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Cat. No. ARG1994

OGFR Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The OGFR Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with disruption of the OGFR gene. Raji cells are an EBV-positive Burkitt's lymphoma model, and OGFR encodes the receptor for opioid growth factor (OGF), which mediates growth inhibition through upregulation of p21 and p27 cyclin-dependent kinase inhibitors. This knockout tool is suitable for studying OGF-OGFr signaling, cell cycle arrest, and B cell malignancy mechanisms. Applications include western blotting, proliferation assays, and screening for opioid receptor modulators.

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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

    OGFR

    Gene Identifier

    NCBI Gene ID 11054

    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 OGFR Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt’s lymphoma B lymphocyte line Raji, designed to ablate functional expression of the opioid growth factor receptor (OGFR) gene. This polyclonal format provides a heterogeneous pool of edited cells that collectively lack OGFR signaling, enabling robust loss-of-function studies without clonal bias.

The Raji parental line is an Epstein-Barr virus (EBV)-positive lymphoblastoid B cell line established from a Burkitt’s lymphoma patient. It retains key features of malignant B cells, including high proliferative capacity and antigen-presenting properties, making it a valuable model for investigating B cell malignancies and the molecular determinants of lymphoma cell growth.

OGFR is a receptor that transduces signals from opioid growth factor (OGF, [Met5]-enkephalin) to negatively regulate cell proliferation. Ligand engagement promotes nuclear translocation of the receptor and transcriptional induction of cyclin-dependent kinase inhibitors CDKN1A (p21) and CDKN1B (p27). Consequently, CDK2/cyclin E activity is suppressed, leading to hypophosphorylation of retinoblastoma protein (RB1) and G1/S cell cycle arrest. Disruption of OGFR removes these inhibitory constraints, allowing dysregulated progression through the cell cycle.

In the context of Raji B lymphocytes, endogenous OGF-OGFr signaling may act as a tumor-suppressive checkpoint. Knocking out OGFR provides a direct means to interrogate how loss of this growth-inhibitory pathway contributes to the aggressive proliferation typical of Burkitt’s lymphoma and other B cell malignancies.

Researchers can employ this model to explore OGF-OGFr-mediated cell cycle regulation, screen small molecules targeting opioid signaling, or investigate crosstalk with oncogenic pathways. Experimental readouts include immunoblotting for p21, p27, and phospho-RB1; quantitative RT-PCR; flow cytometry with propidium iodide staining; and BrdU incorporation assays. OGF treatment and immunoprecipitation experiments can be used to validate receptor-specific responses. For inquiries, please contact Ascent Research.

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