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Cat. No. ARG1943

MOCOS Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The MOCOS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal Raji B lymphocyte population with targeted disruption of MOCOS, encoding molybdenum cofactor sulfurase. This enzyme is critical for activating xanthine oxidase and aldehyde oxidase, which drive purine catabolism and xenobiotic oxidation. Loss of MOCOS is expected to impair uric acid production and alter drug metabolism, making these cells a powerful model for type II xanthinuria research, purine metabolism studies, and B-cell lymphoma drug sensitivity screening.

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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

    MOCOS

    Gene Identifier

    NCBI Gene ID 55034

    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

MOCOS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the MOCOS gene. This loss-of-function model enables investigation of molybdenum cofactor sulfurase biology in a lymphoblastoid context without clonal selection. The Raji cell line, derived from Burkitt’s lymphoma, is a suspension-adapted, EBV-positive line expressing B-cell markers CD19 and CD20, widely used in immunology and cancer research.

Raji cells serve as a robust model for B-cell function, exhibiting antigen presentation capabilities and antibody production. Their genetic stability and ease of manipulation make them ideal for CRISPR/Cas9-mediated gene disruption and subsequent phenotypic analyses. Key features include suspension growth, expression of hallmark B-cell receptors, and retention of signaling pathways relevant to lymphomagenesis.

The MOCOS protein catalyzes the sulfurylation of the molybdenum cofactor (MoCo), an essential step for the activation of xanthine oxidase and aldehyde oxidase. Activated xanthine oxidase drives the conversion of hypoxanthine to xanthine and xanthine to uric acid in purine catabolism, generating superoxide. Aldehyde oxidase mediates xenobiotic oxidation. Interacting factors include xanthine dehydrogenase and aldehyde oxidase 1. Regulation of MOCOS in B cells may involve the transcription factor PAX5.

Disruption of MOCOS in Raji cells impairs MoCo-dependent oxidases, leading to accumulation of purine intermediates and reduced uric acid production. This metabolic shift affects nucleotide balance and redox homeostasis, potentially altering cell proliferation and drug sensitivity. The model is relevant to type II xanthinuria and for studying the role of purine metabolism and aldehyde oxidase activity in B-cell lymphoma drug resistance and toxicity.

Typical applications include Western blotting and RT-qPCR for MOCOS expression analysis, xanthine oxidase activity assays, and uric acid quantification. Drug sensitivity profiling with aldehyde oxidase substrates, flow cytometry for B-cell markers, and cell proliferation assays are also facilitated. For additional information, please contact Ascent Research.

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