https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46767 HIST1H3B/C and H3F3A), altering the epigenetic landscape of primitive oligodendrocyte or astrocyte precursor cells of the pontine region of the brainstem. Lysine‐to‐methionine point mutations at amino acid 27 (H3K27M) co‐occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR/KIT/VEGFR/MET/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K/AKT/mTOR), cyclin‐dependent kinases (CDKs1/4/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN/TP53). This cooperation drives gene expression signatures that inhibit cellular differentiation (ID1/2, Hedgehog) and promotes malignant transformation. Unique to DIPG, is the frequency of co‐occurring sets of genomic insults. However, mapping of the oncogenic signaling pathways activated in response to recurring mutations is unresolved. Herein, known oncogenic signal pathways activated in response to recurring somatic mutations and gene amplifications in DIPG are reviewed. Additionally, an important role for high‐resolution quantitative proteomics/phosphoproteomics in the characterization of signaling cascades are highlighted. These regulate the cell cycle, epigenetics and anti‐apoptotic processes, information critical for the development of improved treatment strategies for DIPG.]]> Wed 30 Nov 2022 11:45:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19659 Wed 27 Jul 2022 13:52:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53345 Wed 22 Nov 2023 10:19:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48596 Wed 22 Mar 2023 08:46:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54801 Wed 13 Mar 2024 11:41:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42381 Wed 13 Mar 2024 09:40:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13745 Wed 11 Apr 2018 16:02:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16473 Wed 11 Apr 2018 15:33:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27600 Wed 11 Apr 2018 14:31:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11905 Wed 11 Apr 2018 10:56:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23271 Wed 11 Apr 2018 10:32:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18017 Wed 11 Apr 2018 09:35:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54081 Wed 06 Mar 2024 14:35:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39125 p-value thresholds by summing methylation beta-values weighted by individual-CpG effect sizes from the meta-analysis of a previously published schizophrenia EWAS (comprising three separate cohorts with 675 [353 SZ and 322 HC] discovery cohort participants, 847 [414 SZ and 433 HC] replication cohort participants, and 96 monozygotic twin-pairs discordant for SZ). All SZ PMPSs were elevated in SZ participants relative to HCs, with the score calculated at a p-value threshold of 1 x 10⁻⁵ accounting for the greatest amount of variance. All PMPSs were elevated in SZ relative to BD and none of the PMPSs were increased in BD, or in a combined cohort of BD and SZ cases, relative to HCs. PMPSs were also not associated with positive or negative symptom severity. That this SZ-derived PMPSs was elevated in SZ, but not BD, suggests that epigenome-wide methylation patterns may represent distinct pathophysiology that is yet to be elucidated.]]> Wed 01 May 2024 12:58:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33632 Tue 27 Nov 2018 16:39:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54524 Tue 27 Feb 2024 19:29:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32623 Tue 26 Jun 2018 11:28:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21455 PR gene and (ii) identified the histone-modifying enzymes that target the H3K4me3 mark at the PR promoters in term and preterm human myometrial tissues obtained before and after labour onset. Bisulphite sequencing showed that despite overall low levels of PR CpG island methylation, there was a significant decrease in methylated CpGs with labour in both preterm (P < 0.05) and term (P < 0.01) groups downstream of the PR-B transcription start site. This methylation change was not associated with altered PR-B expression, but may contribute to the increase in PR-A expression with labour. Chromatin immunoprecipitation revealed that the histone methyltransferase, SET and MYND domain-containing protein 3 (SMYD3), bound to the PR gene at significantly higher levels at the PR-A promoter compared with the PR-B promoter (P < 0.010), with no labour-associated changes observed. The H3K4 demethylase, Jumonji AT-rich interactive domain 1A (JARID1A), also bound to the PR-A, but not to the PR-B promoter prior to term labour, and decreased significantly at the onset of labour (P = 0.014), providing a mechanism for the previously reported increase in H3K4me3 level and PR-A expression with labour. Our studies suggest that epigenetic changes mediated by JARID1A, SMYD3 and DNA methylation may be responsible, at least in part, for the functional progesterone withdrawal that precipitates human labour.]]