https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46784 Wed 30 Nov 2022 13:21:59 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51830 Wed 15 May 2024 15:34:41 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4526 Wed 11 Apr 2018 16:51:00 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25775 Wed 11 Apr 2018 13:20:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9196 Wed 11 Apr 2018 10:54:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14544 Wed 11 Apr 2018 10:15:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4527 Wed 11 Apr 2018 10:09:59 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53700 Wed 10 Jan 2024 10:48:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24126 in vivo use.]]> Wed 09 Mar 2022 15:58:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34679 Trichinella spiralis-infected mice. In contrast, the constitutive HP⁺ MCs in the tongues of mMCP-5-null mice were poorly granulated and lacked mMC-CPA protein. Bone marrow-derived MCs were readily developed from the transgenic mice using IL-3. Although these MCs contained high levels of mMC-CPA mRNA, they also lacked the latter exopeptidase. mMCP-5 protein is therefore needed to target translated mMC-CPA to the secretory granule along with HP-containing serglycin proteoglycans. Alternately, mMCP-5 is needed to protect mMC-CPA from autolysis in the cell's granules. Fibronectin was identified as a target of mMCP-5, and the exocytosis ofmMCP-5from theMCs in the mouse's peritoneal cavity resulted in the expression of metalloproteinase protease-9, which has been implicated in arthritis. In support of the latter finding, experimental arthritis was markedly reduced in mMCP-5-null mice relative to wildtype mice in two disease models.]]> Wed 04 Sep 2019 09:38:57 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17324 Tue 31 Mar 2020 08:15:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35957 Tue 21 Jan 2020 11:08:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42974 Tue 14 May 2024 11:55:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43344 Thu 15 Sep 2022 15:19:01 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35956 Thu 14 May 2020 15:11:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11888 Sat 24 Mar 2018 10:31:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7528 Sat 24 Mar 2018 08:38:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1955 Sat 24 Mar 2018 08:33:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1973 Sat 24 Mar 2018 08:33:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1966 Sat 24 Mar 2018 08:33:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1318 Sat 24 Mar 2018 08:32:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1619 Sat 24 Mar 2018 08:30:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:3111 Sat 24 Mar 2018 08:29:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1215 Sat 24 Mar 2018 08:28:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1185 Sat 24 Mar 2018 08:28:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18116 2+-mediated activation of the anaphase-promoting complex/cyclosome (APC/C). Although the loss in activity of the M-phase kinase CDK1 is known to be an essential downstream event of this process, the contribution of phosphatases to arrest and meiotic resumption is less apparent, especially in mammals. Therefore, we explored the role of protein phosphatase 2A (PP2A) in mouse eggs using pharmacological inhibition and activation as well as a functionally dominant-negative catalytic PP2A subunit (dn-PP2Ac-L199P) coupled with live cell imaging. We observed that PP2A inhibition using okadaic acid induced events normally observed at fertilization: degradation of the APC/C substrates cyclin B1 and securin resulting from loss of the APC/C inhibitor Emi2. Although sister chromatids separated, chromatin remained condensed, and polar body extrusion was blocked as a result of a rapid spindle disruption, which could be ameliorated by non-degradable cyclin B1, suggesting that spindle integrity was affected by CDK1 loss. Similar cell cycle effects to okadaic acid were also observed using dominant-negative PP2Ac. Preincubation of eggs with the PP2A activator FTY720 could block many of the actions of okadaic acid, including Emi2, cyclin B1, and securin degradation and sister chromatid separation. Therefore, in conclusion, we used okadaic acid, dn-PP2Ac-L199P, and FTY720 on mouse eggs to demonstrate that PP2A is needed to for both continued metaphase arrest and successful exit from meiosis.]]> Sat 24 Mar 2018 08:04:35 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17478 −/−-deficient mice. In the caput epididymis of Ido1^−/− animals, the lack of IDO activity was not compensated by other tryptophan-catabolizing enzymes and led to the loss of kynurenine production. The absence of IDO generated an inflammatory state in the caput epididymis as revealed by an increased accumulation of various inflammation markers. The absence of IDO also increased the tryptophan content of the caput epididymis and generated a parallel increase in caput epididymal protein content as a consequence of deficient proteasomal activity. Surprisingly, the lack of IDO expression had no noticeable impact on overall male fertility but did induce highly significant increases in both the number and the percentage of abnormal spermatozoa. These changes coincided with a significant decrease in white blood cell count in epididymal fluid compared with wild type mice. These data provide support for IDO playing a hitherto unsuspected role in sperm quality control in the epididymis involving the ubiquitination of defective spermatozoa and their subsequent removal.]]