Institution
University of Dundee
Education•Dundee, United Kingdom•
About: University of Dundee is a education organization based out in Dundee, United Kingdom. It is known for research contribution in the topics: Population & Protein kinase A. The organization has 19258 authors who have published 39640 publications receiving 1919433 citations. The organization is also known as: Universitas Dundensis & Dundee University.
Topics: Population, Protein kinase A, Phosphorylation, Kinase, Health care
Papers published on a yearly basis
Papers
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TL;DR: This paper reviews the various methods available for irrigation scheduling, contrasting traditional water-balance and soil moisture-based approaches with those based on sensing of the plant response to water deficits, and indicating the strengths and weaknesses of different approaches and highlighting their suitability over different spatial and temporal scales.
Abstract: This paper reviews the various methods available for irrigation scheduling, contrasting traditional water-balance and soil moisture-based approaches with those based on sensing of the plant response to water deficits. The main plant-based methods for irrigation scheduling, including those based on direct or indirect measurement of plant water status and those based on plant physiological responses to drought, are outlined and evaluated. Specific plant-based methods include the use of dendrometry, fruit gauges, and other tissue water content sensors, while measurements of growth, sap flow, and stomatal conductance are also outlined. Recent advances, especially in the use of infrared thermometry and thermography for the study of stomatal conductance changes, are highlighted. The relative suitabilities of different approaches for specific crop and climatic situations are discussed, with the aim of indicating the strengths and weaknesses of different approaches, and highlighting their suitability over different spatial and temporal scales. The potential of soil- and plant-based systems for automated irrigation control using various scheduling techniques is also discussed.
880 citations
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TL;DR: The aim of the present work is to promote global convergence without the need to use a penalty function, so a new concept of a “filter” is introduced which allows a step to be accepted if it reduces either the objective function or the constraint violation function.
Abstract: In this paper the solution of nonlinear programming problems by a Sequential Quadratic Programming (SQP) trust-region algorithm is considered. The aim of the present work is to promote global convergence without the need to use a penalty function. Instead, a new concept of a “filter” is introduced which allows a step to be accepted if it reduces either the objective function or the constraint violation function. Numerical tests on a wide range of test problems are very encouraging and the new algorithm compares favourably with LANCELOT and an implementation of Sl1QP.
879 citations
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University of Texas Health Science Center at Houston1, Harvard University2, Broad Institute3, University of Wisconsin–Milwaukee4, University of Washington5, Washington University in St. Louis6, University of North Carolina at Chapel Hill7, Icahn School of Medicine at Mount Sinai8, University of Michigan9, Lund University10, University of Leicester11, Queen Mary University of London12, University of Oxford13, University of Milan14, University of Verona15, Merck & Co.16, National Institutes of Health17, Levanger Hospital18, Norwegian University of Science and Technology19, University of Ottawa20, Stanford University21, University of Iowa22, George Washington University23, Umeå University24, University of Dundee25, Cambridge University Hospitals NHS Foundation Trust26, Technische Universität München27, University of Kiel28, University of Lübeck29, University of Bonn30, Group Health Cooperative31, Houston Methodist Hospital32, Baylor College of Medicine33, IMDEA34, Tufts University35, University of Leeds36, King Abdulaziz University37, Wellcome Trust Sanger Institute38, University of Mississippi39, Fred Hutchinson Cancer Research Center40, University of Virginia41, University of Vermont42, Boston University43
TL;DR: Rare mutations that disrupt AP OC3 function were associated with lower levels of plasma triglycerides and APOC3, and carriers of these mutations were found to have a reduced risk of coronary heart disease.
Abstract: Background Plasma triglyceride levels are heritable and are correlated with the risk of coronary heart disease. Sequencing of the protein-coding regions of the human genome (the exome) has the potential to identify rare mutations that have a large effect on phenotype. Methods We sequenced the protein-coding regions of 18,666 genes in each of 3734 participants of European or African ancestry in the Exome Sequencing Project. We conducted tests to determine whether rare mutations in coding sequence, individually or in aggregate within a gene, were associated with plasma triglyceride levels. For mutations associated with triglyceride levels, we subsequently evaluated their association with the risk of coronary heart disease in 110,970 persons. Results An aggregate of rare mutations in the gene encoding apolipoprotein C3 (APOC3) was associated with lower plasma triglyceride levels. Among the four mutations that drove this result, three were loss-of-function mutations: a nonsense mutation (R19X) and two splice-site mutations (IVS2+1G→A and IVS3+1G→T). The fourth was a missense mutation (A43T). Approximately 1 in 150 persons in the study was a heterozygous carrier of at least one of these four mutations. Triglyceride levels in the carriers were 39% lower than levels in noncarriers (P<1×10 − 20 ), and circulating levels of APOC3 in carriers were 46% lower than levels in noncarriers (P = 8×10 − 10 ). The risk of coronary heart disease among 498 carriers of any rare APOC3 mutation was 40% lower than the risk among 110,472 noncarriers (odds ratio, 0.60; 95% confidence interval, 0.47 to 0.75; P = 4×10 − 6 ). Conclusions Rare mutations that disrupt APOC3 function were associated with lower levels of plasma triglycerides and APOC3. Carriers of these mutations were found to have a reduced risk of coronary heart disease. (Funded by the National Heart, Lung, and Blood Institute and others.)
