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Cat. No. ARG1355

FBXO38 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The FBXO38 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from Raji B lymphocytes, enabling loss-of-function studies. FBXO38, the substrate recognition subunit of the SCF E3 ubiquitin ligase complex, regulates degradation of proteins including the immune checkpoint receptor PD-1. This knockout model in an EBV-positive Burkitt's lymphoma background supports research into ubiquitin-mediated proteolysis and immune signaling. Typical applications encompass functional analysis of FBXO38 in B cell biology, substrate identification via co-immunoprecipitation, and investigation of SCF complex dynamics. Assays such as Western blotting, flow cytometry, and ubiquitination assays are applicable, with potential for disease modeling in lymphoma and distal hereditary motor neuronopathy.

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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

    FBXO38

    Gene Identifier

    NCBI Gene ID 81545

    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 FBXO38 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the FBXO38 gene in the human Raji B lymphocyte cell line. This heterogeneous pool of edited cells enables loss-of-function investigations without the bias of single-cell cloning. The product is designed for researchers studying FBXO38-dependent ubiquitin pathways in a polyclonal context, preserving natural genetic variation.

The host Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma B lymphocyte model extensively used in immunology and cancer research.

Raji cells display key B cell characteristics, including surface immunoglobulin expression, major histocompatibility complex (MHC)-mediated antigen presentation, and participation in humoral immunity. Their lymphoma origin provides a relevant background for exploring oncogenic mechanisms and immune checkpoint regulation.

FBXO38 serves as the substrate recognition subunit of the SKP1-CUL1-F-box protein (SCF) E3 ubiquitin ligase complex, which also comprises SKP1, CUL1, and RBX1. This complex catalyzes the transfer of ubiquitin to specific substrate proteins, targeting them for 26S proteasome-mediated degradation.

Among its targets, FBXO38 regulates the stability of programmed cell death protein 1 (PD-1), a critical immune checkpoint receptor. Through PD-1 ubiquitination, FBXO38 modulates immune receptor expression and signaling output. Upstream regulation of FBXO38 is achieved through transcriptional control and post-translational modifications, though the full landscape remains to be elucidated.

In the context of Raji B lymphocytes, loss of FBXO38 function is predicted to impair normal substrate degradation, leading to accumulation of proteins such as PD-1.

This dysregulation may alter immune checkpoint signaling, cell cycle progression, and apoptotic responses. Given Raji’s Burkitt’s lymphoma derivation, this knockout model offers a valuable tool to investigate how defects in the ubiquitin-proteasome system contribute to lymphoma pathogenesis and immune evasion strategies. It also facilitates studies on the interplay between protein homeostasis and B cell function.

Typical applications for these polyclonal knockout cells encompass the dissection of ubiquitin-mediated proteolysis in B lymphocytes, functional interrogation of FBXO38 in lymphoma, and substrate discovery through co-immunoprecipitation coupled with mass spectrometry.

Additional uses include analyzing SCF complex dynamics and modeling distal hereditary motor neuronopathy. Common experimental assays include Western blotting, RT-qPCR, flow cytometry, ubiquitination assays, and cell proliferation or apoptosis measurements. For technical details or ordering, please contact Ascent Research.

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