https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37515 Wed 23 Aug 2023 09:36:21 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37757 ARF in human and p19^ARF in mouse) that binds to and inhibits mouse double minute 2 homolog (MDM2) leading to p53 activation, whereas p53 suppresses c-Myc through a combination of mechanisms involving transcriptional inactivation and microRNA-mediated repression. Nonetheless, the regulatory interactions between c-Myc and p53 are not retained by cancer cells as is evident from the often-imbalanced expression of c-Myc over wildtype p53. Although p53 repression in cancer cells is frequently associated with the loss of ARF, we disclose here an alternate mechanism whereby c-Myc inactivates p53 through the actions of the c-Myc-Inducible Long noncoding RNA Inactivating P53 (MILIP). MILIP functions to promote p53 polyubiquitination and turnover by reducing p53 SUMOylation through suppressing tripartite-motif family-like 2 (TRIML2). MILIP upregulation is observed amongst diverse cancer types and is shown to support cell survival, division and tumourigenicity. Thus our results uncover an inhibitory axis targeting p53 through a pan-cancer expressed RNA accomplice that links c-Myc to suppression of p53.]]> Wed 17 Nov 2021 16:28:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32982 Wed 17 Nov 2021 16:28:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50273 Wed 12 Jul 2023 14:18:12 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52417 Wed 11 Oct 2023 11:58:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10319 Wed 11 Apr 2018 16:15:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18837 Wed 11 Apr 2018 15:08:53 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12729 Wed 11 Apr 2018 15:05:34 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26195 Wed 11 Apr 2018 15:00:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20844 TP53INP1 was found to be one of the genes most significantly repressed by HDAC2 and N-Myc according to Affymetrix microarray gene expression datasets. HDAC2 and N-Myc reduced TP53INP1 gene expression by direct binding to the TP53INP1 gene promoter, leading to transcriptional repression of TP53INP1, p53 protein de-phosphorylation at serine 46, neuroblastoma cell proliferation and survival. Moreover, low levels of TP53INP1 expression in human neuroblastoma tissues correlated with high levels of N-Myc expression and poor patient outcome, and the BET bromodomain inhibitors JQ1 and I-BET151 reduced N-Myc expression and reactivated TP53INP1 expression in neuroblastoma cells. These findings identify TP53INP1 repression as an important co-factor for N-Myc oncogenesis, and provide further evidence for the potential application of BET bromodomain inhibitors in the therapy of N-Myc-induced neuroblastoma.]]> Wed 11 Apr 2018 13:01:58 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14353 Wed 11 Apr 2018 11:50:58 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15100 Wed 11 Apr 2018 11:36:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22865 Wed 11 Apr 2018 09:31:09 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48318 Tue 14 Mar 2023 15:37:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32680 Tue 10 Jul 2018 15:38:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35745 chromosome 9 open reading frame 3 gene that was transcriptionally activated by p53. Similarly, the host gene of miRNA-455-3p, collagen alpha-1 (XXVII) chain, was also a p53 transcriptional target. Collectively, our results identify miRNA-27b-3p and miRNA-455-3p as important regulators of cancer cell quiescence in response to p53 and suggest that manipulating miRNA-27b-3p and miRNA-455-3p may constitute novel therapeutic avenues for improving outcomes of cancer treatment. Significance: Two novel p53-responsive microRNAs whose distinct mechanisms of action both stabilize p27 to promote cell quiescence and may serve as therapeutic avenues for improving outcomes of cancer treatment.]]> Thu 28 Oct 2021 12:36:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45318 Thu 27 Oct 2022 13:56:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37758 regenerating islet-derived (REG) gene family are important regulators of many cellular processes. Here we functionally characterise a non-protein coding product of the family, the long noncoding RNA (lncRNA) REG1CP that is transcribed from a DNA fragment at the family locus previously thought to be a pseudogene. REG1CP forms an RNA–DNA triplex with a homopurine stretch at the distal promoter of the REG3A gene, through which the DNA helicase FANCJ is tethered to the core promoter of REG3A where it unwinds double stranded DNA and facilitates a permissive state for glucocorticoid receptor α (GRα)-mediated REG3A transcription. As such, REG1CP promotes cancer cell proliferation and tumorigenicity and its upregulation is associated with poor outcome of patients. REG1CP is also transcriptionally inducible by GRα, indicative of feedforward regulation. These results reveal the function and regulation of REG1CP and suggest that REG1CP may constitute a target for cancer treatment.]]> Thu 27 Jan 2022 15:55:02 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33114 Thu 24 Mar 2022 11:29:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27851 Thu 17 Mar 2022 14:39:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34713 2.5) has been linked to increased stroke. Few studies, however, have examined the effects of long-term exposure. Methods: A total of 45 625 participants were interviewed and included in this study, the participants came from the Study on Global Ageing and Adult Health, a prospective cohort in 6 low- and middle-income countries. Ambient PM_2.5 levels were estimated for participants' communities using satellite data. A multilevel logistic regression model was used to examine the association between long-term PM_2.5 exposure and stroke. Potential effect modification by physical activity and consumption of fruit and vegetables was assessed. Results: The odds of stroke were 1.13 (95% confidence interval, 1.04-1.22) for each 10 µg/m³ increase in PM_2.5. This effect remained after adjustment for confounding factors including age, sex, smoking, and indoor air pollution (adjusted odds ratio=1.12; 95% confidence interval, 1.04-1.21). Further stratified analyses suggested that participants with higher levels of physical activity had greater odds of stroke, whereas those with higher consumption of fruit and vegetables had lower odds of stroke. These effects remained robust in sensitivity analyses. We further estimated that 6.55% (95% confidence interval, 1.97%-12.01%) of the stroke cases could be attributable to ambient PM_2.5 in the study population. Conclusions: This study suggests that ambient PM_2.5 may increase the risk of stroke and may be responsible for the astounding stroke burden in low- and middle-income countries. In addition, greater physical activity may enhance, whereas greater consumption of fruit and vegetables may mitigate the effect.]]> Thu 04 Nov 2021 10:40:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31488 Sat 24 Mar 2018 08:43:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10285 Sat 24 Mar 2018 08:09:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20754 Sat 24 Mar 2018 08:00:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17996 Sat 24 Mar 2018 07:56:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26799 Sat 24 Mar 2018 07:36:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22195 Sat 24 Mar 2018 07:16:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52505 Mon 16 Oct 2023 10:10:51 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55358 Fri 17 May 2024 16:04:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49407 Fri 12 May 2023 14:55:16 AEST ]]>