The FXR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Raji B lymphocytes, with targeted disruption of the FXR1 gene. This loss-of-function model abrogates FXR1-mediated post-transcriptional regulation while preserving the genetic heterogeneity of the parental line, thus minimizing clonal selection artifacts.
The Raji host cell line is an EBV-positive mature B lymphocyte line established from a Burkitt lymphoma patient, serving as a well-characterized model for B-cell malignancies and lymphomagenesis. Raji cells exhibit constitutive activation of survival and proliferation pathways, including NF-??B and PI3K-AKT, and are amenable to genetic manipulation, making them an ideal platform for studying gene function in a lymphoblastoid context.
FXR1 encodes a protein that binds RNA and regulates its transport, stability, and translation, thereby shaping gene expression in lymphocytes and neurons. It is a component of messenger ribonucleoprotein complexes and interacts with FMRP, FXR2, AGO2, DICER, and ribosomal proteins. FXR1 activity is governed by upstream regulators such as mTORC1, MAPK, and NF-??B, linking nutrient and stress signals to post-transcriptional control. Downstream, it modulates the expression of target mRNAs including CYR61, TNF-??, IL-6, and transcripts encoding cell cycle regulators. Through these interactions, FXR1 contributes to the mTOR/PI3K-AKT and MAPK signaling networks, the RNA interference pathway, and cellular stress responses.
In the Raji Burkitt lymphoma model, FXR1 knockout provides a powerful system to examine the role of RNA-binding proteins in B-cell transformation and function. Dysregulation of mRNA metabolism is a hallmark of malignant B cells, and FXR1 has been linked to cancer and neurodevelopmental disorders such as Fragile X syndrome. The abrogation of FXR1 in this polyclonal population allows investigation of its impact on oncogenic signaling, proliferation, apoptosis, and stress adaptation, as well as its interplay with EBV-driven lymphoproliferation.
Researchers can employ this knockout model in diverse assays, including Western blotting, RT-qPCR, RNA-seq, flow cytometry, reporter assays, co-immunoprecipitation, phospho-signaling analysis, and migration assays. It facilitates functional annotation of FXR1 in B-cell biology, exploration of RNA regulatory mechanisms in lymphomagenesis, compound screening for FXR1 modulation, and examination of Fragile X-related pathways in lymphocytes. The polyclonal design avoids clonal bias, enabling detection of robust phenotypic trends. For technical inquiries, please contact Ascent Research.
