Institution
University of Cambridge
Education•Cambridge, United Kingdom•
About: University of Cambridge is a education organization based out in Cambridge, United Kingdom. It is known for research contribution in the topics: Population & Galaxy. The organization has 118293 authors who have published 282289 publications receiving 14497093 citations. The organization is also known as: Cambridge University & Cambridge.
Topics: Population, Galaxy, Context (language use), Gene, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors proposed a method for matching the next-to-leading order (NLO) calculation of a given QCD process with a parton shower Monte Carlo (MC) simulation.
Abstract: We propose a method for matching the next-to-leading order (NLO) calculation of a given QCD process with a parton shower Monte Carlo (MC) simulation. The method has the following features: fully exclusive events are generated, with hadronization according to the MC model; total exclusive rates are accurate to NLO; NLO results for distributions are recovered upon expansion in ?s; hard emissions are treated as in NLO computations while soft/collinear emissions are handled by the MC simulation, with the same logarithmic accuracy as the MC; and matching between the hard- and soft/collinear-emission regions is smooth. A fraction of events with negative weight is generated, but unweighting remains possible with reasonable efficiency. The method is clarified using a simple toy model, and illustrated by application to the hadroproduction of W+W? pairs.
2,101 citations
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TL;DR: It is found that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis, which has important implications for the origins of genomic remodeling and temporal emergence of cancer.
2,099 citations
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TL;DR: It is shown here that RHD2 is an NADPH oxidase, a protein that transfers electrons from NADPH to an electron acceptor leading to the formation of reactive oxygen species (ROS) and that ROS accumulate in growing wild-type (WT) root hairs but their levels are markedly decreased in rhd2 mutants.
Abstract: Cell expansion is a central process in plant morphogenesis, and the elongation of roots and root hairs is essential for uptake of minerals and water from the soil. Ca2+ influx from the extracellular store is required for (and sets the rates of) cell elongation in roots. Arabidopsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromised--rhd2 mutants have short root hairs and stunted roots. To determine the regulation of Ca2+ acquisition in growing root cells we show here that RHD2 is an NADPH oxidase, a protein that transfers electrons from NADPH to an electron acceptor leading to the formation of reactive oxygen species (ROS). We show that ROS accumulate in growing wild-type (WT) root hairs but their levels are markedly decreased in rhd2 mutants. Blocking the activity of the NADPH oxidase with diphenylene iodonium (DPI) inhibits ROS formation and phenocopies Rhd2-. Treatment of rhd2 roots with ROS partly suppresses the mutant phenotype and stimulates the activity of plasma membrane hyperpolarization-activated Ca2+ channels, the predominant root Ca2+ acquisition system. This indicates that NADPH oxidases control development by making ROS that regulate plant cell expansion through the activation of Ca2+ channels.
2,098 citations
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TL;DR: A rational and dynamic virus nomenclature that uses a phylogenetic framework to identify those lineages that contribute most to active spread and is designed to provide a real-time bird’s-eye view of the diversity of the hundreds of thousands of genome sequences collected worldwide.
Abstract: The ongoing pandemic spread of a new human coronavirus, SARS-CoV-2, which is associated with severe pneumonia/disease (COVID-19), has resulted in the generation of tens of thousands of virus genome sequences. The rate of genome generation is unprecedented, yet there is currently no coherent nor accepted scheme for naming the expanding phylogenetic diversity of SARS-CoV-2. Here, we present a rational and dynamic virus nomenclature that uses a phylogenetic framework to identify those lineages that contribute most to active spread. Our system is made tractable by constraining the number and depth of hierarchical lineage labels and by flagging and delabelling virus lineages that become unobserved and hence are probably inactive. By focusing on active virus lineages and those spreading to new locations, this nomenclature will assist in tracking and understanding the patterns and determinants of the global spread of SARS-CoV-2.
2,093 citations
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McGill University1, German Cancer Research Center2, Montreal Children's Hospital3, National Research Council4, Russian Academy5, Semmelweis University6, University of Debrecen7, University of Tübingen8, Boston Children's Hospital9, Augsburg College10, University of Würzburg11, Martin Luther University of Halle-Wittenberg12, Heidelberg University13, University of Toronto14, University of Düsseldorf15, University of Cambridge16, University Hospital Heidelberg17
TL;DR: The presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles, suggesting that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.
Abstract: Glioblastoma multiforme (GBM) is a lethal brain tumour in adults and children. However, DNA copy number and gene expression signatures indicate differences between adult and paediatric cases. To explore the genetic events underlying this distinction, we sequenced the exomes of 48 paediatric GBM samples. Somatic mutations in the H3.3-ATRX-DAXX chromatin remodelling pathway were identified in 44% of tumours (21/48). Recurrent mutations in H3F3A, which encodes the replication-independent histone 3 variant H3.3, were observed in 31% of tumours, and led to amino acid substitutions at two critical positions within the histone tail (K27M, G34R/G34V) involved in key regulatory post-translational modifications. Mutations in ATRX (α-thalassaemia/mental retardation syndrome X-linked) and DAXX (death-domain associated protein), encoding two subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres, were identified in 31% of samples overall, and in 100% of tumours harbouring a G34R or G34V H3.3 mutation. Somatic TP53 mutations were identified in 54% of all cases, and in 86% of samples with H3F3A and/or ATRX mutations. Screening of a large cohort of gliomas of various grades and histologies (n = 784) showed H3F3A mutations to be specific to GBM and highly prevalent in children and young adults. Furthermore, the presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles. This is, to our knowledge, the first report to highlight recurrent mutations in a regulatory histone in humans, and our data suggest that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.
2,091 citations
Authors
Showing all 119522 results
Name | H-index | Papers | Citations |
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Albert Hofman | 267 | 2530 | 321405 |
Zhong Lin Wang | 245 | 2529 | 259003 |
Solomon H. Snyder | 232 | 1222 | 200444 |
Trevor W. Robbins | 231 | 1137 | 164437 |
George Davey Smith | 224 | 2540 | 248373 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
Cyrus Cooper | 204 | 1869 | 206782 |
Eric B. Rimm | 196 | 988 | 147119 |
Martin White | 196 | 2038 | 232387 |
Simon D. M. White | 189 | 795 | 231645 |
Michael Rutter | 188 | 676 | 151592 |
George Efstathiou | 187 | 637 | 156228 |
Mark Hallett | 186 | 1170 | 123741 |
David H. Weinberg | 183 | 700 | 171424 |
Paul G. Richardson | 183 | 1533 | 155912 |