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  • 1
    Publication Date: 2015-08-01
    Description: Intracellular energy distribution has attracted much interest and has been proposed to occur in skeletal muscle via metabolite-facilitated diffusion; however, genetic evidence suggests that facilitated diffusion is not critical for normal function. We hypothesized that mitochondrial structure minimizes metabolite diffusion distances in skeletal muscle. Here we demonstrate a mitochondrial reticulum providing a conductive pathway for energy distribution, in the form of the proton-motive force, throughout the mouse skeletal muscle cell. Within this reticulum, we find proteins associated with mitochondrial proton-motive force production preferentially in the cell periphery and proteins that use the proton-motive force for ATP production in the cell interior near contractile and transport ATPases. Furthermore, we show a rapid, coordinated depolarization of the membrane potential component of the proton-motive force throughout the cell in response to spatially controlled uncoupling of the cell interior. We propose that membrane potential conduction via the mitochondrial reticulum is the dominant pathway for skeletal muscle energy distribution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glancy, Brian -- Hartnell, Lisa M -- Malide, Daniela -- Yu, Zu-Xi -- Combs, Christian A -- Connelly, Patricia S -- Subramaniam, Sriram -- Balaban, Robert S -- Intramural NIH HHS/ -- England -- Nature. 2015 Jul 30;523(7562):617-20. doi: 10.1038/nature14614.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26223627" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/biosynthesis/metabolism ; Animals ; Diffusion ; *Energy Metabolism ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Mitochondria, Muscle/*metabolism ; Mitochondrial Proteins/metabolism ; Muscle, Skeletal/*cytology/*metabolism ; Proton-Motive Force
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Surface and Interface Analysis 20 (1993), S. 140-148 
    ISSN: 0142-2421
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Physics
    Notes: The linewidths of x-ray photoelectron spectra have been correlated with dislocation densities in a shock-damaged crystal of ammonium perchlorate (AP). A centimeter-size AP crystal was non-uniformly damaged by a rapidly decaying shock (peak pressure of 24.4 kbar at the entry surface), recovered intact and cleaved. The cleaved planes permitted interior analysis of the crystal by x-ray photoelectron spectroscopy (XPS) over a pattern of 1 mm × 1 mm areas. The linewidth of the Cl 2p3/2 peak ranged from 1.70 eV for the region of greatest damage to 1.22 eV for the region demonstrating no visible damage, the same linewidth as that for unshocked AP (control). The correlation between dislocation density and XPS linewidth was quantitatively established by chemically etching and counting dislocations on cleaved planes from the shocked crystal. By this technique, a 100 × increase in dislocation density was determined for the region of greatest shock damage relative to undamaged crystal. Molecular orbital energy variation caused by distortion of the lattice in the vicinity of a dislocation is the physical mechanism responsible for the broadening of the photoelectron lines. Ab initio calculations of the Cl 2p energy level from various distorted perchlorate anion geometries have predicted orbital energy shifts sufficient to produce the observed linewidth broadening.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2012-10-01
    Print ISSN: 0005-2728
    Electronic ISSN: 1879-2650
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Published by Elsevier
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