https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50850 Wed 09 Aug 2023 09:39:07 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43322 Thu 15 Sep 2022 14:43:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30005 Mon 17 Oct 2022 12:06:14 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44716 Fri 21 Oct 2022 09:04:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33850 Fri 18 Jan 2019 14:48:51 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53114 Fri 17 Nov 2023 11:41:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35929 MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated ( > 1.5-fold) and downregulated ( < 0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.]]> Fri 17 Jan 2020 11:35:08 AEDT ]]>