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Cat. No. ARG1111

FEZ2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The FEZ2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of Raji B lymphocytes, providing a loss-of-function model for the FEZ2 gene. FEZ2 is a scaffold protein that interacts with PKC?? and DISC1, key components of signaling pathways associated with schizophrenia. This model enables investigation of FEZ2 function in non-neuronal immune cells, supporting studies of PKC??-DISC1 signaling and neuropsychiatric disorder mechanisms. Applications include co-immunoprecipitation, Western blot, and functional assays in B-cell contexts.

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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

    FEZ2

    Gene Identifier

    NCBI Gene ID 9637

    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 FEZ2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, derived from the Raji B lymphocyte cell line, designed for targeted disruption of the FEZ2 gene. This product provides a robust loss-of-function model to study FEZ2-mediated molecular interactions and signaling in a non-neuronal, immune-cell context. The polyclonal nature ensures a diverse pool of gene-disrupted alleles, suitable for reproducible functional analyses across multiple experimental formats.

The Raji cell line is a well-characterized lymphoblastoid line established from a Burkitt??s lymphoma patient, positive for Epstein-Barr virus (EBV) and expressing the B-cell marker CD19. Widely utilized in immunological and oncological research, its stable phenotype and robust growth facilitate consistent experimental outcomes. In this knockout setting, Raji cells offer a distinctive platform to investigate FEZ2, a gene classically linked to neuronal development, within B lymphocytes, potentially revealing uncharacterized roles in immune signaling.

FEZ2 (fasciculation and elongation protein zeta 2) functions as a scaffold protein integral to axonal outgrowth and fasciculation. It directly interacts with protein kinase C zeta (PKC??) and disrupted in schizophrenia 1 (DISC1), placing it centrally within the DISC1 interactome, a network associated with neuropsychiatric disorders. Regulated by neurotrophic factors and PKC?? activators, FEZ2 acts downstream of PKC?? to modulate actin cytoskeleton dynamics and neuronal differentiation markers. It forms complexes with FEZ1, PKC??, and DISC1, coordinately influencing intracellular signaling cascades. Knockout of FEZ2 is anticipated to disrupt these protein interactions and downstream cellular responses.

Although FEZ2 canonical functions are rooted in neuronal systems, its expression in Raji B cells implies broader physiological roles. This model enables dissection of FEZ2-dependent molecular pathways in an immune context, thereby furnishing a valuable tool to examine schizophrenia-associated protein interactions outside the nervous system. The EBV-positive B-cell background may also illuminate intersections between viral latency and FEZ2 signaling, and facilitate studies on how neuropsychiatric risk genes influence immune cell biology. Such insights are critical for understanding neuroimmune crosstalk in disease.

Researchers can employ the FEZ2 Knockout Raji Polyclonal Cells in co-immunoprecipitation assays to delineate protein interaction networks, or in Western blot and RT-qPCR experiments to validate expression changes in downstream targets such as cytoskeletal regulators. Functional assays including cell proliferation and apoptosis measurements can assess FEZ2??s impact on B-cell physiology. Immunofluorescence techniques can visualize alterations in actin organization. Furthermore, these cells serve as a model to study the PKC??-DISC1 signaling axis in immune contexts, relevant to schizophrenia and neuropsychiatric conditions. For further information, please contact Ascent Research.

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