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  • 1
    Publication Date: 2004-01-13
    Description: Wnt signaling has recently emerged as a key factor in controlling stem cell expansion. In contrast, we show here that Wnt/beta-catenin signal activation in emigrating neural crest stem cells (NCSCs) has little effect on the population size and instead regulates fate decisions. Sustained beta-catenin activity in neural crest cells promotes the formation of sensory neural cells in vivo at the expense of virtually all other neural crest derivatives. Moreover, Wnt1 is able to instruct early NCSCs (eNCSCs) to adopt a sensory neuronal fate in a beta-catenin-dependent manner. Thus, the role of Wnt/beta-catenin in stem cells is cell-type dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Hye-Youn -- Kleber, Maurice -- Hari, Lisette -- Brault, Veronique -- Suter, Ueli -- Taketo, Makoto M -- Kemler, Rolf -- Sommer, Lukas -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):1020-3. Epub 2004 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell Biology, Department of Biology, Swiss Federal Institute of Technology, ETH-Honggerberg, CH-8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cadherins/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Movement ; Cells, Cultured ; Central Nervous System/embryology ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/metabolism ; Mice ; Models, Neurological ; Multipotent Stem Cells/*physiology ; Mutation ; Nerve Tissue Proteins/metabolism ; Neural Crest/*cytology/embryology/physiology ; Neurons, Afferent/*cytology/physiology ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; Trans-Activators/*metabolism ; Transcription Factor Brn-3 ; Transcription Factors/metabolism ; Wnt Proteins ; Wnt1 Protein ; *Zebrafish Proteins ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2012-05-25
    Description: Oligodendrocytes, the myelin-forming glial cells of the central nervous system, maintain long-term axonal integrity. However, the underlying support mechanisms are not understood. Here we identify a metabolic component of axon-glia interactions by generating conditional Cox10 (protoheme IX farnesyltransferase) mutant mice, in which oligodendrocytes and Schwann cells fail to assemble stable mitochondrial cytochrome c oxidase (COX, also known as mitochondrial complex IV). In the peripheral nervous system, Cox10 conditional mutants exhibit severe neuropathy with dysmyelination, abnormal Remak bundles, muscle atrophy and paralysis. Notably, perturbing mitochondrial respiration did not cause glial cell death. In the adult central nervous system, we found no signs of demyelination, axonal degeneration or secondary inflammation. Unlike cultured oligodendrocytes, which are sensitive to COX inhibitors, post-myelination oligodendrocytes survive well in the absence of COX activity. More importantly, by in vivo magnetic resonance spectroscopy, brain lactate concentrations in mutants were increased compared with controls, but were detectable only in mice exposed to volatile anaesthetics. This indicates that aerobic glycolysis products derived from oligodendrocytes are rapidly metabolized within white matter tracts. Because myelinated axons can use lactate when energy-deprived, our findings suggest a model in which axon-glia metabolic coupling serves a physiological function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613737/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funfschilling, Ursula -- Supplie, Lotti M -- Mahad, Don -- Boretius, Susann -- Saab, Aiman S -- Edgar, Julia -- Brinkmann, Bastian G -- Kassmann, Celia M -- Tzvetanova, Iva D -- Mobius, Wiebke -- Diaz, Francisca -- Meijer, Dies -- Suter, Ueli -- Hamprecht, Bernd -- Sereda, Michael W -- Moraes, Carlos T -- Frahm, Jens -- Goebbels, Sandra -- Nave, Klaus-Armin -- 078415/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Apr 29;485(7399):517-21. doi: 10.1038/nature11007.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Experimental Medicine, Department of Neurogenetics, Hermann-Rein-Strasse 3, D-37075 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622581" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alkyl and Aryl Transferases/deficiency/genetics/metabolism ; Animals ; Axons/*physiology ; Brain/cytology/metabolism ; Cell Respiration ; Cell Survival ; Demyelinating Diseases/enzymology/genetics/metabolism/pathology ; Electron Transport Complex IV/antagonists & inhibitors/genetics/metabolism ; *Glycolysis ; Lactic Acid/metabolism ; Magnetic Resonance Spectroscopy ; Membrane Proteins/deficiency/genetics/metabolism ; Mice ; Mitochondria/enzymology/genetics/metabolism/pathology ; Mutant Proteins/genetics/metabolism ; Myelin Sheath/*metabolism ; Oligodendroglia/cytology/drug effects/enzymology/*metabolism ; Protons ; Schwann Cells/enzymology/metabolism ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2012-12-04
