Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1

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Loss of mitochondrial function and proteostasis typify aging and age-associated degenerative disorders such as Alzheimer's disease and muscle aging. To date, no cure or preventive measure is available to manage these conditions. Alterations of cellular pro ...

Alpha-synuclein aggregation and mitochondrial dysfunction are main pathological hallmarks of Parkinson's disease (PD) and several other neurodegenerative diseases, collectively known as synucleinopathies. However, increasing evidence suggests that they may ...

Redox homeostasis is essential for cell function and its disruption is associated with multiple pathologies. Redox balance is largely regulated by the relative concentrations of reduced and oxidized glutathione. In eukaryotic cells, this ratio is different ...

Sociality has profound evolutionary roots and is observed from unicellular organisms to multicellular animals. In line with the view that social principles apply across levels of biological complexity, a growing body of data highlights the remarkable socia ...

Mitochondrial dysfunction was highlighted as a crucial vulnerability factor for the development of depression. However, systemic studies assessing stress-induced changes in mitochondria-associated genes in brain regions relevant to depression symptomatolog ...

Hunter's syndrome (mucopolysaccharidosis type II) is a rare X-linked lysosomal storage disorder caused by mutations in the iduronate-2-sulfatase (IDS) gene. Motivated by the case of a child affected by this syndrome, we compared the intracellular fate of w ...

Fluorescence super-resolution microscopy has allowed unprecedented insight into the workings of biological systems below the diffraction limit of light. Over the past decade, it has overcome several challenges to deliver 3D, multi-color and faster imaging ...

Ho and colleagues report that mitochondrial dysfunction and impaired mitophagy triggered by the tumor microenvironment lead to subsequent epigenetic changes and cause permanent T cell exhaustion and dysfunction. The metabolic challenges present in tumors a ...

Transient associations between numerous organelles-e.g., the endoplasmic reticulum and the mitochondria-forge highly-coordinated, particular environments essential for cross-compartment information flow. Our perspective summarizes chemical-biology tools th ...

Primary prostate tumor heterogeneity is poorly understood, leaving research efforts with challenges regarding the initiation and advancement of the disease. The growth of tumor cells is accompanied by mutations in nuclear and in mitochondrial genomes. Thus ...

Increasing evidence suggests that crosstalk between α-synuclein pathology formation and mitochondrial dysfunction plays a central role in the pathogenesis of Parkinson’s disease and related synucleinopathies. While mitochondrial dysfunction is a well-studi ...

Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1

Chattez avec Graph Search

Enhancing mitochondrial quality control to fight neuromuscular degeneration in aging and disease

Fatal attraction-The role of hypoxia when alpha-synuclein gets intimate with mitochondria

Disruption of mitochondrial redox homeostasis by enzymatic activation of a trialkylphosphine probe

The social nature of mitochondria: Implications for human health

Mitochondrial gene signature in the prefrontal cortex for differential susceptibility to chronic stress

Endoplasmic Reticulum and Lysosomal Quality Control of Four Nonsense Mutants of Iduronate 2-Sulfatase Linked to Hunter's Syndrome

High-throughput and adaptive super-resolution fluorescence microscopy of organelles

Disturbed mitochondrial dynamics in CD8(+)TILs reinforce T cell exhaustion

Neighborhood watch: tools for defining locale-dependent subproteomes and their contextual signaling activities

Somatic Mitochondrial DNA Point Mutations Used as Biomarkers to Demonstrate Genomic Heterogeneity in Primary Prostate Cancer

Pronounced α-synuclein pathology in a seeding-based mouse model is not sufficient to induce mitochondrial respiration deficits in the striatum and amygdala