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Cat. No. ARG1396

CREG1 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

CREG1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population modeling loss of the tumor suppressor CREG1 in an EBV-positive B-cell lymphoma background. CREG1 is a secreted glycoprotein that represses E2F1 transcription of cyclin A and cdc2 via Rb interaction, and promotes lysosomal biogenesis through LAMP1 and cathepsin regulation. This model is suitable for investigating B-cell lymphoma pathogenesis, tumor suppression, lysosomal biogenesis, and differentiation. Typical assays include proliferation, apoptosis, flow cytometry, Western blotting of downstream targets, and reporter assays for ??-catenin or E2F activity. It also facilitates drug screening and oncogene cooperation studies.

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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

    CREG1

    Gene Identifier

    NCBI Gene ID 8804

    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 CREG1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, in which the gene encoding CREG1 (Cellular Repressor of E1A-stimulated Genes 1) has been disrupted via CRISPR/Cas9-mediated gene targeting. This polyclonal knockout pool provides a loss-of-function model for studying the tumor-suppressive and differentiation-promoting functions of CREG1 in a B-cell lymphoma background.

The Raji host cell line, originally isolated from a patient with Burkitt??s lymphoma, represents an Epstein?CBarr virus (EBV)-positive B-cell model that retains key features of aggressive B-cell malignancies. Raji cells are widely used for investigating oncogenic mechanisms, viral pathogenesis, and therapeutic responses in B-cell lymphoma research.

CREG1 encodes a secreted glycoprotein that acts as a transcriptional repressor and negatively regulates cell proliferation. Mechanistically, CREG1 antagonizes E1A-mediated transformation by interacting with Rb and p300/CBP, thereby inhibiting E2F1-driven transcription of cell cycle genes such as cyclin A and cdc2. Additionally, CREG1 promotes lysosomal biogenesis by upregulating LAMP1 and cathepsins, and it enhances cellular differentiation. Upstream, CREG1 expression is modulated by p53, E2F1, MEF2 transcription factors, TGF-??, and insulin, while downstream it influences ??-catenin stabilization and insulin receptor substrate (IRS) signaling. CREG1 also binds to the mannose-6-phosphate/IGF2 receptor (IGF2R), linking its function to lysosomal enzyme trafficking.

In the context of Raji cells, disruption of CREG1 eliminates its growth-inhibitory and pro-differentiation activities, potentially accelerating cell-cycle progression and attenuating lysosomal function. This knockout model is particularly relevant for dissecting the role of CREG1 in B-cell lymphoma pathogenesis, as loss of CREG1 expression has been associated with enhanced proliferation and impaired differentiation in various cancers. Furthermore, the EBV-driven background of Raji cells provides a platform to study the interplay between viral oncoproteins and host tumor suppressors such as CREG1.

The CREG1 Knockout Raji Polyclonal Cells are suitable for a range of research applications, including investigation of tumor suppressor mechanisms, lysosomal biogenesis, and B-cell lymphoma biology. Researchers can employ this model in proliferation and apoptosis assays, flow cytometric cell cycle analysis, RT-qPCR and Western blotting for E2F target genes and lysosomal markers (e.g., LAMP1, cathepsin D), co-immunoprecipitation of CREG1-interacting partners (such as Rb or p300/CBP), and reporter assays to assess ??-catenin/TCF or E2F activity. Additionally, the cells can be used in drug sensitivity screens and oncogene cooperation studies to evaluate genetic interactions relevant to lymphoma. For further information, please contact Ascent Research.

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