https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54520 5% O2. Through the generation of a germline-specific Epas1 knockout mouse line, and through modulation of EPAS1 levels in primary cultures of spermatogonia with the small drug molecule Daprodustat, we have demonstrated that EPAS1 is required for robust SSC function in regenerative conditions (post-transplantation and post-chemotherapy), via the regulation of key cellular processes such as metabolism. These findings shed light on the relationship between hypoxia and male fertility and will potentially facilitate optimization of in vitro culture conditions for infertility treatment pipelines using SSCs, such as those directed at pediatric cancer survivors.]]> Wed 28 Feb 2024 16:12:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47000 Wed 26 Jul 2023 09:22:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24909 Wed 12 Aug 2020 09:08:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22037 Wed 11 Apr 2018 14:21:26 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47613 Tue 24 Jan 2023 11:43:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51622 Tue 12 Sep 2023 14:30:56 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39106 Tue 10 May 2022 09:39:30 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36571 Tue 09 Jun 2020 11:40:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44824 Thu 27 Oct 2022 12:44:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45372 Chd4 expression significantly impairs SSC regenerative capacity, causing a ∼50% reduction in colonization of recipient testes. An scRNA-seq comparison revealed reduced expression of “self-renewal” genes following Chd4 knockdown, along with increased expression of signature progenitor genes. Co-immunoprecipitation analyses demonstrated that CHD4 regulates gene expression in spermatogonia not only through its traditional association with the remodeling complex NuRD, but also via interaction with the GDNF-responsive transcription factor SALL4. Cumulatively, the results of this study depict a previously unappreciated role for CHD4 in controlling fate decisions in the spermatogonial pool.]]> Thu 27 Oct 2022 12:14:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20252 Sat 24 Mar 2018 07:59:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19945 Sat 24 Mar 2018 07:58:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27766 Sat 24 Mar 2018 07:40:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26581 Sat 24 Mar 2018 07:26:12 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22263 in vitro induction of acrosomal exocytosis by progesterone, but not by the calcium ionophore A23187, and elicited a concomitant reduction of in vitro fertilization. In vivo treatment with these inhibitors also resulted in spermatozoa displaying reduced acrosome reaction potential. Dynamin 1 and 2 phosphorylation increased on progesterone treatment, and this was also selectively blocked by dynasore. On the basis of our collective data, we propose that dynamin could regulate specific membrane fusion events necessary for acrosomal exocytosis in mouse spermatozoa.]]> Sat 24 Mar 2018 07:17:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51259 Mon 28 Aug 2023 13:50:03 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32871 in vitro fertilisation, though displayed reduced developmental competence beyond the 2-cell stage (P=0.02). To account for these findings, we analysed the efficacy of DSB resolution, revealing a significant reduction in DSB lesions 4 h post-ETP treatment. Notably, this response was completely abrogated by pharmacological inhibition of key elements (DNA-PKcs and DNA ligase IV) of the canonical non-homologous end joining DNA repair pathway, thus providing the first evidence implicating this reparative cascade in the protection of the maternal genome.]]> Mon 23 Sep 2019 10:15:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40758 Mon 18 Jul 2022 13:54:17 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51228 Fri 25 Aug 2023 11:51:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49362 Fri 12 May 2023 12:35:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46098 Fri 11 Nov 2022 11:26:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55287 Fri 10 May 2024 16:22:11 AEST ]]>