Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11325
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dc.contributor.authorPang, Tammy P Sen
dc.contributor.authorClarke, Michele Ven
dc.contributor.authorGhasem-Zadeh, Alien
dc.contributor.authorLee, Nicole K Len
dc.contributor.authorDavey, Rachel Aen
dc.contributor.authorMacLean, Helen Een
dc.date.accessioned2015-05-16T00:54:52Z
dc.date.available2015-05-16T00:54:52Z
dc.date.issued2011-08-22en
dc.identifier.citationMolecular and Cellular Endocrinology 2011; 348(1): 189-97en
dc.identifier.govdoc21872641en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11325en
dc.description.abstractWe tested the hypothesis that androgens have physiological actions via non-DNA binding-dependent androgen receptor (AR) signaling pathways in males, using our genetically modified mice that express a mutant AR with deletion of the 2nd zinc finger of the DNA binding domain (AR(ΔZF2)) that cannot bind DNA. In cultured genital skin fibroblasts, the mutant AR(ΔZF2) has normal ligand binding ability, phosphorylates ERK-1/2 in response to 1 min DHT treatment (blocked by the AR antagonist bicalutamide), but has reduced androgen-dependent nuclear localization compared to wildtype (WT). AR(ΔZF2) males have normal baseline ERK-1/2 phosphorylation, with a 1.5-fold increase in Akt phosphorylation in AR(ΔZF2) muscle vs WT. To identify physiological actions of non-DNA binding-dependent AR signaling, AR(ΔZF2) males were treated for 6 weeks with dihydrotestosterone (DHT). Cortical bone growth was suppressed by DHT in AR(ΔZF2) mice (6% decrease in periosteal and 7% decrease in medullary circumference vs untreated AR(ΔZF2) males). In conclusion, these data suggest that non-DNA binding dependent AR actions suppress cortical bone growth, which may provide a mechanism to fine-tune the response to androgens in bone.en
dc.language.isoenen
dc.subject.otherAndrogens.pharmacology.physiologyen
dc.subject.otherAnimalsen
dc.subject.otherCell Nucleus.metabolismen
dc.subject.otherDNA.metabolismen
dc.subject.otherDihydrotestosterone.pharmacologyen
dc.subject.otherFemur.anatomy & histology.drug effects.metabolismen
dc.subject.otherGene Expressionen
dc.subject.otherGene Expression Regulationen
dc.subject.otherKidney.metabolismen
dc.subject.otherMAP Kinase Signaling Systemen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherModels, Biologicalen
dc.subject.otherMuscle, Skeletal.metabolismen
dc.subject.otherOrgan Specificityen
dc.subject.otherProtein Bindingen
dc.subject.otherProtein Transporten
dc.subject.otherReceptors, Androgen.genetics.metabolismen
dc.subject.otherResponse Elementsen
dc.subject.otherSequence Deletionen
dc.subject.otherSubcutaneous Fat.metabolismen
dc.subject.otherTestis.metabolismen
dc.titleA physiological role for androgen actions in the absence of androgen receptor DNA binding activity.en
dc.typeJournal Articleen
dc.identifier.journaltitleMolecular and cellular endocrinologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin Health, Heidelberg, Vic. 3084, Australiaen
dc.identifier.doi10.1016/j.mce.2011.08.017en
dc.description.pages189-97en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/21872641en
dc.type.austinJournal Articleen
local.name.researcherGhasem-Zadeh, Ali
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
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