Institution
Institute for Systems Biology
Nonprofit•Seattle, Washington, United States•
About: Institute for Systems Biology is a nonprofit organization based out in Seattle, Washington, United States. It is known for research contribution in the topics: Population & Proteomics. The organization has 1277 authors who have published 2777 publications receiving 353165 citations.
Topics: Population, Proteomics, Gene, Proteome, Systems biology
Papers published on a yearly basis
Papers
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University of Amsterdam1, St John's Innovation Centre2, Philips3, Yale University4, University of Rome Tor Vergata5, Università Campus Bio-Medico6, Institute for Systems Biology7, University of Bergen8, University of Catania9, Aix-Marseille University10, National Institutes of Health11, AstraZeneca12, University of Nottingham13, Karolinska Institutet14, University of Southampton15, Semmelweis University16, Fraunhofer Society17, Jagiellonian University Medical College18, Imperial College London19, GlaxoSmithKline20, Umeå University21, Catholic University of the Sacred Heart22, University of Manchester23, Lancashire Teaching Hospitals NHS Foundation Trust24
TL;DR: Exhaled molecular phenotypes of severe asthma were identified and followed up, which were associated with changing inflammatory profile and oral steroid use and suggests that breath analysis can contribute to the management ofsevere asthma.
Abstract: Background: Severe asthma is a heterogeneous condition, as shown by independent cluster analyses based on demographic, clinical, and inflammatory characteristics. A next step is to identify molecularly driven phenotypes using “omics” technologies. Molecular fingerprints of exhaled breath are associated with inflammation and can qualify as noninvasive assessment of severe asthma phenotypes. Objectives: We aimed (1)to identify severe asthma phenotypes using exhaled metabolomic fingerprints obtained from a composite of electronic noses (eNoses)and (2)to assess the stability of eNose-derived phenotypes in relation to within-patient clinical and inflammatory changes. Methods: In this longitudinal multicenter study exhaled breath samples were taken from an unselected subset of adults with severe asthma from the U-BIOPRED cohort. Exhaled metabolites were analyzed centrally by using an assembly of eNoses. Unsupervised Ward clustering enhanced by similarity profile analysis together with K-means clustering was performed. For internal validation, partitioning around medoids and topological data analysis were applied. Samples at 12 to 18 months of prospective follow-up were used to assess longitudinal within-patient stability. Results: Data were available for 78 subjects (age, 55 years [interquartile range, 45-64 years]; 41% male). Three eNose-driven clusters (n = 26/33/19)were revealed, showing differences in circulating eosinophil (P =.045)and neutrophil (P =.017)percentages and ratios of patients using oral corticosteroids (P =.035). Longitudinal within-patient cluster stability was associated with changes in sputum eosinophil percentages (P =.045). Conclusions: We have identified and followed up exhaled molecular phenotypes of severe asthma, which were associated with changing inflammatory profile and oral steroid use. This suggests that breath analysis can contribute to the management of severe asthma.
72 citations
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TL;DR: Genetic analysis shows that elevated CO2 causes downregulation of these mechanisms, resulting in metabolic rearrangement and energy savings in marine diatoms.
Abstract: Carbon fixation by marine diatoms, which dominate ocean primary productivity, is energetically expensive. Now genetic analysis shows that elevated CO2 causes downregulation of these mechanisms, resulting in metabolic rearrangement and energy savings.
72 citations
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TL;DR: Toll-like receptors are key components of effective innate immunity and pathogenic microorganisms must evade recognition by TLRs, manipulate the consequences ofTLR activation, or contend with the inflammatory consequences of TLR activation.
71 citations
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71 citations
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TL;DR: This work presents a screening method that comprehensively explores the parameters affecting the stability of interactions in affinity-captured complexes, enabling the discovery of physiological binding partners in unparalleled detail.
Abstract: We must reliably map the interactomes of cellular macromolecular complexes in order to fully explore and understand biological systems. However, there are no methods to accurately predict how to capture a given macromolecular complex with its physiological binding partners. Here, we present a screening method that comprehensively explores the parameters affecting the stability of interactions in affinity-captured complexes, enabling the discovery of physiological binding partners in unparalleled detail. We have implemented this screen on several macromolecular complexes from a variety of organisms, revealing novel profiles for even well-studied proteins. Our approach is robust, economical and automatable, providing inroads to the rigorous, systematic dissection of cellular interactomes.
71 citations
Authors
Showing all 1292 results
Name | H-index | Papers | Citations |
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Younan Xia | 216 | 943 | 175757 |
Ruedi Aebersold | 182 | 879 | 141881 |
David Haussler | 172 | 488 | 224960 |
Steven P. Gygi | 172 | 704 | 129173 |
Nahum Sonenberg | 167 | 647 | 104053 |
Leroy Hood | 158 | 853 | 128452 |
Mark H. Ellisman | 117 | 637 | 55289 |
Wei Zhang | 112 | 1189 | 93641 |
John Ralph | 109 | 442 | 39238 |
Eric H. Davidson | 106 | 454 | 47058 |
James R. Heath | 103 | 425 | 58548 |
Alan Aderem | 99 | 246 | 46682 |
Anne-Claude Gingras | 97 | 336 | 40714 |
Trey Ideker | 97 | 306 | 72276 |
Michael H. Gelb | 94 | 506 | 34714 |