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Cat. No. ARG40222

Dcaf11 Knockout RAW 264.7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Mus musculus (Mouse)

  • Tissue Source:

    Ascites

  • Disease:

    Leukemia

The Dcaf11 Knockout RAW 264.7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from murine RAW 264.7 macrophages, with disrupted DCAF11, a substrate receptor of the CRL4 E3 ligase that targets NRF2 for degradation. Knockout leads to constitutive NRF2 stabilization and upregulation of antioxidant genes such as NQO1 and HMOX1. This model is ideal for studying NRF2-mediated oxidative stress responses, macrophage inflammatory signaling, and the ubiquitin-proteasome system. Applications include western blotting, RT-qPCR, ARE-reporter assays, ROS measurement, phagocytosis, and cytokine secretion analyses.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    RAW 264.7

    Cell Type

    Macrophage cell line

    Sex of Donor

    Male

    Age

    Adult

    Derived From Site

    In situ; Ascites

    Gene Name

    DCAF11

    Gene Identifier

    NCBI Gene ID 28199

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 Dcaf11 Knockout RAW 264.7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the murine RAW 264.7 macrophage line, featuring disruption of the Dcaf11 gene. This polyclonal pool provides a heterogeneous knockout model, avoiding clonal selection bias while enabling robust loss-of-function studies. The cells are supplied as a ready-to-use tool for dissecting DCAF11-dependent pathways in a macrophage context.

The RAW 264.7 host line is an Abelson virus-transformed macrophage cell line from BALB/c mice that retains key innate immune functions, including phagocytosis and secretion of inflammatory cytokines such as TNF-?? and IL-6. Its well-characterized signaling networks and genetic tractability make it a standard model for macrophage biology, inflammation, and immune surveillance research.

DCAF11 functions as a substrate receptor for the Cullin4-RING E3 ubiquitin ligase (CRL4) complex, interacting with DDB1, CUL4A/B, and RBX1. It recruits the transcription factor NRF2 (NFE2L2) for ubiquitin-dependent proteasomal degradation, thus negatively regulating the antioxidant response. Under oxidative stress or electrophile challenge, DCAF11-mediated degradation is inhibited, allowing NRF2 to accumulate and activate antioxidant response element (ARE)-driven genes, including NQO1, HMOX1, and GCLM. Dcaf11 knockout therefore stabilizes NRF2 and constitutively induces antioxidant gene expression.

In RAW 264.7 macrophages, loss of DCAF11 disrupts redox homeostasis and can alter inflammatory responses due to crosstalk between NRF2 and NF-??B pathways. This polyclonal knockout model permits examination of how sustained NRF2 activation affects phagocytosis, ROS handling, and cytokine secretion, providing insights into macrophage regulation in oxidative stress-related conditions such as cancer and neurodegeneration.

These cells are suited for a variety of assays, including western blotting for DCAF11 and NRF2, RT-qPCR of Nqo1 and Hmox1, ARE-luciferase reporter assays, and ROS measurement. They also enable co-immunoprecipitation studies of CRL4 complex interactions and functional assays for phagocytic activity and inflammatory cytokine production. Applications include NRF2 pathway investigation, ubiquitin-proteasome research, macrophage redox biology, and screening for NRF2 modulators. For further information, contact Ascent Research.

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