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Cat. No. ARG1428

NCOA2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

CRISPR/Cas9-edited polyclonal knockout of NCOA2 in Raji Burkitt lymphoma cells provides a loss-of-function model to interrogate transcriptional coactivator function in B cell malignancies. NCOA2, a p160 coactivator, integrates signals from nuclear receptors (ER??, GR) and transcription factors (MYC, STAT3) to drive proliferative and survival gene programs, including CCND1 and BCL2. This polyclonal knockout population avoids clonal artifacts and enables studies of coactivator-dependent oncogenic networks, including NF-??B and MYC pathways. Applications range from ChIP-qPCR and RNA-seq profiling to proliferation and apoptosis assays, supporting both mechanistic research and drug target validation in lymphoma.

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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

    NCOA2

    Gene Identifier

    NCBI Gene ID 10499

    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 NCOA2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the NCOA2 gene is disrupted in Raji B lymphoblastoid cells. This mixture of edited cells provides a loss-of-function model to study coactivator biology without clonal selection bias, suitable for functional genomics and drug target evaluation.

Raji is an Epstein-Barr virus-positive Burkitt lymphoma cell line, widely used as a model for B cell malignancies and immune signaling. These B lymphocytes exhibit constitutive NF-??B and MYC activity, reflecting key oncogenic pathways. Their robust growth and ease of genetic manipulation make them ideal for investigating lymphoma-driving genes.

NCOA2 is a p160 transcriptional coactivator that links nuclear receptors and transcription factors to basal machinery. It is activated by estrogen receptor, glucocorticoid receptor, and thyroid hormone receptor, and interacts with MYC, STAT3, and CBP/p300. Downstream targets include CCND1, BCL2, MYC, and SLC2A1, driving proliferation and survival. In B cells, NCOA2 integrates B cell receptor?CBTK?CNF-??B signaling to promote gene expression.

In Raji cells, NCOA2 supports oncogenic programs mediated by MYC and NF-??B. Its disruption likely impairs expression of CCND1 and BCL2, reducing proliferation and sensitizing cells to apoptosis. The model thus reveals coactivator dependencies in aggressive lymphoma and allows examination of cross-talk among hormone, growth factor, and immune signaling pathways converging on NCOA2.

Applications include transcriptomic profiling by RNA-seq, chromatin occupancy analysis via ChIP-qPCR, and functional assays such as proliferation/apoptosis and MYC reporter assays. The cells facilitate studies of nuclear receptor coactivator roles in hematopoietic cancers and preclinical testing of coactivator-targeting agents. For further information, please contact Ascent Research.

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