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Institution

University of Basel

EducationBasel, 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.


Papers
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
01 Jul 1986-Nature
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

NameH-indexPapersCitations
Yang Yang1712644153049
Martin Karplus163831138492
Frank J. Gonzalez160114496971
Paul Emery1581314121293
Matthias Egger152901184176
Don W. Cleveland15244484737
Ashok Kumar1515654164086
Kurt Wüthrich143739103253
Thomas J. Smith1401775113919
Robert Huber13967173557
Peter Robmann135143897569
Ernst Detlef Schulze13367069504
Michael Levine12958655963
Claudio Santoni129102780598
Pablo Garcia-Abia12698978690
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023146
2022552
20213,395
20203,227
20192,984
20182,775