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Cat. No. ARG1386

GALNT2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The GALNT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited B lymphoblastoid cell population with disruption of GALNT2, the initiating O-glycosyltransferase that adds GalNAc to serine/threonine residues of substrates like MUC1 and EGFR. This model enables study of O-glycosylation-dependent signaling and adhesion in an EBV-positive Burkitt lymphoma background. Applications include lectin-based glycan detection, flow cytometry profiling, and functional assays to investigate GALNT2??s role in apoptosis, migration, and immune recognition, supporting cancer and glycosylation disorder research.

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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

    GALNT2

    Gene Identifier

    NCBI Gene ID 2590

    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

The GALNT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the GALNT2 gene has been disrupted. This heterogeneous pool of Raji cells provides a loss-of-function model of GALNT2, the enzyme that initiates mucin-type O-glycosylation in the Golgi apparatus by transferring N-acetylgalactosamine (GalNAc) to serine/threonine residues of target proteins. The polyclonal format captures a range of gene-editing events, making it suitable for functional genomics studies without clonal artifacts.

The parental Raji cell line is an Epstein-Barr virus (EBV)-positive human B lymphoblastoid line originally isolated from a Nigerian Burkitt lymphoma patient. Raji cells are widely employed in hematological cancer research due to their expression of B-cell surface markers and constitutive EBV-driven growth. This cellular model provides a relevant context for studying how glycosylation influences proliferation, apoptosis, and immune interactions in B-cell lymphomas.

GALNT2 functions under the transcriptional control of SP1, TGF-??, and hypoxia-inducible factors, and acts on key substrates including MUC1, MUC4, EGFR, and the insulin receptor. It collaborates with other glycosyltransferases such as GALNT1, GALNT3, C1GALT1, and B3GNT6 within the Golgi to elaborate O-glycan structures. Through these modifications, GALNT2 influences receptor stability, ligand binding, cell adhesion, and downstream signaling, linking O-glycosylation to cancer progression, dyslipidemia, and congenital disorders of glycosylation.

In the Raji Burkitt lymphoma context, GALNT2 knockout allows dissection of mucin-type O-glycosylation’s role in B-cell malignancy. Raji cells exhibit aberrant glycosylation linked to EBV transformation; depletion of GALNT2 alters the O-glycoproteome, potentially impacting surface receptor dynamics, adhesion properties, and apoptotic thresholds. The polyclonal knockout population mirrors heterogeneous glycosylation responses, enabling investigation of how variable GALNT2 disruption affects oncogenic signaling and immune evasion at the population level.

This knockout cell product supports lectin blotting with Vicia villosa or Helix pomatia agglutinins to assess O-glycan changes, flow cytometry for cell surface glycan profiling, and Annexin V apoptosis assays. Additional applications include cell adhesion and migration/invasion assays to probe metastatic behavior, as well as glycoproteomic and RNA-seq analyses to map glycosylation-related gene networks. For detailed product information or assistance, please contact Ascent Research.

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