877 citations
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TL;DR: It is demonstrated that SGK1 hydrophobic motif phosphorylation and activity is ablated in knockout fibroblasts possessing mTORC1 activity, but lacking the m TORC2 subunits rictor, Sin1, Sin2, or mLST8 or SEC13 protein 8.
Abstract: SGK1 (serum- and glucocorticoid-induced protein kinase 1) is a member of the AGC (protein kinase A/protein kinase G/protein kinase C) family of protein kinases and is activated by agonists including growth factors. SGK1 regulates diverse effects of extracellular agonists by phosphorylating regulatory proteins that control cellular processes such as ion transport and growth. Like other AGC family kinases, activation of SGK1 is triggered by phosphorylation of a threonine residue within the T-loop of the kinase domain and a serine residue lying within the C-terminal hydrophobic motif (Ser(422) in SGK1). PDK1 (phosphoinositide-dependent kinase 1) phosphorylates the T-loop of SGK1. The identity of the hydrophobic motif kinase is unclear. Recent work has established that mTORC1 [mTOR (mammalian target of rapamycin) complex 1] phosphorylates the hydrophobic motif of S6K (S6 kinase), whereas mTORC2 (mTOR complex 2) phosphorylates the hydrophobic motif of Akt (also known as protein kinase B). In the present study we demonstrate that SGK1 hydrophobic motif phosphorylation and activity is ablated in knockout fibroblasts possessing mTORC1 activity, but lacking the mTORC2 subunits rictor (rapamycin-insensitive companion of mTOR), Sin1 (stress-activated-protein-kinase-interacting protein 1) or mLST8 (mammalian lethal with SEC13 protein 8). Furthermore, phosphorylation of NDRG1 (N-myc downstream regulated gene 1), a physiological substrate of SGK1, was also abolished in rictor-, Sin1- or mLST8-deficient fibroblasts. mTORC2 immunoprecipitated from wild-type, but not from mLST8- or rictor-knockout cells, phosphorylated SGK1 at Ser(422). Consistent with mTORC1 not regulating SGK1, immunoprecipitated mTORC1 failed to phosphorylate SGK1 at Ser(422), under conditions which it phosphorylated the hydrophobic motif of S6K. Moreover, rapamycin treatment of HEK (human embryonic kidney)-293, MCF-7 or HeLa cells suppressed phosphorylation of S6K, without affecting SGK1 phosphorylation or activation. The findings of the present study indicate that mTORC2, but not mTORC1, plays a vital role in controlling the hydrophobic motif phosphorylation and activity of SGK1. Our findings may explain why in previous studies phosphorylation of substrates, such as FOXO (forkhead box O), that could be regulated by SGK, are reduced in mTORC2-deficient cells. The results of the present study indicate that NDRG1 phosphorylation represents an excellent biomarker for mTORC2 activity.
875 citations
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TL;DR: Despite the many groups of organisms capable of fixing N, and the very different ecosystems in which the process is important, it is suggested that common controls provide a foundation for the development of regional and global models that incorporate ecological controls of biological N fixation.
Abstract: N limitation to primary production and other ecosystem processes is widespread. To understand the causes and distribution of N limitation, we must understand the controls of biological N fixation. The physiology of this process is reasonably well characterized, but our understanding of ecological controls is sparse, except in a few cultivated ecosystems. We review information on the ecological controls of N fixation in free-living cyanobacteria, vascular plant symbioses, and heterotrophic bacteria, with a view toward developing improved conceptual and simulation models of ecological controls of biological N fixation.
874 citations
Authors
Showing all 19404 results
Name | H-index | Papers | Citations |
---|---|---|---|
Matthias Mann | 221 | 887 | 230213 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Stefan Schreiber | 178 | 1233 | 138528 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Salvador Moncada | 164 | 495 | 138030 |
Jorge E. Cortes | 163 | 2784 | 124154 |
Andrew P. McMahon | 162 | 415 | 90650 |
Philip Cohen | 154 | 555 | 110856 |
Dirk Inzé | 149 | 647 | 74468 |
Andrew T. Hattersley | 146 | 768 | 106949 |
Antonio Lanzavecchia | 145 | 408 | 100065 |
Kim Nasmyth | 142 | 294 | 59231 |
David Price | 138 | 1687 | 93535 |
Dario R. Alessi | 136 | 354 | 74753 |