The FTO Knockout Raji Polyclonal Cells represent a polyclonal population of Raji B lymphoblastoid cells engineered via CRISPR/Cas9-mediated gene disruption at the FTO locus. This knockout model provides a genetically modified cell pool with heterogeneous editing events across the FTO gene, enabling functional interrogation of FTO-dependent epitranscriptomic regulation without clonal isolation. The cells are supplied as a live, ready-to-use product for immediate downstream applications.
Raji cells are an Epstein-Barr virus (EBV)-positive B lymphoblastoid cell line derived from a Burkitt’s lymphoma patient. As a B lymphocyte model, they retain key features of humoral immunity, including antigen presentation and antibody production. Their robust proliferation in suspension culture and well-characterized signaling networks make them a versatile system for studying B cell biology, lymphomagenesis, and immune responses.
FTO encodes an RNA N6-methyladenosine (m6A) demethylase that catalyzes the oxidative removal of m6A marks on target mRNAs, thereby controlling their stability, splicing, and translation. The enzyme is regulated by upstream signals such as insulin, AMPK, and FOXO1, and it interacts with RNA-binding proteins like YTHDF2 and ELAVL1. Key downstream targets include the oncogenic transcription factor MYC and the signal transducer STAT3, as well as metabolic regulators PPARG and CEBPA. Dysregulation of FTO impacts major signaling cascades, including mTOR, JAK-STAT, NF-??B, and MAPK pathways.
In the Raji lymphoma context, FTO knockout remodels the m6A epitranscriptome, leading to altered post-transcriptional control of MYC and STAT3 expression. This disruption can perturb proliferative, survival, and immune-related pathways, mirroring aspects of FTO’s role in obesity-associated cancers and metabolic disorders. The model thus offers a relevant platform to dissect how m6A modifications govern malignant B cell phenotypes and how FTO contributes to lymphomagenesis.
Typical applications include investigating m6A-dependent gene regulation in B cell lymphoma, validating FTO as a therapeutic target for metabolic and malignant diseases, and screening for epitranscriptomic modulators. Researchers can perform MeRIP-seq and RNA-seq to map transcriptome-wide m6A changes and gene expression profiles, western blotting and RT-qPCR to quantify FTO targets such as MYC and PPARG, and functional assays for proliferation, apoptosis, and glucose uptake. Drug sensitivity studies with FTO inhibitors like rhein can assess target engagement. For further information or custom requests, please contact Ascent Research.
