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Related Concept Videos

Electron Transport Chain: Complex I and II01:46

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Related Experiment Video

Updated: Aug 6, 2025

Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes
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Identification of chemotherapy targets reveals a nucleus-to-mitochondria ROS sensing pathway.

Junbing Zhang, Claire M Simpson, Jacqueline Berner

    Biorxiv : the Preprint Server for Biology
    |March 22, 2023
    PubMed
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    Chemotherapies increase reactive oxygen species (ROS), but how cells sense and respond remains unclear. This study identifies a nucleus-to-mitochondria pathway involving CHK1 and SSBP1 that resolves ROS and mediates resistance to platinum-based chemotherapy in ovarian cancer.

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    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Cancer Research

    Background:

    • Chemotherapies induce cell death partly via reactive oxygen species (ROS), but the precise mechanisms of ROS function and sensing are poorly understood.
    • Identifying ROS-modified proteins and their roles in chemotherapy sensitivity or resistance is crucial for developing effective cancer treatments.

    Approach:

    • Utilized an integrated proteogenomic approach to analyze 11 chemotherapies.
    • Identified both unique and shared protein targets, including ribosomal components, suggesting a role in translation regulation.
    • Focused on CHK1 as a key nuclear hydrogen peroxide (H2O2) sensor.

    Key Points:

    • CHK1 acts as a nuclear H2O2 sensor, initiating an anti-ROS cellular program.
    • CHK1 phosphorylates SSBP1, inhibiting its mitochondrial import and reducing nuclear H2O2 levels.
    • This nucleus-to-mitochondria signaling pathway is essential for resolving nuclear ROS accumulation.

    Conclusions:

    • Discovered a druggable pathway for sensing and resolving nuclear ROS.
    • This pathway is critical for mediating resistance to platinum-based chemotherapies in ovarian cancers.
    • Findings offer potential therapeutic targets for overcoming chemotherapy resistance.