Institution
University of Groningen
Education•Groningen, Groningen, Netherlands•
About: University of Groningen is a education organization based out in Groningen, Groningen, Netherlands. It is known for research contribution in the topics: Population & Context (language use). The organization has 36346 authors who have published 69116 publications receiving 2940370 citations. The organization is also known as: Rijksuniversiteit Groningen & RUG.
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TL;DR: Investigation of the branching phenotype revealed that in branching cells nucleoid organization, divisome formation and peptidoglycan incorporation were disrupted, and Xac with minC deleted exhibited the classic Δmin phenotype observed in other bacteria deleted for min components.
Abstract: Xanthomonas citri (Xac) is the causal agent of citrus canker, a disease that affects citrus crops and causes economic impact worldwide. To further characterize cell division in this plant pathogen, we investigated the role of the protein MinC in cell division, chromosome segregation, and peptidoglycan incorporation by deleting the gene minC using allele exchange. Xac with minC deleted exhibited the classic Δmin phenotype observed in other bacteria deleted for min components: minicells and short filamentation. In addition we noticed the formation of branches, which is similar to what was previously described for Escherichia coli deleted for either min or for several low molecular weight penicillin-binding proteins (PBPs). The branching phenotype was medium dependent and probably linked to gluconeogenic growth. We complemented the minC gene by integrating gfp-minC into the amy locus. Xac complemented strains displayed a wild-type phenotype. In addition, GFP-MinC oscillated from pole to pole, similar to MinCD oscillations observed in E. coli and more recently in Synechococcus elongatus. Further investigation of the branching phenotype revealed that in branching cells nucleoid organization, divisome formation and peptidoglycan incorporation were disrupted.
768 citations
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TL;DR: This Perspective presents the reader with the current state and outlook on photopharmacology, in particular the principles behind photoregulation of bioactivity, the challenges of molecular design, and the possible therapeutic scenarios are discussed.
Abstract: Pharmacotherapy is often severely hindered by issues related to poor drug selectivity, including side effects, environmental toxicity, and the emergence of resistance. Lack of selectivity is caused by the inability to control drug activity in time and space. Photopharmacology aims at solving this issue by incorporating photoswitchable groups into the molecular structure of bioactive compounds. These switching units allow for the use of light as an external control element for pharmacological activity, which can be delivered with very high spatiotemporal precision. This Perspective presents the reader with the current state and outlook on photopharmacology. In particular, the principles behind photoregulation of bioactivity, the challenges of molecular design, and the possible therapeutic scenarios are discussed.
765 citations
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TL;DR: It is shown that oxidation–reduction cycles of peroxiredoxin proteins constitute a universal marker for circadian rhythms in all domains of life, by characterizing their oscillations in a variety of model organisms and exploring the interconnectivity between these metabolic cycles and transcription–translation feedback loops of the clockwork in each system.
Abstract: Cellular life emerged ∼3.7 billion years ago. With scant exception, terrestrial organisms have evolved under predictable daily cycles owing to the Earth’s rotation. The advantage conferred on organisms that anticipate such environmental cycles has driven the evolution of endogenous circadian rhythms that tune internal physiology to external conditions. The molecular phylogeny of mechanisms driving these rhythms has been difficult to dissect because identified clock genes and proteins are not conserved across the domains of life: Bacteria, Archaea and Eukaryota. Here we show that oxidation–reduction cycles of peroxiredoxin proteins constitute a universal marker for circadian rhythms in all domains of life, by characterizing their oscillations in a variety of model organisms. Furthermore, we explore the interconnectivity between these metabolic cycles and transcription–translation feedback loops of the clockwork in each system. Our results suggest an intimate co-evolution of cellular timekeeping with redox homeostatic mechanisms after the Great Oxidation Event ∼2.5 billion years ago. Daily oxidation–reduction cycles of peroxiredoxin proteins are shown to be conserved in all domains of life, including Bacteria, Archaea and Eukaryota. Most living organisms possess an endogenous circadian clock that ties their metabolism to a 24-hour day–night cycle. 'Clock genes' have been studied in many organisms and their variety has encouraged the view that each clock evolved independently. But there is a unifying factor: a non-transcriptionally based form of circadian oscillation, involving the oxidation–reduction cycles of peroxiredoxin proteins, has been identified in human red blood cells and algae. This study demonstrates that these redox cycles are conserved in all domains of life, including Bacteria, Archaea and Eukaryota, pointing to the possibility that this type of cellular timekeeping has co-evolved with redox homeostatic mechanisms across organisms for billions of years. The link may go back 2.5 billion years, to the Great Oxidation Event that consigned anaerobic metabolism to the margins of evolutionary history.
765 citations
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Christian R. Marshall1, Daniel P. Howrigan2, Daniele Merico1, Bhooma Thiruvahindrapuram1 +252 more•Institutions (87)
TL;DR: A collaborative effort in which a centralized analysis pipeline is applied to a SCZ cohort, finding support at a suggestive level for nine additional candidate susceptibility and protective loci, which consist predominantly of CNVs mediated by non-allelic homologous recombination (NAHR).
Abstract: Genomic copy number variants (CNVs) have been strongly implicated in the etiology of schizophrenia (SCZ). However, apart from a small number of risk variants, elucidation of the CNV contribution to risk has been difficult due to the rarity of risk alleles, all occurring in less than 1% of cases. We sought to address this obstacle through a collaborative effort in which we applied a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. We observed a global enrichment of CNV burden in cases (OR=1.11, P=5.7e-15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7e-6). CNV burden is also enriched for genes associated with synaptic function (OR = 1.68, P = 2.8e-11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3e-5). We identified genome-wide significant support for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. We find support at a suggestive level for nine additional candidate susceptibility and protective loci, which consist predominantly of CNVs mediated by non-allelic homologous recombination (NAHR).
764 citations
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Katholieke Universiteit Leuven1, Vita-Salute San Raffaele University2, Ghent University Hospital3, Institut Jules Bordet4, Maastricht University Medical Centre5, Erasmus University Rotterdam6, University of Groningen7, University Hospital of Basel8, European Organisation for Research and Treatment of Cancer9
TL;DR: Results at median follow-up of 10·6 years show that conventional postoperative irradiation significantly improves biochemical progression-free survival and local control compared with a wait-and-see policy, supporting results at 5 year follow- up; however, improvements in clinical progression- free survival were not maintained.
764 citations
Authors
Showing all 36692 results
Name | H-index | Papers | Citations |
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Ronald C. Kessler | 274 | 1332 | 328983 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Lei Jiang | 170 | 2244 | 135205 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Richard H. Friend | 169 | 1182 | 140032 |
Panos Deloukas | 162 | 410 | 154018 |
Jerome I. Rotter | 156 | 1071 | 116296 |
Christopher M. Dobson | 150 | 1008 | 105475 |
Dirk Inzé | 149 | 647 | 74468 |
Scott T. Weiss | 147 | 1025 | 74742 |
Dieter Lutz | 139 | 671 | 67414 |
Wilmar B. Schaufeli | 137 | 513 | 95718 |
Cisca Wijmenga | 136 | 668 | 86572 |
Arnold B. Bakker | 135 | 506 | 103778 |