response.
In Raji cells, EBV-driven transformation causes aberrant signaling, making PAIP2 knockout a powerful tool to examine how loss of translational repression affects the oncogenic phenotype. The EBV-positive background facilitates studies of viral latency interplay with host translation control, while the B cell origin enables investigation of PAIP2??s role in lymphomagenesis. This model allows probing the consequences of unregulated protein synthesis on proliferation, apoptosis, and stress responses.
Research applications include translation regulation studies, lymphomagenesis mechanism dissection, RNA-binding protein analysis, cancer translational control, and drug target validation for translation inhibitors. Assays such as polysome profiling, luciferase reporters, western blotting, co-immunoprecipitation, RNA-seq, ribosome profiling, and functional proliferation/apoptosis assays are highly suitable. For additional information, contact Ascent Research.
