University Library
  • Login
A gateway to Melbourne's research publications
Minerva Access is the University's Institutional Repository. It aims to collect, preserve, and showcase the intellectual output of staff and students of the University of Melbourne for a global audience.
View Item 
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Medical Biology
  • Medical Biology - Research Publications
  • View Item
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Medical Biology
  • Medical Biology - Research Publications
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

    Rapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells

    Thumbnail
    Download
    Published version (5.773Mb)

    Citations
    Scopus
    Altmetric
    10
    Author
    Ushiki, T; Huntington, ND; Glaser, SP; Kiu, H; Georgiou, A; Zhang, J-G; Metcalf, D; Nicola, NA; Roberts, AW; Alexander, WS
    Date
    2016-09-01
    Source Title
    PLoS One
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Huntington, Nicholas; Alexander, Warren; Zhang, Jian-Guo; Glaser, Stephan; Nicola, Nicos; Roberts, Andrew
    Affiliation
    Medical Biology (W.E.H.I.)
    Centre for Cancer Research
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Ushiki, T., Huntington, N. D., Glaser, S. P., Kiu, H., Georgiou, A., Zhang, J. -G., Metcalf, D., Nicola, N. A., Roberts, A. W. & Alexander, W. S. (2016). Rapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells. PLOS ONE, 11 (9), https://doi.org/10.1371/journal.pone.0162111.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/260162
    DOI
    10.1371/journal.pone.0162111
    Abstract
    The Suppressors of Cytokine Signalling (SOCS) proteins are negative regulators of cytokine signalling required to prevent excess cellular responses. SOCS1 and SOCS3 are essential to prevent inflammatory disease, SOCS1 by attenuating responses to IFNγ and gamma-common (γc) cytokines, and SOCS3 via regulation of G-CSF and IL-6 signalling. SOCS1 and SOCS3 show significant sequence homology and are the only SOCS proteins to possess a KIR domain. The possibility of overlapping or redundant functions was investigated in inflammatory disease via generation of mice lacking both SOCS1 and SOCS3 in hematopoietic cells. Loss of SOCS3 significantly accelerated the pathology and inflammatory disease characteristic of SOCS1 deficiency. We propose a model in which SOCS1 and SOCS3 operate independently to control specific cytokine responses and together modulate the proliferation and activation of lymphoid and myeloid cells to prevent rapid inflammatory disease.

    Export Reference in RIS Format     

    Endnote

    • Click on "Export Reference in RIS Format" and choose "open with... Endnote".

    Refworks

    • Click on "Export Reference in RIS Format". Login to Refworks, go to References => Import References


    Collections
    • Minerva Elements Records [52609]
    • Centre for Cancer Research - Research Publications [83]
    • Medical Biology - Research Publications [1412]
    Minerva AccessDepositing Your Work (for University of Melbourne Staff and Students)NewsFAQs

    BrowseCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
    My AccountLoginRegister
    StatisticsMost Popular ItemsStatistics by CountryMost Popular Authors