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Cat. No. ARG1299

MerTK Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The MerTK Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population from EBV-positive Burkitt lymphoma B lymphocytes, designed to disrupt MerTK receptor tyrosine kinase function. MerTK, activated by Gas6 and Protein S, mediates efferocytosis and anti-inflammatory signaling through PI3K/AKT and ERK pathways. Loss of MerTK in these cells abrogates apoptotic cell clearance and may enhance pro-inflammatory responses, making them valuable for studying B cell immunology, tumor microenvironment interactions, and autoimmune diseases such as lupus. Applications include phagocytosis assays, cytokine profiling, and phospho-signaling analysis.

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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

    MERTK

    Gene Identifier

    NCBI Gene ID 10461

    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 MerTK Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function studies of the MerTK receptor tyrosine kinase in a B lymphocyte context. This product comprises a heterogeneous pool of Raji cells with targeted MerTK gene disruption, providing a robust model free from clonal bias, suitable for high-throughput functional assays and pathway analysis.

Raji cells are EBV-positive Burkitt lymphoma-derived B lymphocytes that maintain features of humoral immunity and antigen presentation. Their high transfection efficiency and rapid growth facilitate CRISPR engineering, while the oncogenic and viral background offers a relevant system to study MerTK-mediated immune regulation in lymphoma and tumor microenvironment research.

MerTK activates upon binding of Gas6 or Protein S, leading to autophosphorylation and recruitment of adaptors such as CrkII and DOCK180?CElmo, which stimulate Rac1 to drive phagocytosis. Downstream PI3K/AKT and ERK signaling promotes phosphorylation of AKT, ERK1/2, and STAT3, and transcriptional upregulation of SOCS1 and anti-inflammatory cytokines IL-10 and TGF-??. This pathway mediates efferocytosis and immune quiescence, with regulation by apoptotic cell exposure and TLR stimulation.

In Raji cells, MerTK knockout abrogates efferocytosis and may induce heightened inflammatory signaling, providing a platform to dissect B cell-intrinsic immune checkpoints. The model is valuable for studies on autoimmune diseases like systemic lupus erythematosus and retinitis pigmentosa, as well as cancer immunology, enabling investigation of how MerTK loss alters cytokine secretion and antigen presentation in an EBV-positive background.

Typical assays include Western blotting for MerTK and phospho-MerTK, flow cytometry-based phagocytosis assays, RT-qPCR of MerTK and downstream targets (e.g., SOCS1, IL-10), immunofluorescence, and ELISA for cytokine secretion. Phospho-signaling profiling and drug sensitivity screens targeting TAM pathways further expand its utility. This product supports research in atherosclerosis, autoimmune disorders, and therapeutic development. For additional information, please contact Ascent Research.

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