> Tue 24 Apr 2018 11:46:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54378 Tue 20 Feb 2024 20:24:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44611 Tue 18 Oct 2022 08:44:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52573 Tue 17 Oct 2023 15:48:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53822 Tue 16 Jan 2024 15:19:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47078 Tue 13 Dec 2022 16:28:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51636 Tue 12 Sep 2023 20:14:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50245 Tue 11 Jul 2023 12:10:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45586 Tue 08 Nov 2022 15:02:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45857 p level: 1.06 × 10^-7), that were associated with maternal smoking during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), CYP1A1 (detoxification), MYO1G (cell signalling) and FRMD4A (nicotine dependence). A sensitivity analysis showed a dose dependent relationship between maternal smoking and offspring methylation. These results changed little following adjustment for paternal, passive or offspring smoking and there were no CpGs identified that associated with these variables. Two of the 23 identified CpGs (cg00253568 (FTO) and cg00213123 (CYP1A1)) were associated with either TG (males and females), diastolic blood pressure (females only) or HDL-C (males only), after Bonferroni correction. Discussion: This study demonstrates a critical timing of cigarette smoke exposure over the life-course for establishing persistent changes in DNA methylation into adolescence in a dose dependent manner. There were significant associations between offspring CpG methylation and adolescent cardiovascular risk factors, namely TG, HDL-C and diastolic blood pressure. Future studies on current smoking habits and DNA methylation should consider the importance of maternal smoking during pregnancy and explore how the persistent DNA methylation effects of in utero smoke exposure increase cardiometabolic risk.]]> Tue 08 Nov 2022 08:25:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53494 Thu 30 Nov 2023 15:44:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39670 Thu 28 Jul 2022 08:10:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51627 Thu 23 Nov 2023 14:26:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45991 Thu 10 Nov 2022 10:14:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30829 Thu 09 Dec 2021 11:04:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9702 Sat 24 Mar 2018 08:34:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7268 Sat 24 Mar 2018 08:33:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20202 Sat 24 Mar 2018 08:06:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21387 Catechol-O-methyltransferase (COMT) Val¹⁵⁸Met polymorphism, a common genetic variant known to affect cognition and prefrontal dopamine levels. Participants were 429 schizophrenia/schizoaffective cases from the Australian Schizophrenia Research Bank (ASRB). Cognitive performance was assessed using the Repeatable Battery for Assessment of Neuropsychological Status (RBANS), Controlled Oral Word Association Test (COWAT), Letter Number Sequencing (LNS) test, and the Wechsler Test of Adult Reading (WTAR). Hierarchical regression was used to test the main effects and additive interaction effects of genotype and childhood trauma in the domains of physical abuse, emotional abuse, and emotional neglect, on cognition and symptom profiles of clinical cases. Consistent with previous findings, COMT Val homozygotes performed worse on cognitive measures in the absence of childhood adversity. In addition, a significant interaction between COMT genotype and physical abuse was associated with better executive function in Val homozygotes, relative to those of the same genotype with no history of abuse. Finally, the severity of positive symptoms was greater in Met carriers who had experienced physical abuse, and the severity of negative symptoms in Met carriers was greater in the presence of emotional neglect. These results suggest that the possible epigenetic modulation of the expression of the COMT Val¹⁵⁸Met polymorphism and consequent effects on cognition and symptoms in schizophrenia, with worse outcomes associated with adverse childhood experiences in Met carriers.]]> Sat 24 Mar 2018 08:05:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21346 Sat 24 Mar 2018 07:51:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29000 Sat 24 Mar 2018 07:41:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29322 Sat 24 Mar 2018 07:34:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27253 Sat 24 Mar 2018 07:29:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22021 Mon 24 Sep 2018 13:40:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33803 Mon 23 Sep 2019 13:59:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32020 Mon 23 Sep 2019 12:12:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42366 Mon 22 Aug 2022 14:08:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49910 Mon 19 Jun 2023 11:07:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52306 Mon 09 Oct 2023 10:16:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38008 Fri 23 Jul 2021 15:13:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44510 Fri 14 Oct 2022 09:11:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48913 Fri 14 Apr 2023 18:21:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52991 Fri 03 Nov 2023 16:05:35 AEDT ]]>