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dc.contributor.authorUshiki, T
dc.contributor.authorHuntington, ND
dc.contributor.authorGlaser, SP
dc.contributor.authorKiu, H
dc.contributor.authorGeorgiou, A
dc.contributor.authorZhang, J-G
dc.contributor.authorMetcalf, D
dc.contributor.authorNicola, NA
dc.contributor.authorRoberts, AW
dc.contributor.authorAlexander, WS
dc.date.accessioned2021-02-05T00:48:59Z
dc.date.available2021-02-05T00:48:59Z
dc.date.issued2016-09-01
dc.identifierpii: PONE-D-16-26149
dc.identifier.citationUshiki, 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.
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11343/260162
dc.description.abstractThe 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.
dc.languageEnglish
dc.publisherPUBLIC LIBRARY SCIENCE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleRapid Inflammation in Mice Lacking Both SOCS1 and SOCS3 in Hematopoietic Cells
dc.typeJournal Article
dc.identifier.doi10.1371/journal.pone.0162111
melbourne.affiliation.departmentMedical Biology (W.E.H.I.)
melbourne.affiliation.departmentCentre for Cancer Research
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titlePLoS One
melbourne.source.volume11
melbourne.source.issue9
dc.rights.licenseCC BY
melbourne.elementsid1094589
melbourne.contributor.authorHuntington, Nicholas
melbourne.contributor.authorAlexander, Warren
melbourne.contributor.authorZhang, Jian-Guo
melbourne.contributor.authorGlaser, Stephan
melbourne.contributor.authorNicola, Nicos
melbourne.contributor.authorRoberts, Andrew
dc.identifier.eissn1932-6203
melbourne.accessrightsOpen Access


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