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Cat. No. ARG1864

LGALS2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The LGALS2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited knockout population derived from Raji B lymphocytes, targeting the LGALS2 gene, which encodes galectin-2. Galectin-2 is a carbohydrate-binding protein that interacts with lymphotoxin alpha (LTA) and modulates NF-??B signaling, influencing T-cell apoptosis and inflammatory cytokine production. This model leverages the Raji cell line (human Burkitt lymphoma, EBV-positive) to provide a relevant system for studying B cell biology, immune regulation, and lymphoma pathogenesis. Applications include apoptosis assays, NF-??B reporter analysis, cytokine profiling, and co-immunoprecipitation studies, enabling detailed investigation of galectin-2-dependent mechanisms in inflammation and autoimmunity.

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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

    LGALS2

    Gene Identifier

    NCBI Gene ID 3957

    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 LGALS2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji cells, designed for loss-of-function studies of the LGALS2 gene. This product consists of a heterogeneous pool of cells harboring CRISPR/Cas9-mediated disruptions in the LGALS2 locus, providing a robust genetic background for functional analyses. The polyclonal format avoids clonal selection bias, making it suitable for population-level investigations of gene function in B lymphocyte models.

Raji cells are a human B lymphocyte line established from a Burkitt lymphoma patient and are characterized by Epstein-Barr virus (EBV) positivity and growth in suspension. These cells are widely employed in biomedical research to study antibody production, antigen presentation, and immune response regulation. Their malignant origin and EBV association make them particularly relevant for exploring mechanisms of lymphomagenesis and immune dysregulation.

The LGALS2 gene encodes galectin-2, a carbohydrate-binding protein that interacts with lymphotoxin alpha (LTA) and modulates NF-??B signaling. Galectin-2 functions downstream of TNF-?? and NF-??B and influences the extrinsic apoptotic pathway via regulation of caspase activation and Bcl-2 family proteins. Mechanistically, galectin-2 binding to LTA affects the IKK complex, driving I??B?? phosphorylation and NF-??B nuclear translocation, subsequently controlling expression of pro-inflammatory cytokines including IL-1?? and IL-6. Disruption of LGALS2 thereby perturbs these interconnected signaling cascades.

In Raji B cells, knockout of LGALS2 is anticipated to impair galectin-2-mediated regulation of T-cell apoptosis and inflammatory cytokine production, potentially altering B?CT cell interactions and NF-??B-dependent transcriptional programs. This cellular model is highly relevant for dissecting the molecular underpinnings of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus, as well as inflammatory bowel disease and lymphoma, where dysregulated galectin-2 and NF-??B activity have been reported.

Researchers can utilize these polyclonal knockout cells in a wide array of experimental approaches. Western blotting and RT-qPCR enable confirmation of LGALS2 disruption and assessment of downstream gene expression changes. Flow cytometry facilitates profiling of cell surface markers and apoptosis assays (e.g., Annexin V staining) to evaluate programmed cell death. NF-??B reporter assays and cytokine ELISAs provide quantitative readouts of signaling pathway activity. Co-immunoprecipitation experiments can probe altered protein interactions, particularly with LTA and glycoprotein ligands. These applications support in-depth investigations of B cell biology, inflammation, and lymphoma pathogenesis. For further information, please contact Ascent Research.

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