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Results for "

mitochondrial respiratory chain Complexes IV

" in MedChemExpress (MCE) Product Catalog:

4

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Biochemical Assay Reagents

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Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-Y1366

    Mitochondrial Metabolism Reactive Oxygen Species (ROS) Arp2/3 Complex Apoptosis Inflammation/Immunology
    Hydroxyacetone is a toxic compound. Hydroxyacetone can be isolated from e-cigarette aerosols. Hydroxyacetone reduces the activity of cellular Mitochondrial reductase (with an IC50 of 5.53 mg/mL for mitochondrial reductase in BEAS-2B cells) and increases ROS levels. Hydroxyacetone induces mitochondrial stress and oxidative damage. Hydroxyacetone induces destabilization of F-actin. At high concentrations, Hydroxyacetone promotes cell rounding and Apoptotic body formation. Hydroxyacetone exerts toxic effects on cells including airway epithelial cells and possesses respiratory toxicity potential .\n


    Hydroxyacetone
  • HY-125857B

    Biochemical Assay Reagents Apoptosis Caspase Metabolic Disease
    Cytochrome C (Saccharomyces cerevisiae) is a type C cytochrome located in the intermembrane space of the mitochondria. As an electron carrier, Cytochrome C (Saccharomyces cerevisiae) transfers electrons between complex III (cytochrome c reductase) and complex IV (cytochrome c oxidase, CIV) of the respiratory chain. Cytochrome C (Saccharomyces cerevisiae) can play a crucial role in triggering apoptosis by being released from the mitochondria into the cytosol .
    Cytochrome C (Saccharomyces cerevisiae)
  • HY-132178B

    Biochemical Assay Reagents Metabolic Disease
    Cytochrome C oxidase (complex IV) (EC 7.1.1.9) is the unique terminal oxidase of the mitochondrial respiratory chain (RC) in mammals. Cytochrome C oxidase is made up of thirteen subunits that catalyze the transfer of electrons from ferro-cytochrome c to molecular oxygen .
    Cytochrome C oxidase
  • HY-131453

    Mitochondrial Metabolism Cardiovascular Disease Inflammation/Immunology
    Mitochondrial respiration-IN-1 is a mitochondrial respiratory inhibitor. Mitochondrial respiration-IN-1 reduces platelet aggregation, adhesion, and platelet-induced coagulation responses. Mitochondrial respiration-IN-1 induces adaptive glycolysis, decreases mitochondrial membrane potential, selectively reduces ATP production derived from oxidative phosphorylation, and exerts bidirectional regulatory effects on cell proliferation. Mitochondrial respiration-IN-1 activates UPRmt and upregulates the expression of SDHA-1 and MT-CO1. Mitochondrial respiration-IN-1 restores metabolic homeostasis in type 2 diabetic mice. Mitochondrial respiration-IN-1 can be used to investigate diseases mediated by inappropriate platelet activation/aggregation and type 2 diabetes .
    Mitochondrial respiration-IN-1

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