Institution
University of Basel
Education•Basel, Basel-Stadt, Switzerland•
About: University of Basel is a education organization based out in Basel, Basel-Stadt, Switzerland. It is known for research contribution in the topics: Population & Transplantation. The organization has 25084 authors who have published 52975 publications receiving 2388002 citations. The organization is also known as: Universität Basel & Basel University.
Topics: Population, Transplantation, Gene, Poison control, Quantum dot
Papers published on a yearly basis
Papers
More filters
••
TL;DR: This review is concerned with the influence of structural parameters, such as peptide helicity, hydrophobicity,hydrophobic moment, peptide charge and the size of the hydrophobic/hydrophilic domain, on membrane activity and selectivity of natural and model peptides.
675 citations
••
TL;DR: The anatomical distribution of serotonin-2 receptors in the human brain was studied by light microscopic autoradiography, using [3H]ketanserin as a ligand and the receptor densities were quantified by microdensitometry with the aid of a computer-assisted image-analysis system.
674 citations
••
TL;DR: Mice with a Crem−/− background and lacking Creb in the central nervous system during development show extensive apoptosis of postmitotic neurons, and mice in which both Creb1 and Crem are disrupted in the postnatal forebrain show progressive neurodegeneration in the hippocampus and in the dorsolateral striatum.
Abstract: Control of cellular survival and proliferation is dependent on extracellular signals and is a prerequisite for ordered tissue development and maintenance. Activation of the cAMP responsive element binding protein (CREB) by phosphorylation has been implicated in the survival of mammalian cells. To define its roles in the mouse central nervous system, we disrupted Creb1 in brain of developing and adult mice using the Cre/loxP system. Mice with a Crem(-/-) background and lacking Creb in the central nervous system during development show extensive apoptosis of postmitotic neurons. By contrast, mice in which both Creb1 and Crem are disrupted in the postnatal forebrain show progressive neurodegeneration in the hippocampus and in the dorsolateral striatum. The striatal phenotype is reminiscent of Huntington disease and is consistent with the postulated role of CREB-mediated signaling in polyglutamine-triggered diseases.
670 citations
••
TL;DR: Non-equilibrium approaches involving frequency-dependence, density-Dependence, evolutionary game theory, adaptive dynamics, and explicit population dynamics have supplanted optimization as the preferred approach and may soon extend the impact of life history theory into population dynamics and interspecific interactions in coevolving communities.
Abstract: Life history theory tries to explain how evolution designs organisms to achieve reproductive success. The design is a solution to an ecological problem posed by the environment and subject to constraints intrinsic to the organism. Work on life histories has expanded the role of phenotypes in evolutionary theory, extending the range of predictions from genetic patterns to whole-organism traits directly connected to fitness. Among the questions answered are the following: Why are organisms small or large? Why do they mature early or late? Why do they have few or many offspring? Why do they have a short or a long life? Why must they grow old and die? The classical approach to life histories was optimization; it has had some convincing empirical success. Recently non-equilibrium approaches involving frequency-dependence, density-dependence, evolutionary game theory, adaptive dynamics, and explicit population dynamics have supplanted optimization as the preferred approach. They have not yet had as much empirical success, but there are logical reasons to prefer them, and they may soon extend the impact of life history theory into population dynamics and interspecific interactions in coevolving communities.
670 citations
••
TL;DR: Methotrexate, a folate antagonist, blocks import into mitochondria of mouse dihydrofolate reductase fused to a mitochondrial presequence, suggesting that diHydrofolates must at least partly unfold in order to be transported across mitochondrial membranes.
Abstract: Methotrexate, a folate antagonist, blocks import into mitochondria of mouse dihydrofolate reductase fused to a mitochondrial presequence. Methotrexate does not mask the presequence, but stabilizes the dihydrofolate reductase moiety. It does not inhibit import of the authentic precursor from which the presequence is derived. This suggests that dihydrofolate reductase must at least partly unfold in order to be transported across mitochondrial membranes.
667 citations
Authors
Showing all 25374 results
Name | H-index | Papers | Citations |
---|---|---|---|
Yang Yang | 171 | 2644 | 153049 |
Martin Karplus | 163 | 831 | 138492 |
Frank J. Gonzalez | 160 | 1144 | 96971 |
Paul Emery | 158 | 1314 | 121293 |
Matthias Egger | 152 | 901 | 184176 |
Don W. Cleveland | 152 | 444 | 84737 |
Ashok Kumar | 151 | 5654 | 164086 |
Kurt Wüthrich | 143 | 739 | 103253 |
Thomas J. Smith | 140 | 1775 | 113919 |
Robert Huber | 139 | 671 | 73557 |
Peter Robmann | 135 | 1438 | 97569 |
Ernst Detlef Schulze | 133 | 670 | 69504 |
Michael Levine | 129 | 586 | 55963 |
Claudio Santoni | 129 | 1027 | 80598 |
Pablo Garcia-Abia | 126 | 989 | 78690 |