    Description: Mechanisms controlling the proliferative activity of neural stem and progenitor cells (NSPCs) have a pivotal role to ensure life-long neurogenesis in the mammalian brain. How metabolic programs are coupled with NSPC activity remains unknown. Here we show that fatty acid synthase (Fasn), the key enzyme of de novo lipogenesis, is highly active in adult NSPCs and that conditional deletion of Fasn in mouse NSPCs impairs adult neurogenesis. The rate of de novo lipid synthesis and subsequent proliferation of NSPCs is regulated by Spot14, a gene previously implicated in lipid metabolism, that we found to be selectively expressed in low proliferating adult NSPCs. Spot14 reduces the availability of malonyl-CoA, which is an essential substrate for Fasn to fuel lipogenesis. Thus, we identify here a functional coupling between the regulation of lipid metabolism and adult NSPC proliferation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587167/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587167/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knobloch, Marlen -- Braun, Simon M G -- Zurkirchen, Luis -- von Schoultz, Carolin -- Zamboni, Nicola -- Arauzo-Bravo, Marcos J -- Kovacs, Werner J -- Karalay, Ozlem -- Suter, Ueli -- Machado, Raquel A C -- Roccio, Marta -- Lutolf, Matthias P -- Semenkovich, Clay F -- Jessberger, Sebastian -- P30 DK020579/DK/NIDDK NIH HHS/ -- R01 DK076729/DK/NIDDK NIH HHS/ -- R01 DK088083/DK/NIDDK NIH HHS/ -- England -- Nature. 2013 Jan 10;493(7431):226-30. doi: 10.1038/nature11689. Epub 2012 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Institute, Faculty of Medicine, University of Zurich, 8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23201681" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/cytology/*metabolism ; Animals ; Cell Proliferation ; Dentate Gyrus/metabolism ; Fatty Acid Synthases/deficiency/genetics/*metabolism ; Gene Expression Profiling ; Hippocampus/cytology/metabolism ; *Lipogenesis ; Malonyl Coenzyme A/metabolism ; Mice ; Mice, Transgenic ; Neural Stem Cells/cytology/*metabolism ; Neurogenesis ; Nuclear Proteins/genetics/metabolism ; Transcription Factors/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2014-08-01
    Description: Mesenchymal stem cells occupy niches in stromal tissues where they provide sources of cells for specialized mesenchymal derivatives during growth and repair. The origins of mesenchymal stem cells have been the subject of considerable discussion, and current consensus holds that perivascular cells form mesenchymal stem cells in most tissues. The continuously growing mouse incisor tooth offers an excellent model to address the origin of mesenchymal stem cells. These stem cells dwell in a niche at the tooth apex where they produce a variety of differentiated derivatives. Cells constituting the tooth are mostly derived from two embryonic sources: neural crest ectomesenchyme and ectodermal epithelium. It has been thought for decades that the dental mesenchymal stem cells giving rise to pulp cells and odontoblasts derive from neural crest cells after their migration in the early head and formation of ectomesenchymal tissue. Here we show that a significant population of mesenchymal stem cells during development, self-renewal and repair of a tooth are derived from peripheral nerve-associated glia. Glial cells generate multipotent mesenchymal stem cells that produce pulp cells and odontoblasts. By combining a clonal colour-coding technique with tracing of peripheral glia, we provide new insights into the dynamics of tooth organogenesis and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaukua, Nina -- Shahidi, Maryam Khatibi -- Konstantinidou, Chrysoula -- Dyachuk, Vyacheslav -- Kaucka, Marketa -- Furlan, Alessandro -- An, Zhengwen -- Wang, Longlong -- Hultman, Isabell -- Ahrlund-Richter, Lars -- Blom, Hans -- Brismar, Hjalmar -- Lopes, Natalia Assaife -- Pachnis, Vassilis -- Suter, Ueli -- Clevers, Hans -- Thesleff, Irma -- Sharpe, Paul -- Ernfors, Patrik -- Fried, Kaj -- Adameyko, Igor -- G0901599/Medical Research Council/United Kingdom -- MC_U117537087/Medical Research Council/United Kingdom -- England -- Nature. 