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Cat. No. ARG1936

FGFR1 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The FGFR1 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout model of the FGFR1 receptor tyrosine kinase in the human EBV-positive Burkitt lymphoma B lymphoblast line Raji. FGFR1, activated by FGF ligands such as FGF1 and FGF2, signals through MAPK/ERK and PI3K-AKT cascades, mediated by adaptors like FRS2 and GRB2, to regulate proliferation and survival. This knockout population is designed for studying FGFR1-dependent pathways in B-cell lymphoma, target validation, and signal transduction research. Representative applications include phospho-signaling analysis, proliferation and apoptosis assays, and migration studies, supported by the suspension culture format of Raji cells. For technical inquiries, please contact Ascent Research.

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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

    FGFR1

    Gene Identifier

    NCBI Gene ID 2260

    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 FGFR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast line. This product provides a loss-of-function model for the human FGFR1 gene, encoding fibroblast growth factor receptor 1, in a well-characterized hematopoietic suspension cell background. The polyclonal composition reflects a pooled knockout approach, suitable for population-level studies.

Raji cells are an EBV-positive B lymphoblast line established from a Burkitt lymphoma patient. They grow in suspension and exhibit B lymphocyte features including antigen presentation and immunoglobulin production, making them a standard model for B-cell malignancy and lymphocyte signaling research.

FGFR1 is a receptor tyrosine kinase that transduces signals from fibroblast growth factors (FGFs) including FGF1, FGF2, FGF4, FGF8, and FGF23, with heparan sulfate proteoglycans as obligate coreceptors. Ligand engagement induces receptor dimerization and autophosphorylation, creating docking sites for adaptor proteins FRS2, GRB2, SOS1, GAB1, and SHC1. These interactions initiate downstream cascades: the RAS-RAF-MEK-ERK pathway leading to phosphorylation of MAPK1/3, the PI3K-AKT pathway activating AKT1, and the PLC?? pathway with PLCG1 generating second messengers. These signals converge on transcription factors such as FOS, JUN, and STAT1, regulating gene expression programs that control cell proliferation, differentiation, migration, and survival. In the knockout model, disruption of FGFR1 abolishes these ligand-dependent signaling events, providing a defined loss-of-function background for mechanistic studies.

Within the Raji B lymphoblast context, FGFR1 is implicated in the proliferation and survival pathways that sustain malignant B cells. Aberrant FGF signaling has been documented in B-cell lymphomas, and this knockout model allows researchers to uncouple FGFR1-specific contributions from other regulatory inputs, such as B-cell receptor signaling and EBV latent gene expression. By eliminating FGFR1, the polyclonal cells offer a versatile platform to examine how this receptor modulates lymphoblast growth, apoptotic thresholds, and chemotactic responses.

Applications encompass target validation for FGFR1-directed therapeutics in B-lymphoma, dissection of FGF-dependent signal transduction, and functional genomics screens. Compatible experimental readouts include western blotting for FGFR1 and downstream phospho-proteins, RT-qPCR for transcriptional targets, flow cytometry for cell cycle and surface markers, proliferation and apoptosis assays, and migration assays. Additional approaches such as phospho-signaling multiplex analysis and inhibitor synergy studies are well suited to this polyclonal knockout system. For detailed product information and technical support, please contact Ascent Research.

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