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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Memorial Sloan Kettering Cancer Center1, Swiss Institute of Bioinformatics2, Harvard University3, Princeton University4, University of Texas at Dallas5, Washington University in St. Louis6, Institute for Systems Biology7, Bilkent University8, Van Andel Institute9, University of Pennsylvania10, University of Texas MD Anderson Cancer Center11, Mayo Clinic12, Columbia University Medical Center13, Fred Hutchinson Cancer Research Center14, University of California, San Francisco15, University of Michigan16, Peter MacCallum Cancer Centre17, Baylor College of Medicine18
TL;DR: This work charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity.
1,841 citations
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TL;DR: The emergence of systems biology is described, as well as several examples of specific systems approaches.
Abstract: ▪ Abstract Systems biology studies biological systems by systematically perturbing them (biologically, genetically, or chemically); monitoring the gene, protein, and informational pathway responses; integrating these data; and ultimately, formulating mathematical models that describe the structure of the system and its response to individual perturbations. The emergence of systems biology is described, as are several examples of specific systems approaches.
1,709 citations
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TL;DR: This finding represents a new component of the innate immune system and the acute phase response to infection and limits bacterial growth by sequestrating the iron-laden siderophore.
Abstract: Although iron is required to sustain life, its free concentration and metabolism have to be tightly regulated. This is achieved through a variety of iron-binding proteins including transferrin and ferritin. During infection, bacteria acquire much of their iron from the host by synthesizing siderophores that scavenge iron and transport it into the pathogen. We recently demonstrated that enterochelin, a bacterial catecholate siderophore, binds to the host protein lipocalin 2 (ref. 5). Here, we show that this event is pivotal in the innate immune response to bacterial infection. Upon encountering invading bacteria the Toll-like receptors on immune cells stimulate the transcription, translation and secretion of lipocalin 2; secreted lipocalin 2 then limits bacterial growth by sequestrating the iron-laden siderophore. Our finding represents a new component of the innate immune system and the acute phase response to infection.
1,622 citations
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TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
Abstract: Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1,2,3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10,11,12,13,14,15,16,17,18.
1,600 citations
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TL;DR: Th17 differentiation is directed by two lineage-specific nuclear receptors, ROR alpha and ROR gamma, and is induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3.
1,589 citations
Authors
Showing all 1292 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |