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 & Gene. 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, Gene, Immune system, Receptor, CAS Registry Number
Papers published on a yearly basis
Papers
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TL;DR: The fulfilment of universal psychological needs, such as competence, relatedness, popularity, stimulation, meaning, security, or autonomy, is considered to be the major source of positive experience with interactive technologies.
646 citations
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TL;DR: Mice with homozygous SMN disruption display massive cell death during early embryonic development, indicating that the SMN gene product is necessary for cellular survival and function.
Abstract: Proximal spinal muscular atrophy is an autosomal recessive human disease of spinal motor neurons leading to muscular weakness with onset predominantly in infancy and childhood. With an estimated heterozygote frequency of 1/40 it is the most common monogenic disorder lethal to infants; milder forms represent the second most common pediatric neuromuscular disorder. Two candidate genes—survival motor neuron (SMN) and neuronal apoptosis inhibitory protein have been identified on chromosome 5q13 by positional cloning. However, the functional impact of these genes and the mechanism leading to a degeneration of motor neurons remain to be defined. To analyze the role of the SMN gene product in vivo we generated SMN-deficient mice. In contrast to the human genome, which contains two copies, the mouse genome contains only one SMN gene. Mice with homozygous SMN disruption display massive cell death during early embryonic development, indicating that the SMN gene product is necessary for cellular survival and function.
646 citations
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TL;DR: The isolation of a complementary DNA from rat kidney is reported that encodes a 556-amino-acid membrane protein, OCT1, which has the functional characteristics of organic cation uptake over the basolateral membrane of renal proximal tubules and of organiccation uptake into hepatocytes.
Abstract: Cationic drugs of different types and structures (antihistaminics, antiarrhythmics, sedatives, opiates, cytostatics and antibiotics, for example) are excreted in mammals by epithelial cells of the renal proximal tubules and by hepatocytes in the liver In the proximal tubules, two functionally disparate transport systems are involved which are localized in the basolateral and luminal plasma membrane and are different from the previously identified neuronal monoamine transporters and ATP-dependent multidrug exporting proteins Here we report the isolation of a complementary DNA from rat kidney that encodes a 556-amino-acid membrane protein, OCT1, which has the functional characteristics of organic cation uptake over the basolateral membrane of renal proximal tubules and of organic cation uptake into hepatocytes OCT1 is not homologous to any other known protein and is found in kidney, liver and intestine As OCT1 translocates hydrophobic and hydrophilic organic cations of different structures, it is considered to be a new prototype of polyspecific transporters that are important for drug elimination
644 citations
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TL;DR: Remaining large arteries in both Notch1 and Hey1/Hey2 knockout mice fail to express the arterial endothelial markers CD44, neuropilin1, and ephrin-B2, which indicates that Hey1 /Hey2 are essential transducers of Notch signals in cardiovascular development that may mediate arterial cell fate decision.
Abstract: The Delta–Notch signaling pathway plays a central role in the development of most vertebrate organs. The Hey family of bHLH transcription factors are direct targets of Notch signaling. Loss of Hey2 in the mouse leads to cardiac defects with high postnatal lethality. We have now generated a mouse Hey1 knockout that has no apparent phenotypic defect. The combined loss of Hey1 and Hey2, however, results in embryonic death after embryonic day 9.5 (E9.5) with a global lack of vascular remodeling and massive hemorrhage. Initial vasculogenesis appears unaffected, but all subsequently developing major vessels in the embryo and yolk sac are either small or absent. Furthermore, the placental labyrinth completely lacks embryonic blood vessels. Similar vascular defects are observed in Jagged1 and Notch1 knockout mice. In the latter we found Hey1 and Hey2 expression in yolk sacs to be strongly reduced. Remaining large arteries in both Notch1 and Hey1/Hey2 knockout mice fail to express the arterial endothelial markers CD44, neuropilin1, and ephrin-B2. This indicates that Hey1/Hey2 are essential transducers of Notch signals in cardiovascular development that may mediate arterial cell fate decision.
644 citations
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TL;DR: In this paper, the effects of traditional and social media strategies on the recipients' perceptions of reputation and reactions of secondary crisis communications were analyzed, and the results indicated that the medium matters more than the message.
641 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 |