CTIF Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line, engineered for loss-of-function studies of the CTIF gene. This product provides a genetically disrupted pool of cells in which CTIF expression is abrogated through CRISPR/Cas9-mediated gene disruption, enabling investigation of CTIF-dependent translation initiation and nonsense-mediated mRNA decay (NMD) pathways in a lymphocytic context. The polyclonal format preserves population-level diversity while ensuring target gene inactivation, suitable for pooled functional genomics and biochemical assays.
The parental Raji cell line is a well-characterized B lymphocyte model originating from a human Burkitt lymphoma. These cells are Epstein-Barr virus (EBV)-positive and maintain surface expression of immunoglobulin M (IgM) along with canonical B cell markers, reflecting their antigen-presenting and adaptive immune effector functions. Raji cells are widely employed in immunology and oncology research to study B cell signaling, lymphomagenesis, and viral transformation, providing a physiologically relevant platform for dissecting mRNA regulatory mechanisms in a cancerous B cell environment.
CTIF acts as a CBP80/20-dependent translation initiation factor, bridging the cap-binding complex (CBP80/CBP20) to the 40S ribosomal subunit via interactions with eIF3 and PABPC1. This facilitates the pioneer round of translation on CBC-bound mRNAs, which is closely coupled to NMD??a surveillance pathway that degrades mRNAs harboring premature termination codons. Within this process, CTIF associates with UPF1, a core NMD factor, and influences the recruitment of decay factors like SMG6 and SMG7. Thus, CTIF integrates translation initiation with mRNA quality control, impacting gene expression fidelity.
In Raji B lymphocytes, CTIF knockout disrupts the initiation of CBC-dependent translation and impairs NMD, making these cells a powerful tool for dissecting how defects in mRNA surveillance contribute to lymphomagenesis. Given that Burkitt lymphoma involves dysregulated gene expression and often evasion of apoptosis, the CTIF-null background can be used to assess the roles of NMD substrates in proliferation, survival, and immune function. Additionally, the EBV-positive status of Raji cells allows exploration of viral?Chost interactions affecting translational control.
These CTIF knockout polyclonal cells are suited for a range of experimental approaches, including RT-qPCR and RNA-seq to quantify NMD substrates, polysome profiling to examine translation initiation dynamics, and western blotting to assess downstream signaling events. Flow cytometry and proliferation/apoptosis assays can delineate functional consequences in lymphoma biology. Researchers investigating cap-dependent translation or NMD in B cell malignancies will find this model invaluable for mechanistic studies and therapeutic target validation. For further technical details, please contact Ascent Research.
