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Cat. No. ARG1830

FGD1 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

FGD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of human Raji B lymphocytes with targeted disruption of FGD1. FGD1 is a Cdc42-specific guanine nucleotide exchange factor that regulates actin cytoskeleton organization, filopodia formation, and cell migration via downstream effectors such as PAK1 and WASP. This loss-of-function model enables investigation of FGD1-dependent B-cell receptor signaling, cytoskeletal dynamics, and cell migration in an EBV-positive Burkitt's lymphoma background, with wide applications in immunology, cancer biology, and drug screening.

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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

    FGD1

    Gene Identifier

    NCBI Gene ID 2245

    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 FGD1 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line, with targeted disruption of the FGD1 gene. This loss-of-function model is designed for investigation of FGD1-dependent signaling and cytoskeletal regulation in a B-cell context.

The Raji cell line originates from a Burkitt’s lymphoma patient and is Epstein-Barr virus (EBV)-positive. As B lymphocytes, Raji cells are widely employed in immunology and cancer research due to their capacity for antigen presentation, antibody production, and robust B-cell receptor (BCR) signaling. Their EBV-transformed background provides a relevant model for studying lymphomagenesis and B-cell malignancies.

FGD1 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPase Cdc42 by promoting its GTP-bound state. Active Cdc42 subsequently stimulates downstream effectors including PAK1, WASP, and the ARP2/3 complex, orchestrating actin cytoskeleton reorganization, filopodia formation, and cell migration. FGD1 activity is regulated by upstream signals from the BCR, CD40 ligand, and integrin-mediated pathways, and may involve interactions with phosphatidylinositol lipids, cortactin, and other actin regulatory proteins. This positions FGD1 at a critical node linking extracellular cues to cytoskeletal dynamics.

In the Raji B lymphocyte model, FGD1 is implicated in BCR-dependent cytoskeletal remodeling, cell polarization, and migration processes essential for immune function. Disruption of FGD1 in these cells allows dissection of its role in B-cell signaling, adhesion, and morphological responses downstream of BCR and CD40 stimulation. Moreover, since FGD1 mutations cause Aarskog-Scott syndrome and faciogenital dysplasia, this polyclonal knockout model offers a platform to explore disease mechanisms associated with Cdc42 dysfunction in an immune cell background.

Researchers can utilize these polyclonal knockout cells to perform detailed studies of B-cell cytoskeletal dynamics, migration/invasion, and BCR signal transduction. Compatible assays include Western blotting, immunofluorescence, flow cytometry, Ca2? flux analysis, RNA-seq, and phospho-signaling interrogation. The polyclonal format ensures a heterogeneous population representative of the knockout effect without clonal biases, suitable for population-level phenotypic screens and drug response profiling. For additional information, please contact Ascent Research.

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