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Deubiquitylases in developmental ubiquitin signaling and congenital diseases

Cell death and differentiation, 2021-02, Vol.28 (2), p.538-556 [Peer Reviewed Journal]

This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020 ;ISSN: 1350-9047 ;EISSN: 1476-5403 ;DOI: 10.1038/s41418-020-00697-5 ;PMID: 33335288

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  • Title:
    Deubiquitylases in developmental ubiquitin signaling and congenital diseases
  • Author: Basar, Mohammed A ; Beck, David B ; Werner, Achim
  • Subjects: Animals ; Cell interactions ; Congenital Abnormalities - enzymology ; Congenital diseases ; Deubiquitinating Enzymes - metabolism ; Deubiquitinating Enzymes - physiology ; Embryogenesis ; Enzymes ; Humans ; Localization ; Lysine ; Mutation ; Protein Processing, Post-Translational ; Review ; Signal Transduction ; Ubiquitin ; Ubiquitin - metabolism ; Ubiquitination
  • Is Part Of: Cell death and differentiation, 2021-02, Vol.28 (2), p.538-556
  • Description: Metazoan development from a one-cell zygote to a fully formed organism requires complex cellular differentiation and communication pathways. To coordinate these processes, embryos frequently encode signaling information with the small protein modifier ubiquitin, which is typically attached to lysine residues within substrates. During ubiquitin signaling, a three-step enzymatic cascade modifies specific substrates with topologically unique ubiquitin modifications, which mediate changes in the substrate's stability, activity, localization, or interacting proteins. Ubiquitin signaling is critically regulated by deubiquitylases (DUBs), a class of ~100 human enzymes that oppose the conjugation of ubiquitin. DUBs control many essential cellular functions and various aspects of human physiology and development. Recent genetic studies have identified mutations in several DUBs that cause developmental disorders. Here we review principles controlling DUB activity and substrate recruitment that allow these enzymes to regulate ubiquitin signaling during development. We summarize key mechanisms of how DUBs control embryonic and postnatal differentiation processes, highlight developmental disorders that are caused by mutations in particular DUB members, and describe our current understanding of how these mutations disrupt development. Finally, we discuss how emerging tools from human disease genetics will enable the identification and study of novel congenital disease-causing DUBs.
  • Publisher: England: Nature Publishing Group
  • Language: English
  • Identifier: ISSN: 1350-9047
    EISSN: 1476-5403
    DOI: 10.1038/s41418-020-00697-5
    PMID: 33335288
  • Source: GFMER Free Medical Journals
    MEDLINE
    PubMed Central
    ProQuest Central
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