https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29220 Wed 19 Jan 2022 15:15:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21727 EL by protein phosphatase 2A (PP2A). However, melanoma cells are largely resistant to ER stress-induced apoptosis, suggesting that Bim activation is suppressed in melanoma cells undergoing ER stress. We show here that ER stress reduces PP2A activity leading to increased ERK activation and subsequent phosphorylation and proteasomal degradation of Bim_EL. Despite sustained upregulation of Bim at the transcriptional level, the Bim_EL protein expression was downregulated after an initial increase in melanoma cells subjected to pharmacological ER stress. This was mediated by increased activity of ERK, whereas the phosphatase activity of PP2A was reduced by ER stress in melanoma cells. The increase in ERK activation was, at least in part, due to reduced dephosphorylation by PP2A, which was associated with downregulation of the PP2A catalytic C subunit. Notably, instead of direct dephosphorylation of Bim_EL, PP2A inhibited its phosphorylation indirectly through dephosphorylation of ERK in melanoma cells. Taken together, these results identify downregualtion of PP2A activity as an important protective mechanism of melanoma cells against ER stress-induced apoptosis.]]> Wed 11 Apr 2018 17:12:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20054 c. By contrast, the main source of CD36+MPs in non-T2DM individuals was endothelial cells (CD105+=40.9±8.3% and 33.9±8.3% for lean and obese controls, respectively). Across the entire cohort, plasma CD36 protein concentration varied from undetectable to 22.9 μg ml⁻¹ and was positively correlated with CD36+MPs measured by flow cytometry (P=0.0006) but only weakly associated with the distribution of controls and T2DM (P=0.021). Multivariate analysis confirmed that plasma CD36+MP levels were a much better biomarker for diabetes than CD36 protein concentration (P=0.009 vs P=0.398, respectively). Conclusions: Both the levels and cellular profile of CD36+MPs differ in T2DM compared with controls, suggesting that these specific vesicles could represent distinct biological vectors contributing to the pathology of the disease.]]> Wed 11 Apr 2018 16:13:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9178 Wed 11 Apr 2018 15:35:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9452 Wed 11 Apr 2018 14:22:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17258 Wed 11 Apr 2018 11:05:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30753 Thu 03 Feb 2022 12:21:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1017 Sat 24 Mar 2018 08:29:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13253 Sat 24 Mar 2018 08:15:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10550 Sat 24 Mar 2018 08:10:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17732 Sat 24 Mar 2018 07:57:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25886 Sat 24 Mar 2018 07:25:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23615 Sat 24 Mar 2018 07:13:28 AEDT ]]>