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Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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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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Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Mitochondrial Membranes01:45

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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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.
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The Inner Mitochondrial Membrane01:28

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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Energy to Drive Translocation01:37

Energy to Drive Translocation

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Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
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Mitochondrial Precursor Proteins01:39

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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[Multiple sclerosis - a mitochondria-mediated disease?]

Kristin N Varhaug1, Christian A Vedeler1, Charalampos Tzoulis1

  • 1Klinisk institutt 1 Universitetet i Bergen og Nevrologisk avdeling Haukeland universitetssykehus.

Tidsskrift for Den Norske Laegeforening : Tidsskrift for Praktisk Medicin, Ny Raekke
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Mitochondrial dysfunction may contribute to neurodegeneration in multiple sclerosis (MS) due to inflammation and increased energy demands from demyelination, potentially leading to chronic energy deficiency in the central nervous system.

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Area of Science:

  • Neuroscience
  • Pathology
  • Mitochondrial Biology

Background:

  • Mitochondria are implicated in neurodegenerative diseases like Parkinson's.
  • Neurodegeneration is an early feature of multiple sclerosis (MS).
  • This review explores the link between mitochondrial dysfunction and MS.

Purpose of the Study:

  • To investigate the potential association between mitochondrial dysfunction and multiple sclerosis.
  • To synthesize current knowledge on the role of mitochondria in MS pathogenesis.

Main Methods:

  • Literature search of PubMed (concluded May 2016) for original and review articles.
  • Selection and full-text review of 71 articles from an initial 2276.
  • Inclusion of additional articles from reference lists and author archives.

Main Results:

  • Mitochondrial alterations are observed in MS-affected brain regions.
  • Observed changes include inflammation-induced damage and compensatory responses to axonal energy demands.
  • The specific type of mitochondrial damage is pathology-dependent.

Conclusions:

  • Inflammation-induced mitochondrial damage and increased energy demands in MS may cause chronic CNS energy deficiency.
  • This energy deficit could drive neurodegeneration in MS.
  • Understanding mitochondrial roles may offer new therapeutic targets for MS.