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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheetham, Seth W -- Brand, Andrea H -- 092096/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 May 17;340(6134):817-8. doi: 10.1126/science.1238525.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN,UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23687033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila Proteins/metabolism ; Drosophila melanogaster/*metabolism ; Insulin/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; *Signal Transduction ; Somatomedins/metabolism ; Stem Cells/metabolism
    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: 2015-10-08
    Description: : DamID is a powerful technique for identifying regions of the genome bound by a DNA-binding (or DNA-associated) protein. Currently, no method exists for automatically processing next-generation sequencing DamID (DamID-seq) data, and the use of DamID-seq datasets with normalization based on read-counts alone can lead to high background and the loss of bound signal. DamID-seq thus presents novel challenges in terms of normalization and background minimization. We describe here damidseq_pipeline, a software pipeline that performs automatic normalization and background reduction on multiple DamID-seq FASTQ datasets. Availability and implementation: Open-source and freely available from http://owenjm.github.io/damidseq_pipeline . The damidseq_pipeline is implemented in Perl and is compatible with any Unix-based operating system (e.g. Linux, Mac OSX). Contact: o.marshall@gurdon.cam.ac.uk Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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  • 3
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2018-04-06
    Description: Quiescent stem cells in adult tissues can be activated for homeostasis or repair. Neural stem cells (NSCs) in Drosophila are reactivated from quiescence in response to nutrition by the insulin signaling pathway. It is widely accepted that quiescent stem cells are arrested in G 0 . In this study, however, we demonstrate that quiescent NSCs (qNSCs) are arrested in either G 2 or G 0 . G 2 -G 0 heterogeneity directs NSC behavior: G 2 qNSCs reactivate before G 0 qNSCs. In addition, we show that the evolutionarily conserved pseudokinase Tribbles (Trbl) induces G 2 NSCs to enter quiescence by promoting degradation of Cdc25 String and that it subsequently maintains quiescence by inhibiting Akt activation. Insulin signaling overrides repression of Akt and silences trbl transcription, allowing NSCs to exit quiescence. Our results have implications for identifying and manipulating quiescent stem cells for regenerative purposes.
    Keywords: Development, Neuroscience
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2018-04-05
    Description: Quiescent stem cells in adult tissues can be activated for homeostasis or repair. Neural stem cells (NSCs) in Drosophila are reactivated from quiescence in response to nutrition by the insulin signaling pathway. It is widely accepted that quiescent stem cells are arrested in G0. In this study, however, we demonstrate that quiescent NSCs (qNSCs) are arrested in either G2 or G0. G2-G0 heterogeneity directs NSC behavior: G2 qNSCs reactivate before G0 qNSCs. In addition, we show that the evolutionarily conserved pseudokinase Tribbles (Trbl) induces G2 NSCs to enter quiescence by promoting degradation of Cdc25String and that it subsequently maintains quiescence by inhibiting Akt activation. Insulin signaling overrides repression of Akt and silences trbl transcription, allowing NSCs to exit quiescence. Our results have implications for identifying and manipulating quiescent stem cells for regenerative purposes.
    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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