Institution
University of Antwerp
Education•Antwerp, Belgium•
About: University of Antwerp is a education organization based out in Antwerp, Belgium. It is known for research contribution in the topics: Population & Context (language use). The organization has 16682 authors who have published 48837 publications receiving 1689748 citations. The organization is also known as: Universiteit Antwerpen & UAntwerp.
Papers published on a yearly basis
Papers
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TL;DR: In this article, a taxonomy of efforts of suppliers in the commoditized electro-technical industry to create new non-price-based customer value is developed, which builds on the competitive strategy and strategic marketing literature.
432 citations
TL;DR: The detection of three interstitial, overlapping 17q21.31 microdeletions in a cohort of 1,200 mentally retarded individuals associated with a clearly recognizable clinical phenotype of mental retardation, hypotonia and a characteristic face is described.
Abstract: Submicroscopic genomic copy number changes have been identified only recently as an important cause of mental retardation. We describe the detection of three interstitial, overlapping 17q21.31 microdeletions in a cohort of 1,200 mentally retarded individuals associated with a clearly recognizable clinical phenotype of mental retardation, hypotonia and a characteristic face. The deletions encompass the MAPT and CRHR1 genes and are associated with a common inversion polymorphism.
432 citations
TL;DR: An increase of α-tubulin acetylation induced by pharmacological inhibition of histone deacetylase 6 (HDAC6) corrected the axonal transport defects caused by HSPB1 mutations and rescued the CMT phenotype of symptomatic mutant H SPB1 mice.
Abstract: Charcot-Marie-Tooth disease (CMT) is the most common inherited disorder of the peripheral nervous system. Mutations in the 27-kDa small heat-shock protein gene (HSPB1) cause axonal CMT or distal hereditary motor neuropathy (distal HMN). We developed and characterized transgenic mice expressing two different HSPB1 mutations (S135F and P182L) in neurons only. These mice showed all features of CMT or distal HMN dependent on the mutation. Expression of mutant HSPB1 decreased acetylated α-tubulin abundance and induced severe axonal transport deficits. An increase of α-tubulin acetylation induced by pharmacological inhibition of histone deacetylase 6 (HDAC6) corrected the axonal transport defects caused by HSPB1 mutations and rescued the CMT phenotype of symptomatic mutant HSPB1 mice. Our findings demonstrate the pathogenic role of α-tubulin deacetylation in mutant HSPB1-induced neuropathies and offer perspectives for using HDAC6 inhibitors as a therapeutic strategy for hereditary axonopathies.
431 citations
Memorial Sloan Kettering Cancer Center1, Keio University2, Beth Israel Deaconess Medical Center3, Mount Sinai Hospital4, Yale University5, Fox Chase Cancer Center6, New Generation University College7, University of Chicago8, New York University9, Imperial College London10, Radboud University Nijmegen11, University of Barcelona12, Peter MacCallum Cancer Centre13, University of Michigan14, University of São Paulo15, Fred Hutchinson Cancer Research Center16, University of Duisburg-Essen17, Northern General Hospital18, University of Caen Lower Normandy19, Churchill Hospital20, Queen's University21, University of Sydney22, Sungkyunkwan University23, Seoul National University24, Kyorin University25, University of Copenhagen26, Nippon Medical School27, Katholieke Universiteit Leuven28, British Hospital29, University of Texas MD Anderson Cancer Center30, University of Antwerp31, Hyogo College of Medicine32, University of Western Australia33, Glenfield Hospital34, Cleveland Clinic35, Icahn School of Medicine at Mount Sinai36, University of Turin37, Université libre de Bruxelles38, Juntendo University39, National Cancer Research Institute40, Mayo Clinic41, Princess Margaret Cancer Centre42, Sinai Grace Hospital43, Netherlands Cancer Institute44, Hiroshima University45, City of Hope National Medical Center46, Georgetown University47, University of Tokushima48, University of Pisa49, Osaka University50
TL;DR: Codes for the primary tumor categories of AIS and minimally invasive adenocarcinoma (MIA) and a uniform way to measure tumor size in part‐solid tumors for the eighth edition of the tumor, node, and metastasis classification of lung cancer are proposed.
431 citations
TL;DR: In this paper, the authors investigated the effects of ash on the burned ecosystem, especially when transported by wind or water, and investigated its control on water and soil losses at slope and catchment scales, and examined its role in the C cycle.
430 citations
Authors
Showing all 16957 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Cornelia M. van Duijn | 183 | 1030 | 146009 |
| John Hardy | 177 | 1178 | 171694 |
| Mark Gerstein | 168 | 751 | 149578 |
| Hannes Jung | 159 | 2069 | 125069 |
| Rui Zhang | 151 | 2625 | 107917 |
| Dirk Inzé | 149 | 647 | 74468 |
| Walter Paulus | 149 | 809 | 86252 |
| Robin Erbacher | 138 | 1721 | 100252 |
| Rupert Leitner | 136 | 1201 | 90597 |
| Alison Goate | 136 | 721 | 85846 |
| Andrea Giammanco | 135 | 1362 | 98093 |
| Maria Spiropulu | 135 | 1455 | 96674 |
| Peter Robmann | 135 | 1438 | 97569 |
| Michael Tytgat | 134 | 1449 | 94133 |
| Matthew Herndon | 133 | 1732 | 97466 |