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Cat. No. ARG1833

FMR1 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

FMR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of Raji B lymphocytes with disruption of the FMR1 gene, resulting in loss of the RNA-binding protein FMRP. FMRP normally represses translation of targets such as MAP1B and ARC and is regulated by mGluR5, CREB1, and the mTOR pathway. These cells enable studies of FMRP-dependent RNA regulation in immune cells, modeling of Fragile X syndrome, and compound screening targeting synaptic-like signaling pathways in B lymphocytes. Applications include RNA immunoprecipitation, RT-qPCR, and flow cytometry.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Raji

    Cell Type

    B cell line

    Sex of Donor

    Male

    Age

    11 years

    Derived From Site

    In situ; Maxilla

    Gene Name

    Fmr1

    Gene Identifier

    NCBI Gene ID 2332

    Morphology

    Lymphoblast-like

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The FMR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line, featuring targeted disruption of the FMR1 gene. This loss-of-function model eliminates FMRP expression, and the polyclonal format provides a heterogeneous mixture of edited cells, reflecting diverse knockout genotypes without clonal selection, ideal for robust population-level analyses.

Derived from an Epstein-Barr virus-positive Burkitt’s lymphoma, Raji B cells serve as a well-established model for antigen presentation and immunoglobulin production. Their stable proliferation, defined surface marker profile, and tractable genetic manipulation make them a powerful platform for studying signal transduction and translational regulation in the immune system. The line is widely used in investigations of EBV-driven lymphomagenesis and B cell receptor signaling.

FMR1 encodes the RNA-binding protein FMRP, a translational repressor that forms complexes with CYFIP1, FXR1P, FXR2P, and Argonaute proteins to control the stability and translation of target mRNAs, including MAP1B, ARC, and BDNF. FMRP activity is regulated upstream by mGluR5, CREB1, and BDNF signaling, and it functions within the mTOR pathway alongside key components such as 4E-BP, eIF4E, PI3K, AKT, TSC1/2, and Rheb. Disruption of FMR1 in this system abolishes FMRP-mediated repression, leading to dysregulation of synaptic-like signaling cascades that are increasingly recognized in lymphocyte biology.

By eliminating FMRP in a B lymphocyte context, this knockout model recapitulates core molecular features of Fragile X syndrome and related disorders, including fragile X-associated tremor/ataxia syndrome, fragile X-associated primary ovarian insufficiency, and autism spectrum disorders. The loss of FMRP-dependent translational control may alter pathways relevant to antigen presentation and antibody production, offering a unique system to dissect connections between mRNA metabolism and immune cell function.

These cells are suited for diverse experimental applications: analyzing FMRP?CRNA interactions via RNA immunoprecipitation and polysome profiling, quantifying FMRP target mRNAs (BDNF, ARC) by RT-qPCR, and performing compound screens against the mGluR5?CPI3K?CAKT?CmTOR axis. Additional assays include Western blotting for FMRP, flow cytometry for B cell markers, and MTT-based viability testing. For further details or custom requests, contact Ascent Research.

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