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  • 1
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    Molecular basis for the differential use of glucose and glutamine in cell proliferation as revealed by synchronized HeLa cells [Cell Biology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-12-28
    Description: During cell division, the activation of glycolysis is tightly regulated by the action of two ubiquitin ligases, anaphase-promoting complex/cyclosome–Cdh1 (APC/C-Cdh1) and SKP1/CUL-1/F-box protein–β-transducin repeat-containing protein (SCF-β-TrCP), which control the transient appearance and metabolic activity of the glycolysis-promoting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, isoform 3 (PFKFB3). We now demonstrate that the breakdown of PFKFB3 during S phase occurs specifically via a distinct residue (S273) within the conserved recognition site for SCF-β-TrCP. Glutaminase 1 (GLS1), the first enzyme in glutaminolysis, is also targeted for destruction by APC/C-Cdh1 and, like PFKFB3, accumulates after the activity of this ubiquitin ligase decreases in mid-to-late G1. However, our results show that GLS1 differs from PFKFB3 in that its recognition by APC/C-Cdh1 requires the presence of both a Lys-Glu-Asn box (KEN box) and a destruction box (D box) rather than a KEN box alone. Furthermore, GLS1 is not a substrate for SCF-β-TrCP and is not degraded until cells progress from S to G2/M. The presence of PFKFB3 and GLS1 coincides with increases in generation of lactate and in utilization of glutamine, respectively. The contrasting posttranslational regulation of PFKFB3 and GLS1, which we have verified by studies of ubiquitination and protein stability, suggests the different roles of glucose and glutamine at distinct stages in the cell cycle. Indeed, experiments in which synchronized cells were deprived of either of these substrates show that both glucose and glutamine are required for progression through the restriction point in mid-to-late G1, whereas glutamine is the only substrate essential for the progression through S phase into cell division.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Using geophysical techniques to trace active faults in the urbanized northern Hueco Bolson, West Texas, USA, and northern Chihuahua, Mexico (2016)
    Geological Society of America (GSA)
    In: Geosphere
    Details
    Publication Date: 2016-01-28
    Description: The Hueco Bolson serves as one of the primary groundwater sources for the El Paso–Ciudad Juárez metropolitan region of over 2.5 million residents. The bolson lies at the point where the strike of the southern Rio Grande rift changes from north-south to northwest-southeast, likely due to its interaction with preexisting Mesozoic and Paleozoic structures. The region is tectonically active with recent (〈750,000 years) movement along basin-bounding faults and low-level (M〈4) seismicity. Over the past five years, we have used a combination of microgravity and water well logs to image the complex structure of this basin within an urbanized environment. Our results indicate the East Franklin Mountains fault, the main boundary fault on the west side of the bolson, extends as much as 30 km south of the end of its mapped surficial trace. Two intrabasin faults that have been mapped at the surface in the less developed portions of the city can be traced into central El Paso and Ciudad Juárez. These faults appear to control the boundary between fresh and saline water within the aquifer system beneath El Paso. Gravity modeling also suggests at least two additional concealed intrabasin faults are located beneath the metropolitan area.
    Electronic ISSN: 1553-040X
    Topics: Geosciences
    Published by Geological Society of America (GSA)
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  • 3
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    Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: Nitric oxide was found to trigger mitochondrial biogenesis in cells as diverse as brown adipocytes and 3T3-L1, U937, and HeLa cells. This effect of nitric oxide was dependent on guanosine 3',5'-monophosphate (cGMP) and was mediated by the induction of peroxisome proliferator-activated receptor gamma coactivator 1alpha, a master regulator of mitochondrial biogenesis. Moreover, the mitochondrial biogenesis induced by exposure to cold was markedly reduced in brown adipose tissue of endothelial nitric oxide synthase null-mutant (eNOS-/-) mice, which had a reduced metabolic rate and accelerated weight gain as compared to wild-type mice. Thus, a nitric oxide-cGMP-dependent pathway controls mitochondrial biogenesis and body energy balance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nisoli, Enzo -- Clementi, Emilio -- Paolucci, Clara -- Cozzi, Valeria -- Tonello, Cristina -- Sciorati, Clara -- Bracale, Renata -- Valerio, Alessandra -- Francolini, Maura -- Moncada, Salvador -- Carruba, Michele O -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):896-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preclinical Sciences, Center for Study and Research on Obesity, Luigi Sacco Hospital, University of Milan, Milan 20157, Italy. enzo.nisoli@unimi.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574632" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Adipocytes/*metabolism/ultrastructure ; Adipose Tissue, Brown/cytology/metabolism/ultrastructure ; Animals ; Cold Temperature ; Cyclic GMP/metabolism ; DNA, Mitochondrial/metabolism ; DNA-Binding Proteins/metabolism ; Eating ; Energy Metabolism ; Female ; HeLa Cells ; High Mobility Group Proteins ; Humans ; Male ; Mice ; Mice, Knockout ; Mitochondria/*metabolism/ultrastructure ; *Mitochondrial Proteins ; Motor Activity ; NF-E2-Related Factor 1 ; Nitric Oxide/*physiology ; Nitric Oxide Synthase/genetics/*metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Nuclear Proteins/metabolism ; Nuclear Respiratory Factors ; Oligonucleotides, Antisense/pharmacology ; Oxadiazoles/pharmacology ; Oxygen Consumption ; Penicillamine/*analogs & derivatives/pharmacology ; Quinoxalines/pharmacology ; RNA, Messenger/genetics/metabolism ; Rats ; Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; U937 Cells ; Weight Gain
