The MTFR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B lymphoblastoid cell line. This product provides a loss-of-function model for the mitochondrial fission regulator 1 (MTFR1) gene, enabling investigation of mitochondrial dynamics and its role in B-cell lymphoma biology. The polyclonal pool contains a heterogeneous mixture of cells with targeted gene disruptions at the MTFR1 locus, providing a robust population-based system for studying gene function without the need for single-cell cloning. This format is particularly suitable for bulk assays that assess average cellular responses and heterogeneity.
The Raji cell line is an EBV-positive B lymphoblastoid line derived from a Burkitt’s lymphoma patient. It serves as a well-established model for B-cell malignancies, including lymphoma and leukemia, and is widely used to study immune cell signaling, apoptosis, and drug responses. Raji cells exhibit constitutive NF-??B activity due to latent EBV infection, making them a valuable tool for investigating the interplay between viral oncogenesis and host cell metabolism. The suspension-growth characteristics and high transfection efficiency of Raji cells further facilitate genetic manipulation and downstream functional assays.
MTFR1 encodes a mitochondrial outer membrane protein that promotes fission by recruiting and activating DNM1L (DRP1) at the mitochondrial surface, working with adaptors FIS1, MFF, and MIEF1. MTFR1 activity is modulated by energy-sensing pathways AMPK and mTOR, and cellular redox status through ROS and HIF1A. Loss of MTFR1 disrupts fission, causing elongated mitochondria, altered ATP synthesis, and apoptosis resistance. Mechanistically, MTFR1 interacts with DNM1L, FIS1, MFF, and OPA1 at ER-mitochondria contact sites to coordinate remodeling and metabolism.
In the context of Raji B lymphoma cells, MTFR1 knockout provides a powerful tool to dissect the role of mitochondrial dynamics in cancer cell survival and chemoresistance. Lymphoma cells often rewire mitochondrial fission/fusion balance to support rapid proliferation and evade apoptosis. Disruption of MTFR1 in this model enables functional studies on how mitochondrial morphology impacts metabolic reprogramming, AMPK/mTOR signaling, and sensitivity to anticancer agents. Given the association between mitochondrial fission and lymphoma progression, this knockout system allows investigation of MTFR1 as a potential therapeutic target and biomarker in B-cell malignancies.
Researchers can employ these cells for molecular and cellular analyses, including Western blotting and RT-qPCR to confirm MTFR1 disruption and downstream targets like DNM1L and FIS1. Immunofluorescence with MitoTracker visualizes elongated mitochondrial networks, while flow cytometry-based apoptosis and ATP assays quantify functional outcomes. Seahorse metabolic flux analysis reveals glycolytic and oxidative phosphorylation changes, and co-immunoprecipitation validates interactions with fission proteins. These applications support lymphoma biology, mitochondrial dynamics, and drug sensitivity research. For further information, contact Ascent Research.
