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Cat. No. ARG2015

MAT2B Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The MAT2B Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human Raji B lymphocytes (Burkitt's lymphoma, EBV-positive) with targeted disruption of MAT2B, which encodes the regulatory subunit of methionine adenosyltransferase II. MAT2B modulates S-adenosylmethionine (SAM) synthesis and functions as a transcriptional corepressor, linking methionine metabolism to epigenetic regulation via interactions with MAT2A, BAF53a, and corepressor complexes. This knockout model is ideal for investigating SAM-dependent methylation, metabolic reprogramming, and oncogenic signaling in B-cell lymphoma. Applications include LC-MS-based SAM measurement, DNA and histone methylation profiling, cell proliferation studies, and drug target validation for MAT2A/MAT2B inhibitors.

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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

    MAT2B

    Gene Identifier

    NCBI Gene ID 27430

    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 MAT2B Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from human Raji B lymphocytes, featuring disruption of the MAT2B gene. This product provides a heterogeneous loss-of-function model without single?cell clonal selection, enabling studies of MAT2B ablation in a lymphoma-relevant background.

Raji is an EBV-positive Burkitt’s lymphoma B-cell line widely used in immunology and oncology research. It retains key features such as antibody production, antigen presentation, and immune memory functions, offering a well-characterized platform for investigating B-cell malignancies and metabolic dysregulation.

MAT2B encodes the regulatory ?? subunit of methionine adenosyltransferase II, which partners with catalytic MAT2A to generate S-adenosylmethionine (SAM) from methionine and ATP. MAT2B senses methionine availability, modulating MAT2A activity, and also acts as a transcriptional corepressor, bridging one-carbon metabolism to epigenetic control. Upstream regulators MYC, SP1, NF-Y, and SREBP1 control MAT2B expression, while downstream effects encompass MAT2A levels, DNA and histone methylation, phosphatidylcholine synthesis, and polyamine production. Through interactions with BAF53a, actin, and corepressor complexes, MAT2B integrates metabolic signals with chromatin remodeling.

In Raji lymphoma cells, MAT2B knockout permits dissection of how methionine metabolism drives malignant phenotypes. Dysregulated SAM synthesis and aberrant methylation are common in cancer, and MAT2B is linked to hepatocellular carcinoma, colorectal cancer, and liver fibrosis. Disrupting MAT2B in this B-cell model allows investigation of altered SAM homeostasis, epigenetic reprogramming by DNA methyltransferases (DNMTs) and histone methyltransferases that depend on SAM, and transcriptional changes that sustain lymphoma growth, providing insights into metabolic vulnerabilities of EBV-driven B-cell malignancies.

Researchers can use these polyclonal knockout cells to measure SAM levels via LC-MS, assess global DNA methylation and histone modification profiles using Western blotting or sequencing-based methods, and evaluate proliferation and apoptosis. Transcriptomic analysis by RNA-seq and protein interaction studies by co-immunoprecipitation further elucidate MAT2B-dependent networks. Applications include drug target validation for MAT2A/MAT2B inhibitors and high-throughput screening of metabolic modulators in lymphoma. For additional information, contact Ascent Research.

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