The PAIP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, designed for functional studies of poly(A)-binding protein interacting protein 1 (PAIP1), a key regulator of translation initiation. This polyclonal format provides a heterogeneous mixture of cells carrying targeted disruptions in the PAIP1 locus, enabling pooled loss-of-function analyses without single-cell cloning.
The Raji host cell line is an EBV-positive Burkitt’s lymphoma-derived B lymphocyte model widely employed in immunology and cancer research. These cells are capable of antibody production, exhibit rapid proliferation, and retain active mTOR signaling, making them an appropriate system for investigating translational control mechanisms in B cell lymphomas.
PAIP1 facilitates translation initiation by bridging the mRNA poly(A) tail, via its interaction with PABPC1, to the cap-binding complex containing eIF4G and eIF4A, thereby enhancing mRNA circularization and ribosomal recruitment. PAIP1 activity is regulated upstream by mTORC1, which phosphorylates 4E-BP1 to release eIF4E and promote eIF4F complex assembly, and functions downstream of growth factor signals to drive translation of proliferation-related mRNAs and global protein synthesis.
In the Raji B lymphocyte context, PAIP1 knockout is predicted to impair oncogene translation and attenuate proliferation, providing a relevant model for studying translational dysregulation in B cell lymphomas. Because Raji cells harbor MYC translocations and depend on high translational output, disruption of PAIP1 disrupts the mRNA circularization step, potentially reducing synthesis of pro-proliferative proteins and sensitizing cells to translation inhibitors.
This polyclonal knockout population is suitable for investigating translation control in lymphoma, examining oncogene expression, and validating drug targets for translation inhibitors. Representative assays include Western blotting and RT-qPCR for confirming PAIP1 disruption and downstream effector analysis, polysome profiling to assess ribosome loading, cell viability and proliferation assays by flow cytometry, and luciferase reporter assays to measure cap-dependent translation efficiency. For further information, please contact Ascent Research.