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Cat. No. ARG1580

CLPP Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

CLPP Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte line, with disrupted expression of the mitochondrial matrix protease CLPP. This model enables study of mitochondrial proteostasis, the UPRmt regulated by ATF5 and CHOP, and apoptosis control. Applications include mitochondrial dysfunction research in B-cell lymphoma, drug screening for mitochondrial protease inhibitors, and apoptosis assays. Western blotting, JC-1 staining, and ATP quantification can be used to characterize CLPP-dependent phenotypes.

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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

    CLPP

    Gene Identifier

    NCBI Gene ID 8192

    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 CLPP Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphocyte line, with disrupted CLPP expression. This product provides a heterogeneous knockout model, avoiding clonal selection and enabling robust functional studies of mitochondrial proteostasis. The polyclonal format supports bulk cell assays such as drug response profiling and metabolic analyses.

Raji is an EBV-positive Burkitt lymphoma cell line widely used in immunology and cancer research due to its rapid proliferation and apoptotic sensitivity. Its suspension growth facilitates high-throughput screening. Combining this B-cell lymphoma model with CLPP knockout offers a unique system to study mitochondrial dysfunction in hematologic cancers.

CLPP encodes a mitochondrial matrix serine protease that forms a proteolytic complex with the hexameric unfoldase CLPX to degrade misfolded or damaged proteins, essential for maintaining mitochondrial proteostasis. This function is central to the mitochondrial unfolded protein response (UPRmt), a stress pathway activated by the accumulation of protein aggregates. Key transcription factors ATF5 and CHOP are induced downstream of mitochondrial stress signals and upregulate chaperones and proteases. Upstream regulators PGC-1??, NRF1, and TFAM link mitochondrial biogenesis to proteostatic capacity. Disruption of CLPP impairs substrate degradation, leading to mitochondrial protein aggregate accumulation, elevated reactive oxygen species (ROS), reduced ATP production, and heightened apoptosis sensitivity. CLPP cooperates with mitochondrial chaperones HSP60 and HSP10, which assist in substrate handling, while alternative proteases such as LONP1 and HTRA2 may partially compensate for CLPP loss.

In the Raji B lymphocyte context, CLPP knockout enables dissection of how mitochondrial proteostasis influences survival, metabolic adaptation, and chemosensitivity of lymphoma cells. The model permits comprehensive characterization using Western blotting for CLPP and CLPX, RT-qPCR for UPRmt markers ATF5 and CHOP, JC-1-based mitochondrial membrane potential measurement, and Annexin V apoptosis detection. It is particularly valuable for drug screening studies targeting mitochondrial proteases and for investigating the UPRmt in lymphomagenesis.

This polyclonal knockout product is suitable for a broad range of applications: studying mitochondrial proteostasis mechanisms in B-cell lymphoma, investigating UPRmt signaling in cancer, and screening chemical libraries for mitochondrial protease modulators. Functional readouts include ROS measurement, ATP quantification, mitochondrial membrane potential assessment, and apoptosis assays. The model can also be used in colony formation assays to evaluate long-term proliferative effects and in drug sensitivity testing with mitochondrial toxins. For co-culture or in vivo studies, these cells provide a starting point to explore how CLPP affects tumor growth and immune interactions. For additional information, please contact Ascent Research.

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