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Cat. No. ARG1271

EXOG Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The EXOG Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human Raji Burkitt lymphoma B cells with targeted disruption of the EXOG gene, which encodes a mitochondrial 5'-3' endo/exonuclease involved in mtDNA repair and apoptosis regulation. EXOG interacts with POLG, TFAM, Endonuclease G, and AIFM1; its loss promotes mtDNA damage and apoptosis susceptibility. This model supports mitochondrial biology, DNA repair, and cancer metabolism research, with applications in mtDNA damage quantification, apoptosis assays, and metabolic profiling.

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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

    EXOG

    Gene Identifier

    NCBI Gene ID 9941

    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 EXOG Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population derived from the human Raji B lymphocyte line, designed to disrupt the EXOG gene encoding a mitochondrial 5′-3′ endo/exonuclease. This polyclonal knockout model enables loss-of-function studies of mtDNA repair and apoptosis pathways without clonal selection, providing a genetically heterogeneous background that better mimics physiological cell culture conditions.

The parental Raji cell line is an EBV-positive human Burkitt lymphoma B lymphocyte model that proliferates in suspension. Widely utilized to investigate B-cell biology and lymphomagenesis, Raji cells exhibit malignant features and serve as a well-characterized system for examining apoptosis, signal transduction, and metabolic reprogramming. Their rapid growth and genetic stability make them suitable for CRISPR/Cas9-mediated gene disruption.

EXOG functions as a mitochondrial endo/exonuclease that cleaves DNA at abasic sites and participates in mtDNA base excision repair and replication. Its activity is modulated by oxidative stress, TFAM, and DNA damage signals, and it interacts with POLG, TFAM, Endonuclease G, and AIFM1. EXOG acts upstream of mtDNA integrity maintenance and mitochondrial function, and its disruption leads to mtDNA damage accumulation and heightened apoptotic susceptibility, partly through AIFM1-mediated execution pathways.

In Raji B lymphoma cells, EXOG knockout compromises mtDNA repair, causing accumulation of mitochondrial lesions, impaired respiratory capacity, and increased sensitivity to apoptotic triggers. This model is particularly valuable for dissecting how mitochondrial dysfunction fuels Burkitt lymphoma malignancy and for identifying metabolic dependencies that could be targeted therapeutically. The EBV-positive status further provides a platform to study viral oncoprotein interactions with mitochondrial homeostasis.

Research applications include quantifying mtDNA damage by qPCR or Comet assay, measuring apoptosis via Annexin V staining and Western blotting for markers such as cleaved caspase-3 and AIFM1, determining mtDNA copy number, and performing metabolic flux analysis with Seahorse analyzers. These polyclonal EXOG knockout cells support investigations in mitochondrial biology, DNA repair, apoptosis regulation, and cancer metabolism. For further inquiries, contact Ascent Research.

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