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Lysosomal activity in response to the incubation of pristine and functionalized carbon nanodots.
iScience
January 2025
Solid State Physics Laboratory, Heinrich Heine University Düsseldorf, 40204 Düsseldorf, Germany.
We present functional studies of lysosomes in human cells after uptake of carbon nanodots (CNDs). Even under high CND concentrations, the lysosomal functionality, as characterized via cathepsins B and L as well as the autophagic markers SQSTM1/p62 and LC3B-II, is maintained. Furthermore, branched polyethylenimine (bPEI) molecules have been coupled to the CNDs as a model functionalization or example of a drug.
View Article and Find Full Text PDFOligodendrocyte precursor cells facilitate neuronal lysosome release.
Nat Commun
January 2025
Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany.
Oligodendrocyte precursor cells (OPCs) shape brain function through many non-canonical regulatory mechanisms beyond myelination. Here we show that OPCs form contacts with their processes on neuronal somata in a neuronal activity-dependent manner. These contacts facilitate exocytosis of neuronal lysosomes.
View Article and Find Full Text PDFThe α- to γ-enolase switch: The role and regulation of γ-enolase during oligodendrocyte differentiation.
Int J Biol Macromol
January 2025
Department of Pharmaceutical Biology, Faculty of Pharmacy, University of Ljubljana, Aškerčeva 7, 1000 Ljubljana, Slovenia. Electronic address:
The glycolytic enzyme γ-enolase is a highly specific neuronal marker that is known to replace ubiquitously expressed α-enolase in the brain. Moreover, γ-enolase has been shown to exert neurotrophic activity, which is regulated by cathepsin X, a lysosomal peptidase. This study investigates the role of γ-enolase and its regulation by cathepsin X during the differentiation of oligodendrocytes, which are essential for normal brain function.
View Article and Find Full Text PDFEstrogen-related receptor gamma is a regulator of mitochondrial, autophagy, and immediate-early gene programs in spiny projection neurons: Relevance for transcriptional changes in Huntington disease.
Neurobiol Dis
January 2025
Department of Neurology and Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Southern Research, Birmingham, AL 35205, USA. Electronic address:
Mitochondrial dysfunction, transcriptional dysregulation, and protein aggregation are hallmarks of multiple neurodegenerative disorders, including Huntington's disease (HD). Strategies are needed to counteract these processes to restore neuronal health and function in HD. Recent evidence indicates that the transcription factor estrogen-related receptor gamma (ERRγ/Esrrg) is required for normal expression of mitochondrial, synaptic, and autophagy genes in neurons.
View Article and Find Full Text PDFAcetylation modification in the regulation of macroautophagy.
Adv Biotechnol (Singap)
June 2024
Shenzhen Key Laboratory of Plant Genetic Engineering and Molecular Design, Institute of Plant and Food Science, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Macroautophagy, commonly referred to as autophagy, is an evolutionarily conserved cellular process that plays a crucial role in maintaining cellular homeostasis. It orchestrates the delivery of dysfunctional or surplus cellular materials to the vacuole or lysosome for degradation and recycling, particularly during adverse conditions. Over the past few decades, research has unveiled intricate regulatory mechanisms governing autophagy through various post-translational modifications (PTMs).
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