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Cat. No. ARG42597

CAT Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The CAT Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the catalase gene (CAT) in the Raji B lymphoblastoid cell line. Catalase is a key antioxidant enzyme that decomposes hydrogen peroxide, protecting cells from oxidative damage. Its expression is regulated by FOXO, NRF2, PPAR??, and HIF-1??, and it interacts with peroxisomal proteins such as PEX5 and PEX14. Disruption of CAT in EBV-positive Raji cells leads to accumulation of reactive oxygen species, sensitizing cells to oxidative stress-induced apoptosis. This model is valuable for investigating catalase-dependent redox regulation in B-cell lymphoma, screening for oxidative stress modulators, and studying the interplay between antioxidant defenses and oncogenic signaling in lymphoblastoid cells.

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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

    CAT

    Gene Identifier

    NCBI Gene ID 847

    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 CAT Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line. This product features targeted disruption of the CAT gene, which encodes catalase, an essential antioxidant enzyme. The polyclonal format provides a heterogeneous pool of cells with loss-of-function mutations in CAT, enabling robust assessment of gene function without clonal selection biases. This knockout model is designed for researchers investigating oxidative stress responses and the role of catalase in B-cell biology.

The Raji cell line is a widely used human B lymphocyte model, originally derived from a Burkitt lymphoma patient. Raji cells are EBV-positive and maintain a lymphoblastoid phenotype, making them suitable for studies in immunology and cancer biology. These suspension cells exhibit rapid proliferation and have been extensively characterized in signaling, apoptosis, and drug response assays. The host cell background provides a relevant context for examining the interplay between EBV latency and cellular antioxidant defenses.

Catalase catalyzes the decomposition of hydrogen peroxide into water and oxygen, thereby protecting cells from oxidative damage. CAT expression is transcriptionally regulated by FOXO transcription factors, NRF2, PPAR??, and HIF-1?? in response to oxidative stress. Catalase interacts with peroxisomal import receptors PEX5 and PEX14, and functionally cooperates with superoxide dismutase and glutathione peroxidase to maintain redox homeostasis. Disruption of CAT leads to accumulation of H2O2, which can modulate redox-sensitive signaling pathways and promote oxidative stress-induced apoptosis.

In the Raji cellular context, CAT knockout results in heightened sensitivity to oxidative stress, potentially impacting lymphoma cell survival and proliferation. The EBV-positive background of Raji cells may synergize with elevated reactive oxygen species (ROS), influencing viral latency and oncogenic signaling. This model enables dissection of catalase-dependent protective mechanisms in B lymphoblastoid cells, providing insights into how oxidative stress contributes to lymphomagenesis and tumor maintenance.

Researchers can employ this polyclonal knockout population to study oxidative stress responses in B cells, screen for modulators of catalase activity or ROS signaling, and investigate the role of catalase in lymphoma biology. Representative assays include catalase activity measurement, H2DCFDA-based ROS detection by flow cytometry, western blotting for catalase, cell viability assays under H2O2 challenge, Annexin V apoptosis staining, and qRT-PCR for oxidative stress markers. For further information or to inquire about this product, please contact Ascent Research.

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