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Cat. No. ARG1844

GMEB2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The GMEB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human Raji B lymphocytes. GMEB2 is a transcriptional coregulator that modulates glucocorticoid receptor and TGF-beta/Smad signaling through interactions with factors such as the glucocorticoid receptor, Smad2/3, PARP-1, and CBP/p300. In this Burkitt lymphoma-derived line, GMEB2 knockout impairs glucocorticoid-induced apoptosis and TGF-beta-mediated gene regulation, making it a valuable model for lymphoma research and drug screening. Typical applications include Western blotting, apoptosis assays, and reporter gene studies with GRE-luciferase or TGF-beta-responsive constructs.

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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

    GMEB2

    Gene Identifier

    NCBI Gene ID 26205

    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 GMEB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the GMEB2 gene, enabling loss-of-function studies without clonal selection. It serves as a versatile research tool for investigating glucocorticoid and TGF-beta signaling in a B-cell context.

Raji cells are a lymphoblastoid cell line established from a Burkitt lymphoma patient, representing mature B lymphocytes with characteristics of the germinal center stage. These cells express surface immunoglobulins and are widely used to study humoral immunity, B-cell malignancies, and apoptosis signaling. Their derivation from an aggressive lymphoma makes them particularly relevant for cancer biology and drug sensitivity screening.

GMEB2 functions as a transcriptional coregulator that fine-tunes gene expression by interacting with the glucocorticoid receptor (GR) and Smad2/3 transcription factors. It participates in the assembly of transcriptional complexes containing PARP-1 and CBP/p300, integrating signals from glucocorticoids and TGF-beta. Upon ligand activation, the GR translocates to the nucleus and recruits GMEB2 to glucocorticoid-responsive gene promoters, while TGF-beta receptor-mediated phosphorylation of Smad2/3 enables their association with GMEB2 at TGF-beta-responsive elements. Through these interactions, GMEB2 modulates the transcription of downstream targets, including members of the Bcl-2 family and caspases, thereby exerting control over apoptosis and cell proliferation.

In Raji B lymphocytes, GMEB2 plays a critical role in mediating glucocorticoid-induced apoptosis and TGF-beta-driven gene regulation. Disruption of GMEB2 in these polyclonal knockout cells abrogates the normal transcriptional responses to glucocorticoids and TGF-beta, leading to altered cell survival and proliferative capacity. This model is particularly informative for dissecting the mechanisms of glucocorticoid resistance and TGF-beta signaling in B-cell lymphoma, offering a platform to explore pathways that govern immune cell fate and oncogenic transformation.

The GMEB2 Knockout Raji Polyclonal Cells are suited for a range of functional assays, including Western blotting and RT-qPCR for protein and mRNA expression analysis, RNA-seq for transcriptome profiling, ChIP-qPCR for assessing GMEB2 occupancy at target promoters, immunofluorescence for subcellular localization, flow cytometry for surface marker and cell cycle analysis, apoptosis assays using Annexin V/PI staining, and co-immunoprecipitation to probe protein?Cprotein interactions. Additionally, reporter assays with GRE-luciferase or TGF-beta-responsive constructs allow quantitative assessment of pathway activity, and drug sensitivity studies enable screening of compounds targeting glucocorticoid or TGF-beta pathways. For further technical information, please contact Ascent Research.

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