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Cat. No. ARG1723

COPS7A Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

COPS7A Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population targeting COPS7A in the Raji B lymphocyte line. This model enables loss-of-function studies of a core COP9 signalosome subunit involved in cullin-RING ligase deneddylation, with downstream effects on p53 and ??-catenin stability. Disruption of COPS7A perturbs ubiquitin-dependent signaling pathways, including NF-??B and JAK-STAT, making these cells suitable for investigating protein degradation mechanisms in Burkitt??s lymphoma. Applications include CRL activity assays, drug screening for proteasome inhibitors, and functional dissection of the ubiquitin-proteasome system in B cell malignancies.

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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

    COPS7A

    Gene Identifier

    NCBI Gene ID 50813

    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

COPS7A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the COPS7A gene has been disrupted. This loss-of-function model provides a pooled Raji cell background for studying the COP9 signalosome (CSN) without requiring clonal isolation. The polyclonal format enables robust population-based assays and screening campaigns.

The Raji host cell line originates from a human Burkitt??s lymphoma, is Epstein-Barr virus (EBV) positive, and expresses B lymphocyte surface markers. Raji cells serve as a well-established model for B cell biology, lymphomagenesis, and immune response studies, and their EBV positivity offers additional relevance for viral oncology research.

COPS7A is a core subunit of the COP9 signalosome, which catalyzes the deneddylation of cullin-RING E3 ubiquitin ligases (CRLs). By removing NEDD8 from cullin scaffolds such as CUL1, CUL3, and CUL4, the CSN inactivates CRLs and stabilizes substrates including p53, ??-catenin, and cyclin E. This regulatory node connects protein ubiquitination and degradation to JAK-STAT, NF-??B, and MAPK/ERK signaling pathways. COPS7A interacts with other CSN subunits (COPS1?C8), CUL1-Rbx1, NEDD8, and USP15, and its activity is modulated by CDK/cyclin kinases, NEDD8 conjugation machinery, and DNA damage signals.

Disruption of COPS7A in Raji B lymphocytes alters CRL-mediated ubiquitination, likely affecting cell cycle progression, apoptosis, and NF-??B-driven survival programs. This perturbation creates a valuable system for dissecting the role of the ubiquitin-proteasome system in Burkitt??s lymphoma, especially in the context of EBV-driven oncogenesis, and for identifying vulnerabilities to proteasome inhibitors.

Key applications include functional analysis of the CSN/CRL axis, mechanistic investigation of ubiquitin-dependent signaling in B cell malignancies, and drug screening for proteasome-modulating agents. Researchers can employ ubiquitination assays, Western blotting for substrate stabilization (e.g., p53, ??-catenin), deneddylation activity assays, flow cytometry for cell cycle and apoptosis, co-immunoprecipitation of CSN complexes, and RNA-seq-based transcriptomics. For further experimental guidance or additional product details, contact Ascent Research.

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