85 results found
    1. Cell Biology

    The mitochondrial permeability transition pore activates the mitochondrial unfolded protein response and promotes aging

    Suzanne Angeli et al.
    Loss of the F-ATP synthase c-subunit inhibits a pathological mitochondrial permeability transition pore that is coupled to a maladaptive mitochondrial unfolded protein response while also extending lifespan.
    1. Structural Biology and Molecular Biophysics

    Atomistic simulations indicate the c-subunit ring of the F1Fo ATP synthase is not the mitochondrial permeability transition pore

    Wenchang Zhou et al.
    The notion that the lumen of the ATP synthase membrane rotor is the long-sought megachannel that triggers the onset of the mitochondrial permeability transition is found to be inconsistent with its actual structural and functional properties.
    1. Cell Biology

    Bax and Bak function as the outer membrane component of the mitochondrial permeability pore in regulating necrotic cell death in mice

    Jason Karch et al.
    The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.
    1. Structural Biology and Molecular Biophysics
    2. Cell Biology

    Massive endocytosis triggered by surface membrane palmitoylation under mitochondrial control in BHK fibroblasts

    Donald W Hilgemann et al.
    Mitochondria can trigger massive endocytosis by releasing coenzyme A into the cytoplasm and thereby promoting the addition of fatty acids to surface membrane proteins.
    1. Structural Biology and Molecular Biophysics
    2. Cell Biology

    Massive palmitoylation-dependent endocytosis during reoxygenation of anoxic cardiac muscle

    Mei-Jung Lin et al.
    Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.
    1. Cell Biology

    Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte

    Huiliang Zhang et al.
    The primary respiratory defect seen in aged cardiomyocytes is an elevated proton leak mediated by ANT1, and this is prevented by treatment with SS-31 (elamipretide).
    1. Cell Biology
    2. Neuroscience

    Tissue acidosis induces neuronal necroptosis via ASIC1a channel independent of its ionic conduction

    Yi-Zhi Wang et al.
    An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.
    1. Immunology and Inflammation
    2. Neuroscience

    Differential accumulation of storage bodies with aging defines discrete subsets of microglia in the healthy brain

    Jeremy Carlos Burns et al.
    Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.
    1. Cell Biology
    2. Neuroscience

    C9orf72 arginine-rich dipeptide repeat proteins disrupt karyopherin-mediated nuclear import

    Lindsey R Hayes et al.
    Poly-PR and poly-GR interact with importin β, disrupt importin-cargo loading, and inhibit nuclear import in permeabilized cells in a manner that can be rescued by RNA.
    1. Cancer Biology
    2. Cell Biology

    A novel mitochondrial Kv1.3–caveolin axis controls cell survival and apoptosis

    Jesusa Capera et al.
    The association of caveolin with the potassium channel Kv1.3 fine-tunes cell survival and apoptosis.

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