2014 Sep 25;513(7519):551-4. doi: 10.1038/nature13536. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Neuroscience, Karolinska Institutet, Stockholm 17177, Sweden [2]. ; 1] Department of Dental Medicine, Karolinska Institutet, Stockholm 17177, Sweden [2]. ; Division of Molecular Neurobiology, MRC National Institute for Medical Research, London NW7 1AA, UK. ; 1] Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm 17177, Sweden [2] A.V. Zhirmunsky Institute of Marine Biology of the Far Eastern Branch of the Russian Academy of Sciences, Vladivostok 690041, Russia. ; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm 17177, Sweden. ; Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm 17177, Sweden. ; Department of Craniofacial Development and Stem Cell Biology, King's College London Dental Institute, Guy's Hospital, London SE1 3QD, UK. ; Department of Women's and Children's Health, Karolinska Institutet, Stockholm 17177, Sweden. ; Science for Life Laboratory, Royal Institute of Technology, Stockholm 17177, Sweden. ; Department of Biology, Institute of Molecular Health Sciences, ETH Zurich CH-8093, Switzerland. ; 1] Hubrecht Institute, Koninklijke Nederlandse Akademie van Wetenschappen (KNAW), PO Box 85164, 3508 AD Utrecht, the Netherlands [2] Department of Molecular Genetics, University Medical Center Utrecht, Utrecht 3508 GA, the Netherlands. ; Institute of Biotechnology, Developmental Biology Program, University of Helsinki, Helsinki FI-00014, Finland. ; Department of Neuroscience, Karolinska Institutet, Stockholm 17177, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; *Cell Lineage ; Cell Tracking ; Clone Cells/cytology ; Dental Pulp/cytology ; Female ; Incisor/*cytology/embryology ; Male ; Mesenchymal Stromal Cells/*cytology ; Mice ; Models, Biological ; Neural Crest/cytology ; Neuroglia/*cytology ; Odontoblasts/cytology ; Regeneration ; Schwann Cells/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2010-05-08
    Description: The thickness of the myelin sheath that insulates axons is fitted for optimal nerve conduction velocity. Here, we show that, in Schwann cells, mammalian disks large homolog 1 (Dlg1) interacts with PTEN (phosphatase and tensin homolog deleted on chromosome 10) to inhibit axonal stimulation of myelination. This mechanism limits myelin sheath thickness and prevents overmyelination in mouse sciatic nerves. Removing this brake results also in myelin outfoldings and demyelination, characteristics of some peripheral neuropathies. Indeed, the Dlg1 brake is no longer functional in a mouse model of Charcot-Marie-Tooth disease. Therefore, negative regulation of myelination appears to be essential for optimization of nerve conduction velocity and myelin maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotter, Laurent -- Ozcelik, Murat -- Jacob, Claire -- Pereira, Jorge A -- Locher, Veronica -- Baumann, Reto -- Relvas, Joao B -- Suter, Ueli -- Tricaud, Nicolas -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1415-8. doi: 10.1126/science.1187735. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell Biology, Department of Biology, Eidgenossische Technische Hochschule (ETH) Zurich, CH-8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448149" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Animals ; Axons/physiology ; Coculture Techniques ; Ganglia, Spinal/cytology ; Membrane Proteins/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Myelin Sheath/*physiology/ultrastructure ; Nerve Tissue Proteins/genetics/*metabolism ; Neural Conduction ; Neuregulin-1/metabolism ; PTEN Phosphohydrolase/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Rats ; Schwann Cells/*physiology ; Sciatic Nerve/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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  • 8
    Publication Date: 1983-08-01
    Print ISSN: 0024-9297
    Electronic ISSN: 1520-5835
    Topics: Chemistry and Pharmacology , Physics
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  • 9
    Publication Date: 1998-04-01
    Print ISSN: 0024-9297
    Electronic ISSN: 1520-5835
    Topics: Chemistry and Pharmacology , Physics
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  • 10
    Publication Date: 1991-10-01
    Print ISSN: 0024-9297
    Electronic ISSN: 1520-5835
    Topics: Chemistry and Pharmacology , Physics
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