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Cat. No. ARG1615

CHST3 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

CHST3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited Raji B-lymphocyte pool lacking chondroitin 6-O-sulfotransferase. CHST3, regulated by SOX9 and TGFB1, cooperates with CSGALNACT1 and CHPF in sulfating proteoglycans like versican, affecting cell adhesion and signaling. This model enables dissection of chondroitin sulfation in B-cell lymphoma and tumor microenvironment, and is suitable for HPLC-MS disaccharide analysis, immunofluorescence, adhesion/migration assays, and sulfotransferase inhibitor screening. Contact Ascent Research for technical support.

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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

    CHST3

    Gene Identifier

    NCBI Gene ID 9469

    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% COâ‚‚

  • 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. It 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

CHST3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal Raji B lymphocyte population with targeted disruption of the CHST3 gene. This heterogeneous pool contains diverse CHST3 loss-of-function mutations, providing a genetically averaged knockout model that minimizes clonal bias. By eliminating chondroitin 6-O-sulfotransferase activity, these cells enable robust functional studies of chondroitin sulfate sulfation in a human B-cell context.

Raji cells are an EBV-positive, Burkitt’s lymphoma-derived lymphoblastoid line exhibiting a mature B-cell phenotype with surface immunoglobulin and classic B-cell markers. Their well-characterized signaling networks and rapid proliferation make them a preferred model for B-cell malignancies and glycobiological investigations. This background is ideal for examining how CHST3 deletion impacts chondroitin sulfate metabolism and lymphoma cell behavior.

The CHST3 gene encodes chondroitin 6-O-sulfotransferase, which catalyzes 6-O-sulfation of GalNAc residues in chondroitin sulfate, generating CS-E and CS-D motifs critical for proteoglycan function. CHST3 acts downstream of regulators SOX9, TGFB1, and BMP2, and partners with CSGALNACT1, CHSY1, and CHPF in a biosynthetic complex. The resultant sulfation patterns dictate proteoglycan interactions with extracellular ligands, influencing cell adhesion, migration, and signaling pathways mediated by chondroitin sulfate proteoglycans such as aggrecan and versican.

In Raji B-lymphoma cells, CHST3-mediated sulfation shapes the tumor cell surface proteoglycan repertoire and microenvironmental interactions. Disruption of CHST3 alters sulfation profiles that may affect cell?Cmatrix adhesion, growth factor binding, and cytokine sequestration, thereby impacting lymphoma progression and immune evasion. This polyclonal knockout model offers a physiologically relevant tool to dissect chondroitin sulfate??s role in malignant B-cell biology and tumor microenvironment crosstalk.

Applications include functional investigation of chondroitin sulfate in B-cell lymphoma using RT-qPCR, Western blot, and HPLC-MS-based disaccharide analysis to assess glycosaminoglycan structure. Immunofluorescence, cell adhesion/migration assays, and flow cytometry allow phenotyping of sulfation changes. The polyclonal population is also suited for high-throughput screening of sulfotransferase inhibitors. For inquiries or customized solutions, please contact Ascent Research.

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