https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42661 Wed 31 Aug 2022 13:44:21 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:50844 Wed 09 Aug 2023 09:17:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43489 Tue 20 Sep 2022 12:12:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54704 Thu 28 Mar 2024 11:39:12 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:35094 Thu 20 Jun 2019 15:56:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36692 Thu 13 Jan 2022 10:31:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47931 Thu 09 Feb 2023 12:55:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37125 Thu 03 Feb 2022 12:20:01 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21233 P < 5 × 10⁻⁸) with FVC in or near EFEMP1, BMP6, MIR129-2–HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease.]]> Sat 24 Mar 2018 07:53:01 AEDT ]]>