> Sat 24 Mar 2018 08:04:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20434 −/− C57BL/6 mouse line. The resulting animals exhibited no obvious developmental abnormality, contained normal numbers of granulated MCs in their tissues, and did not compensate for their loss of the membrane tryptase by increasing their expression of other granule proteases. When Prss31-null MCs were activated with a calcium ionophore or by their high affinity IgE receptors, they degranulated in a pattern similar to that of WT MCs. Prss31-null mice had increased baseline airway reactivity to methacholine but markedly reduced experimental chronic obstructive pulmonary disease and colitis, thereby indicating both beneficial and adverse functional roles for the tryptase. In a cigarette smoke-induced model of chronic obstructive pulmonary disease, WT mice had more pulmonary macrophages, higher histopathology scores, and more fibrosis in their small airways than similarly treated Prss31-null mice. In a dextran sodium sulfate-induced acute colitis model, WT mice lost more weight, had higher histopathology scores, and contained more Cxcl-2 and IL-6 mRNA in their colons than similarly treated Prss31-null mice. The accumulated data raise the possibility that inhibitors of this membrane tryptase may provide additional therapeutic benefit in the treatment of humans with these MC-dependent inflammatory diseases.]]> Sat 24 Mar 2018 08:03:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17423 TM, was sufficient to abolish BoNT/A-Hc internalization and BoNT/A-induced SNAP25 cleavage in hippocampal neurons. Dyngo-4a also interfered with BoNT/A-Hc internalization into motor nerve terminals. Furthermore, Dyngo-4a afforded protection against BoNT/A-induced paralysis at the rat hemidiaphragm. A significant delay of >30% in the onset of botulism was observed in mice injected with Dyngo-4a. Dynamin inhibition therefore provides a therapeutic avenue for the treatment of botulism and other diseases caused by pathogens sharing dynamin-dependent uptake mechanisms.]]> Sat 24 Mar 2018 08:01:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17419 Sat 24 Mar 2018 08:01:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17727 − ion conductance). Pharmacological analyses in vitro and in vivo determined that elevated Cl⁻ conductance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activity. Generation of iIL-13Tg/Il13rα1^−/−, iIL-13Tg/Il13rα2^−/−, and iIL-13Tg/Stat6^−/− mice revealed that IL-13-mediated dysregulation of epithelial architecture and Cl⁻ conductance is dependent on IL-13Rα1 and STAT-6. These observations demonstrate a central role for the IL-13/IL-13Rα1 pathway in the regulation of intestinal epithelial cell Cl⁻ secretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an important role for this pathway in secretory diarrhea.]]> Sat 24 Mar 2018 07:57:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17894 Sat 24 Mar 2018 07:56:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20674 Sat 24 Mar 2018 07:55:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20150 Sat 24 Mar 2018 07:51:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6541 Sat 24 Mar 2018 07:48:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28878 Sat 24 Mar 2018 07:40:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:3411 Sat 24 Mar 2018 07:21:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:3455 Sat 24 Mar 2018 07:20:30 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:22251 NTR and the sortilin receptor. Herein, it is shown that proNGF is produced and secreted by breast cancer cells, stimulating their invasion. Using Western blotting and mass spectrometry, proNGF was detected in a panel of breast cancer cells as well as in their conditioned media. Immunohistochemical analysis indicated an overproduction of proNGF in breast tumors, when compared with benign and normal breast biopsies, and a relationship to lymph node invasion in ductal carcinomas. Interestingly, siRNA against proNGF induced a decrease of breast cancer cell invasion that was restored by the addition of non-cleavable proNGF. The activation of TrkA, Akt, and Src, but not the MAP kinases, was observed. In addition, the proNGF invasive effect was inhibited by the Trk pharmacological inhibitor K252a, a kinase-dead TrkA, and siRNA against TrkA sortilin, neurotensin, whereas siRNA against p75^NTR and the MAP kinase inhibitor PD98059 had no impact. These data reveal the existence of an autocrine loop stimulated by proNGF and mediated by TrkA and sortilin, with the activation of Akt and Src, for the stimulation of breast cancer cell invasion.]]> Sat 24 Mar 2018 07:17:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24820 Arabidopsis thaliana produce defects in leaf polarity and shoot apical meristem organization. Although the miR394-LCR node has been documented in Arabidopsis, the identification of proteins targeted by LCR F-box itself has proven problematic. Here, a proteomic analysis of shoot apices from plants with altered LCR levels identified a member of the Latex Protein (MLP) family gene as a potential LCR F-box target. Bioinformatic and molecular analyses also suggested that other MLP family members are likely to be targets for this post-translational regulation. Direct interaction between LCR F-Box and MLP423 was validated. Additional MLP members had reduction in protein accumulation, in varying degrees, mediated by LCR F-Box. Transgenic Arabidopsis lines, in which MLP28 expression was reduced through an artificial miRNA technology, displayed severe developmental defects, including changes in leaf patterning and morphology, shoot apex defects, and eventual premature death. These phenotypic characteristics resemble those of Arabidopsis plants modified to over-express LCR. Taken together, the results demonstrate that MLPs are driven to degradation by LCR, and indicate that MLP gene family is target of miR394-LCR regulatory node, representing potential targets for directly post-translational regulation mediated by LCR F-Box. In addition, MLP28 family member is associated with the LCR regulation that is critical for normal Arabidopsis development.]]> Sat 24 Mar 2018 07:15:12 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22207 R²= 0.89) in untreated populations of human spermatozoa emphasized the pathophysiological significance of these findings. The latter also provide a biochemical explanation for the self-perpetuating nature of oxidative stress in the male germ line, with the products of lipid peroxidation stimulating free radical generation by the sperm mitochondria in a positive feedback loop.]]> Sat 24 Mar 2018 07:11:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42360 Mon 22 Aug 2022 14:01:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17322 Mon 06 Apr 2020 12:14:32 AEST ]]>