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Cat. No. ARG1786

ERF Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The ERF Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the ERF gene in human Raji B lymphocytes. ERF is a transcriptional repressor that regulates ETS target genes such as CCND1 and is phosphorylated by ERK1/2, triggering its nuclear export and degradation. In Raji cells, which are derived from Burkitt??s lymphoma, ERF normally provides negative feedback on the RAS-ERK pathway. This knockout model is valuable for studying tumor suppression in B-cell lymphoma, ERK signaling feedback mechanisms, and drug sensitivity. Researchers can employ assays including Western blotting for ERF and phospho-ERK, RT-qPCR for CCND1 and MYC, cell proliferation assays, and flow cytometry.

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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

    ERF

    Gene Identifier

    NCBI Gene ID 2077

    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 ERF Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population designed to disrupt the ERF gene in the Raji B lymphocyte cell line. This product serves as a loss-of-function model for dissecting ERF-dependent transcriptional repression and its role in RAS-ERK signaling dynamics.

Raji cells are a well-characterized human B lymphoblastoid line established from a Burkitt??s lymphoma. They exhibit B-cell functions including humoral immunity, antigen presentation, and cytokine production. This cellular background is particularly relevant for investigating oncogenic signaling in B-cell malignancies, where the RAS-ERK pathway is frequently activated.

ERF functions as a transcriptional repressor that accumulates in the nucleus under low ERK activity, binding ETS motifs to suppress target genes such as CCND1, MYC, and FOS. Upon activation of upstream receptors (e.g., EGF, FGF), the RAS-ERK cascade??involving GRB2, SOS1, HRAS, RAF1, MEK1/2, and ERK1/2??phosphorylates ERF. This phosphorylation promotes interaction with XPO1, leading to nuclear export and degradation, thereby relieving repression and allowing cell cycle progression. Disruption of ERF removes this critical feedback checkpoint, resulting in constitutive derepression of proliferative targets.

In the Raji lymphoma background, ERF knockout provides a model to study tumor-suppressive mechanisms that are often subverted by aberrant RAS-ERK activity. ERF normally restrains G1/S transition by repressing CCND1; loss of ERF may therefore mimic oncogenic phenotypes observed in aggressive B-cell lymphomas. This polyclonal knockout population enables the examination of how ERF deficiency impacts drug sensitivity, clonal dynamics, and overall malignant behavior in a relevant cellular context.

Typical applications include investigating ERF-mediated tumor suppression, studying feedback regulation of ERK activity, and evaluating drug responses in lymphoid cancers. Compatible assays include Western blotting for ERF and phospho-ERK, RT-qPCR for CCND1 and MYC, cell proliferation assays, flow cytometry for cell cycle analysis, and drug sensitivity screening. For additional technical details, please contact Ascent Research.

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