Institution
University of Würzburg
Education•Wurzburg, Bayern, Germany•
About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & CAS Registry Number. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.
Topics: Population, CAS Registry Number, Immune system, Gene, T cell
Papers published on a yearly basis
Papers
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TL;DR: The combined theoretical and experimental results demonstrate a concept for a quantum spin Hall wide-gap scenario, where the chemical potential resides in the global system gap, ensuring robust edge conductance.
Abstract: Quantum spin Hall materials hold the promise of revolutionary devices with dissipationless spin currents but have required cryogenic temperatures owing to small energy gaps. Here we show theoretically that a room-temperature regime with a large energy gap may be achievable within a paradigm that exploits the atomic spin-orbit coupling. The concept is based on a substrate-supported monolayer of a high–atomic number element and is experimentally realized as a bismuth honeycomb lattice on top of the insulating silicon carbide substrate SiC(0001). Using scanning tunneling spectroscopy, we detect a gap of ~0.8 electron volt and conductive edge states consistent with theory. Our combined theoretical and experimental results demonstrate a concept for a quantum spin Hall wide-gap scenario, where the chemical potential resides in the global system gap, ensuring robust edge conductance.
766 citations
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TL;DR: The present results suggest that the concentrations of IL-1 beta, IL-6, EGF, and TGF-alpha in the dopaminergic, striatal regions were significantly higher in parkinsonian patients than those in controls, whereas those in the cerebral cortex did not show significant differences between parkinsonians and control subjects.
763 citations
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TL;DR: Recent preclinical and clinical data for antibody–drug conjugates and fusion proteins with a special focus on drug components that exert their antitumour effects through normal biological processes are discussed.
Abstract: Targeting drugs specifically to tumour cells to improve efficacy and reduce toxicity is paramount to the future development of anti-cancer agents. Schrama and colleagues critically review current approaches to achieving this and the status of targeted treatments in development. Treatment of cancer is a double-edged sword: it should be as aggressive as possible to completely destroy the tumour, but it is precisely this aggressiveness which often causes severe side effects — a reason why some promising therapeutics can not be applied systemically. In addition, therapeutics such as cytokines that physiologically function in a para- or autocrine fashion require a locally enhanced level to exert their effect appropriately. An elegant way to accumulate therapeutic agents at the tumour site is their conjugation/fusion to tumour-specific antibodies. Here, we discuss recent preclinical and clinical data for antibody–drug conjugates and fusion proteins with a special focus on drug components that exert their antitumour effects through normal biological processes.
758 citations
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National Institutes of Health1, University of Würzburg2, University of Groningen3, Bosch4, University of British Columbia5, University of Arizona6, University of Barcelona7, University of Oslo8, St Mary's Hospital9, University of Rochester10, Oregon Health & Science University11, Cleveland Clinic12, University of Nebraska Medical Center13, University of Birmingham14, United States Department of Health and Human Services15
TL;DR: High-throughput RNA sequencing and RNA interference screening is used to discover essential regulatory pathways in Burkitt's lymphoma that cooperate with MYC, the defining oncogene of this cancer.
Abstract: Burkitt's lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. The normal germinal centre B cell is the presumed cell of origin for both BL and diffuse large B-cell lymphoma (DLBCL), yet gene expression analysis suggests that these malignancies may use different oncogenic pathways. BL is subdivided into a sporadic subtype that is diagnosed in developed countries, the Epstein-Barr-virus-associated endemic subtype, and an HIV-associated subtype, but it is unclear whether these subtypes use similar or divergent oncogenic mechanisms. Here we used high-throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways in BL that cooperate with MYC, the defining oncogene of this cancer. In 70% of sporadic BL cases, mutations affecting the transcription factor TCF3 (E2A) or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival phosphatidylinositol-3-OH kinase pathway in BL, in part by augmenting tonic B-cell receptor signalling. In 38% of sporadic BL cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. These findings suggest opportunities to improve therapy for patients with BL.
757 citations
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TL;DR: It is demonstrated that SLAC1 represents the slow, deactivating, weak voltage-dependent anion channel of guard cells controlled by phosphorylation/dephosphorylation.
Abstract: In response to drought stress the phytohormone ABA (abscisic acid) induces stomatal closure and, therein, activates guard cell anion channels in a calcium-dependent as well as-independent manner. Two key components of the ABA signaling pathway are the protein kinase OST1 (open stomata 1) and the protein phosphatase ABI1 (ABA insensitive 1). The recently identified guard cell anion channel SLAC1 appeared to be the key ion channel in this signaling pathway but remained electrically silent when expressed heterologously. Using split YFP assays, we identified OST1 as an interaction partner of SLAC1 and ABI1. Upon coexpression of SLAC1 with OST1 in Xenopus oocytes, SLAC1-related anion currents appeared similar to those observed in guard cells. Integration of ABI1 into the SLAC1/OST1 complex, however, prevented SLAC1 activation. Our studies demonstrate that SLAC1 represents the slow, deactivating, weak voltage-dependent anion channel of guard cells controlled by phosphorylation/dephosphorylation.
756 citations
Authors
Showing all 31653 results
Name | H-index | Papers | Citations |
---|---|---|---|
Peer Bork | 206 | 697 | 245427 |
Cyrus Cooper | 204 | 1869 | 206782 |
D. M. Strom | 176 | 3167 | 194314 |
George P. Chrousos | 169 | 1612 | 120752 |
David A. Bennett | 167 | 1142 | 109844 |
Marc W. Kirschner | 162 | 457 | 102145 |
Josef M. Penninger | 154 | 700 | 107295 |
William A. Catterall | 154 | 536 | 83561 |
Rui Zhang | 151 | 2625 | 107917 |
Niels Birbaumer | 142 | 835 | 77853 |
Kim Nasmyth | 142 | 294 | 59231 |
James J. Gross | 139 | 529 | 100206 |
Michael Schmitt | 134 | 2007 | 114667 |
Jean-Luc Brédas | 134 | 1026 | 85803 |
Alexander Schmidt | 134 | 1185 | 83879 |