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  • 1
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    Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: Many apoptotic molecules relocate subcellularly in cells undergoing apoptosis. The pro-apoptotic protein BID underwent posttranslational (rather than classic cotranslational) N-myristoylation when cleavage by caspase 8 caused exposure of a glycine residue. N-myristoylation enabled the targeting of a complex of p7 and myristoylated p15 fragments of BID to artificial membranes bearing the lipid composition of mitochondria, as well as to intact mitochondria. This post-proteolytic N-myristoylation serves as an activating switch, enhancing BID-induced release of cytochrome c and cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zha, J -- Weiler, S -- Oh, K J -- Wei, M C -- Korsmeyer, S J -- CA50239-13/CA/NCI NIH HHS/ -- K01 CA82231/CA/NCI NIH HHS/ -- T32 CA72320-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1761-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099414" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Carrier Proteins/chemistry/*metabolism ; Caspase 8 ; Caspase 9 ; Caspases/metabolism ; Cytochrome c Group/metabolism ; Humans ; Intracellular Membranes/*metabolism ; Jurkat Cells ; Liposomes/metabolism ; Mice ; Mitochondria/*metabolism ; Myristic Acid/*metabolism ; Peptide Fragments/metabolism ; Protein Conformation ; Protein Processing, Post-Translational ; Protein Structure, Tertiary ; Protein Transport ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-07
    Description: Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104429/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Manisha -- Jang, Young C -- Oh, Juhyun -- Khong, Danika -- Wu, Elizabeth Y -- Manohar, Rohan -- Miller, Christine -- Regalado, Samuel G -- Loffredo, Francesco S -- Pancoast, James R -- Hirshman, Michael F -- Lebowitz, Jessica -- Shadrach, Jennifer L -- Cerletti, Massimiliano -- Kim, Mi-Jeong -- Serwold, Thomas -- Goodyear, Laurie J -- Rosner, Bernard -- Lee, Richard T -- Wagers, Amy J -- 1DP2 OD004345/OD/NIH HHS/ -- 1R01 AG033053/AG/NIA NIH HHS/ -- 1R01 AG040019/AG/NIA NIH HHS/ -- 5U01 HL100402/HL/NHLBI NIH HHS/ -- DP2 OD004345/OD/NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- R01 AG032977/AG/NIA NIH HHS/ -- R01 AG033053/AG/NIA NIH HHS/ -- R01 AG040019/AG/NIA NIH HHS/ -- R01 AR042238/AR/NIAMS NIH HHS/ -- R01 AR42238/AR/NIAMS NIH HHS/ -- T32 DE007057/DE/NIDCR NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 9;344(6184):649-52. doi: 10.1126/science.1251152. Epub 2014 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Stem Cell Institute and Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24797481" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aging/blood/drug effects/*physiology ; Animals ; Bone Morphogenetic Proteins/administration & dosage/blood/*physiology ; Growth Differentiation Factors/administration & dosage/blood/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*blood supply/drug effects/*physiology ; Myoblasts, Skeletal/drug effects/*physiology ; Parabiosis ; *Regeneration ; *Rejuvenation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Fuel-powered artificial muscles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: Artificial muscles and electric motors found in autonomous robots and prosthetic limbs are typically battery-powered, which severely restricts the duration of their performance and can necessitate long inactivity during battery recharge. To help solve these problems, we demonstrated two types of artificial muscles that convert the chemical energy of high-energy-density fuels to mechanical energy. The first type stores electrical charge and uses changes in stored charge for mechanical actuation. In contrast with electrically powered electrochemical muscles, only half of the actuator cycle is electrochemical. The second type of fuel-powered muscle provides a demonstrated actuator stroke and power density comparable to those of natural skeletal muscle and generated stresses that are over a hundred times higher.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebron, Von Howard -- Yang, Zhiwei -- Seyer, Daniel J -- Kozlov, Mikhail E -- Oh, Jiyoung -- Xie, Hui -- Razal, Joselito -- Hall, Lee J -- Ferraris, John P -- Macdiarmid, Alan G -- Baughman, Ray H -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and NanoTech Institute, University of Texas at Dallas, Richardson, TX 75083-0688, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543453" target="_blank"〉PubMed〈/a〉
    Keywords: *Artificial Organs ; Biomechanical Phenomena ; *Biomimetic Materials ; Bionics ; Electric Power Supplies ; Electrochemistry ; *Electrodes ; Hydrogen/chemistry ; Lifting ; *Muscle, Skeletal/physiology ; *Nanotubes, Carbon ; Oxidation-Reduction ; Oxygen/chemistry ; Robotics ; Stress, Mechanical
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Channel-mediated tonic GABA release from glia (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Synaptic inhibition is based on both tonic and phasic release of the inhibitory transmitter gamma-aminobutyric acid (GABA). Although phasic GABA release arises from Ca(2+)-dependent exocytosis from neurons, the mechanism of tonic GABA release is unclear. Here we report that tonic inhibition in the cerebellum is due to GABA being released from glial cells by permeation through the Bestrophin 1 (Best1) anion channel. We demonstrate that GABA directly permeates through Best1 to yield GABA release and that tonic inhibition is eliminated by silencing of Best1. Glial cells express both GABA and Best1, and selective expression of Best1 in glial cells, after preventing general expression of Best1, fully rescues tonic inhibition. Our results identify a molecular mechanism for tonic inhibition and establish a role for interactions between glia and neurons in mediating tonic inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Soojung -- Yoon, Bo-Eun -- Berglund, Ken -- Oh, Soo-Jin -- Park, Hyungju -- Shin, Hee-Sup -- Augustine, George J -- Lee, C Justin -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):790-6. doi: 10.1126/science.1184334. Epub 2010 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/metabolism ; Calcium/metabolism ; Cerebellum/cytology/*metabolism ; Chlorides/metabolism ; Eye Proteins/genetics/*metabolism ; Female ; HEK293 Cells ; Humans ; Ion Channels/genetics/*metabolism ; Male ; Mice ; *Neural Inhibition ; Neuroglia/*metabolism ; Neurons/*metabolism ; Patch-Clamp Techniques ; Permeability ; RNA Interference ; RNA, Small Interfering/genetics ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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