    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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    Calorie restriction promotes mitochondrial biogenesis by inducing the expression of eNOS (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Calorie restriction extends life span in organisms ranging from yeast to mammals. Here, we report that calorie restriction for either 3 or 12 months induced endothelial nitric oxide synthase (eNOS) expression and 3',5'-cyclic guanosine monophosphate formation in various tissues of male mice. This was accompanied by mitochondrial biogenesis, with increased oxygen consumption and adenosine triphosphate production, and an enhanced expression of sirtuin 1. These effects were strongly attenuated in eNOS null-mutant mice. Thus, nitric oxide plays a fundamental role in the processes induced by calorie restriction and may be involved in the extension of life span in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nisoli, Enzo -- Tonello, Cristina -- Cardile, Annalisa -- Cozzi, Valeria -- Bracale, Renata -- Tedesco, Laura -- Falcone, Sestina -- Valerio, Alessandra -- Cantoni, Orazio -- Clementi, Emilio -- Moncada, Salvador -- Carruba, Michele O -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrated Laboratories Network, Department of Preclinical Sciences, Luigi Sacco Hospital, Milan University, 20157 Milan, Italy. enzo.nisoli@unimi.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224023" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; *Caloric Restriction ; DNA, Mitochondrial/metabolism ; Enzyme Induction ; Female ; GTP Phosphohydrolases/biosynthesis ; Life Expectancy ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/*physiology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/*biosynthesis/genetics ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Oxygen Consumption ; Protein Biosynthesis ; Sirtuin 1 ; Sirtuins/biosynthesis
    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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  • 5
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    Redistribution of intracellular oxygen in hypoxia by nitric oxide: effect on HIF1alpha (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Cells exposed to low oxygen concentrations respond by initiating defense mechanisms, including the stabilization of hypoxia-inducible factor (HIF) 1alpha, a transcription factor that upregulates genes such as those involved in glycolysis and angiogenesis. Nitric oxide and other inhibitors of mitochondrial respiration prevent the stabilization of HIF1alpha during hypoxia. In studies of cultured cells, we show that this effect is a result of an increase in prolyl hydroxylase-dependent degradation of HIF1alpha. With the use of Renilla luciferase to detect intracellular oxygen concentrations, we also demonstrate that, upon inhibition of mitochondrial respiration in hypoxia, oxygen is redistributed toward nonrespiratory oxygen-dependent targets such as prolyl hydroxylases so that they do not register hypoxia. Thus, the signaling consequences of hypoxia may be profoundly modified by nitric oxide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagen, Thilo -- Taylor, Cormac T -- Lam, Francis -- Moncada, Salvador -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671307" target="_blank"〉PubMed〈/a〉
    Keywords: Antioxidants/pharmacology ; *Cell Hypoxia ; Cell Line ; *Cell Respiration/drug effects ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Leupeptins/*pharmacology ; Luciferases/metabolism ; Methacrylates ; Mitochondria/*metabolism ; Nitric Oxide/pharmacology/*physiology ; Nitric Oxide Donors/pharmacology ; Oxygen/*metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thiazoles/pharmacology ; Transcription Factors/*metabolism ; Transfection ; Triazenes/pharmacology
    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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  • 6
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    The role of TH1 and TH2 cells in a rodent malaria infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: CD4+ T cells play a major role in protective immunity against the blood stage of malaria, but the mechanism of protection is unclear. By adoptive transfer of cloned T cell lines, direct evidence is provided that both TH1 and TH2 subsets of CD4+ T cells can protect mice against Plasmodium chabaudi chabaudi infection. TH1 cells protect by a nitric oxide-dependent mechanism, whereas TH2 cells protect by the enhancement and accelerated production of specific immunoglobulin G1 antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor-Robinson, A W -- Phillips, R S -- Severn, A -- Moncada, S -- Liew, F Y -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Laboratories for Experimental Parasitology, University of Glasgow, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/biosynthesis ; Arginine/analogs & derivatives/pharmacology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Female ; Immunoglobulin G/*biosynthesis ; Lymphocyte Depletion ; Malaria/*immunology ; Mice ; Mice, Inbred Strains ; Nitrates/blood ; Nitric Oxide/*metabolism ; Plasmodium chabaudi/*immunology ; T-Lymphocyte Subsets/*immunology ; omega-N-Methylarginine
    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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  • 7
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    The L-Arginine:Nitric Oxide Pathway Is the Major Source of Plasma Nitrite in Fasted Humans (1995)
    Elsevier
    Details
    Publication Date: 1995-06-01
    Print ISSN: 0006-291X
    Electronic ISSN: 1090-2104
    Topics: Biology , Chemistry and Pharmacology , Physics
    Published by Elsevier
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  • 8
    Electronic Resource
    Electronic Resource
    Biosynthesis and Role of the Endothelium-Derived Vasodilator, Nitric Oxide, in the Gastric Mucosa (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 664 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb39755.x
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    The role of nitric oxide and cGMP in platelet adhesion to vascular endothelium
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 148 (1987), S. 1482-1489 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/S0006-291X(87)80299-1
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  • 10
    Electronic Resource
    Electronic Resource
    Glucocorticoids inhibit the induction of nitric oxide synthase in macrophages
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 172 (1990), S. 1246-1252 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0006-291X(90)91583-E
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