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Selective modulation through the glucocorticoid receptor ameliorates muscle pathology in mdx mice

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dc.contributor.authorHuynh, Tony
dc.contributor.authorUaesoontrachoon, Kitipong
dc.contributor.authorQuinn, James
dc.contributor.authorTatem, Kathleen S
dc.contributor.authorHeier, Christopher
dc.contributor.authorVan Der Meulen, Jack H
dc.contributor.authorYu, Qing
dc.contributor.authorHarris, Mark
dc.contributor.authorNolan, Christopher
dc.contributor.authorHaegeman, Guy
dc.contributor.authorGrounds, Miranda D
dc.contributor.authorNagaraju, Kanneboyina
dc.date.accessioned2015-12-10T22:34:49Z
dc.date.issued2013
dc.date.updated2016-02-24T11:31:57Z
dc.description.abstractThe over-expression of NF-κB signalling in both muscle and immune cells contribute to the pathology in dystrophic muscle. The anti-inflammatory properties of glucocorticoids, mediated predominantly through monomeric glucocorticoid receptor inhibition of
dc.identifier.issn0022-3417
dc.identifier.urihttp://hdl.handle.net/1885/56027
dc.publisherJohn Wiley & Sons Inc
dc.sourceJournal of Pathology
dc.subjectKeywords: atrogin 1; cathepsin B; ccl2 protein; creatine kinase; dystrophin; gamma interferon; glucocorticoid receptor; igf1 protein; immunoglobulin enhancer binding protein; interleukin 12p70; interleukin 6; mstn protein; osteopontin; prednisolone; protein; transc compound A; Duchenne muscular dystrophy; glucocorticoid receptor; glucocorticoids; transrepression NF- ? B
dc.titleSelective modulation through the glucocorticoid receptor ameliorates muscle pathology in mdx mice
dc.typeJournal article
local.bibliographicCitation.issue2
local.bibliographicCitation.lastpage235
local.bibliographicCitation.startpage223
local.contributor.affiliationHuynh, Tony, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationUaesoontrachoon, Kitipong, Children’s National Medical Center
local.contributor.affiliationQuinn, James, Children’s National Medical Center
local.contributor.affiliationTatem, Kathleen S, Children’s National Medical Center
local.contributor.affiliationHeier, Christopher, Children’s National Medical Center
local.contributor.affiliationVan Der Meulen, Jack H, Children’s National Medical Center
local.contributor.affiliationYu, Qing, Children’s National Medical Center
local.contributor.affiliationHarris, Mark, Mater Hospital
local.contributor.affiliationNolan, Christopher, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationHaegeman, Guy, University of Gent
local.contributor.affiliationGrounds, Miranda D, University of Western Australia
local.contributor.affiliationNagaraju, Kanneboyina, Children’s National Medical Center
local.contributor.authoruidHuynh, Tony, u4730735
local.contributor.authoruidNolan, Christopher, u1820721
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor110306 - Endocrinology
local.identifier.ariespublicationu4971216xPUB348
local.identifier.citationvolume231
local.identifier.doi10.1002/path.4231
local.identifier.scopusID2-s2.0-84883888613
local.identifier.thomsonID000324092800009
local.type.statusPublished Version

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