https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Endoplasmic reticulum stress enhances the expression of TLR3-induced TSLP by airway epithelium https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55346 Wed 22 May 2024 12:26:00 AEST ]]> Implication of unfolded protein response and autophagy in the treatment of BRAF inhibitor resistant melanoma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28828 V600E mutation, is one of the key alterations in melanoma. Accordingly, two BRAF inhibitors (BRAFi), vemurafenib and dabrafenib are utilized to treat melanoma and resulted in an excellent clinical outcome. However, the clinical success is not long-lasting, and the BRAFi resistance and disease progression inevitably occurs in nearly all patients. Endoplasmic reticulum stress-induced unfolded protein response and autophagy have emerged as potential pro-survival mechanisms adopted by melanoma cells in response to BRAFi. In this review, we discuss the role of unfolded protein response and autophagy that are implicated in the development of BRAFi-resistant melanoma and the corresponding strategy aiming at overcoming the intractable clinical problem.]]> Wed 19 Jan 2022 15:18:22 AEDT ]]> Suppression of PP2A is critical for protection of melanoma cells upon endoplasmic reticulum stress 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 BimEL. Despite sustained upregulation of Bim at the transcriptional level, the BimEL 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 BimEL, 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 ]]> Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2753 Wed 11 Apr 2018 13:06:05 AEST ]]> Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14172 Wed 11 Apr 2018 11:56:01 AEST ]]> Adaptation to ER stress as a driver of malignancy and resistance to therapy in human melanoma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5430 Wed 11 Apr 2018 09:25:36 AEST ]]> Inhibition of MEK blocks GRP78 up-regulation and enhances apoptosis induced by ER stress in gastric cancer cells https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7349 Sat 24 Mar 2018 08:40:16 AEDT ]]> Involvement of endoplasmic reticulum stress in docetaxel-induced JNK-dependent apoptosis of human melanoma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5394 Sat 24 Mar 2018 07:43:57 AEDT ]]> Endoplasmic reticulum stress and the unfolded protein response in the pathogenesis of asthma https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35877 Mon 09 Sep 2024 19:50:03 AEST ]]>