| Field |
Value |
Language |
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dc.contributor.author |
Camaya, I |
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dc.contributor.author |
Hill, M |
|
|
dc.contributor.author |
Sais, D
https://orcid.org/0000-0002-5859-1398
|
|
|
dc.contributor.author |
Tran, N
https://orcid.org/0000-0001-7747-2530
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|
dc.contributor.author |
O'Brien, B
https://orcid.org/0000-0001-5887-2424
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|
dc.contributor.author |
Donnelly, S
https://orcid.org/0000-0003-2005-3698
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dc.contributor.editor |
Sugawara, A |
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dc.date.accessioned |
2024-08-06T03:53:14Z |
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dc.date.available |
2024-06-13 |
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dc.date.available |
2024-08-06T03:53:14Z |
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dc.date.issued |
2024 |
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dc.identifier.citation |
J Diabetes Res, 2024, 2024, (1), pp. 8555211 |
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dc.identifier.issn |
2314-6745 |
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dc.identifier.issn |
2314-6753 |
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dc.identifier.uri |
http://hdl.handle.net/10453/180173
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dc.description.abstract |
We have previously identified a parasite-derived peptide, FhHDM-1, that prevented the progression of diabetes in nonobese diabetic (NOD) mice. Disease prevention was mediated by the activation of the PI3K/Akt pathway to promote β-cell survival and metabolism without inducing proliferation. To determine the molecular mechanisms driving the antidiabetogenic effects of FhHDM-1, miRNA:mRNA interactions and in silico predictions of the gene networks were characterised in β-cells, which were exposed to the proinflammatory cytokines that mediate β-cell destruction in Type 1 diabetes (T1D), in the presence and absence of FhHDM-1. The predicted gene targets of miRNAs differentially regulated by FhHDM-1 mapped to the biological pathways that regulate β-cell biology. Six miRNAs were identified as important nodes in the regulation of PI3K/Akt signaling. Additionally, IGF-2 was identified as a miRNA gene target that mediated the beneficial effects of FhHDM-1 on β-cells. The findings provide a putative mechanism by which FhHDM-1 positively impacts β-cells to permanently prevent diabetes. As β-cell death/dysfunction underlies diabetes development, FhHDM-1 opens new therapeutic avenues. |
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dc.format |
Electronic-eCollection |
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dc.language |
eng |
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dc.publisher |
HINDAWI LTD |
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dc.relation.ispartof |
J Diabetes Res |
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dc.relation.isbasedon |
10.1155/2024/8555211 |
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dc.rights |
info:eu-repo/semantics/openAccess |
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dc.subject |
1116 Medical Physiology |
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dc.subject.classification |
3202 Clinical sciences |
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|
dc.subject.mesh |
MicroRNAs |
|
|
dc.subject.mesh |
Animals |
|
|
dc.subject.mesh |
Insulin-Secreting Cells |
|
|
dc.subject.mesh |
Apoptosis |
|
|
dc.subject.mesh |
Signal Transduction |
|
|
dc.subject.mesh |
Cytokines |
|
|
dc.subject.mesh |
Mice |
|
|
dc.subject.mesh |
Mice, Inbred NOD |
|
|
dc.subject.mesh |
Phosphatidylinositol 3-Kinases |
|
|
dc.subject.mesh |
Proto-Oncogene Proteins c-akt |
|
|
dc.subject.mesh |
Diabetes Mellitus, Type 1 |
|
|
dc.subject.mesh |
Gene Expression Regulation |
|
|
dc.subject.mesh |
Animals |
|
|
dc.subject.mesh |
Mice, Inbred NOD |
|
|
dc.subject.mesh |
Mice |
|
|
dc.subject.mesh |
Diabetes Mellitus, Type 1 |
|
|
dc.subject.mesh |
MicroRNAs |
|
|
dc.subject.mesh |
Cytokines |
|
|
dc.subject.mesh |
Signal Transduction |
|
|
dc.subject.mesh |
Apoptosis |
|
|
dc.subject.mesh |
Gene Expression Regulation |
|
|
dc.subject.mesh |
Insulin-Secreting Cells |
|
|
dc.subject.mesh |
Proto-Oncogene Proteins c-akt |
|
|
dc.subject.mesh |
Phosphatidylinositol 3-Kinases |
|
|
dc.subject.mesh |
MicroRNAs |
|
|
dc.subject.mesh |
Animals |
|
|
dc.subject.mesh |
Insulin-Secreting Cells |
|
|
dc.subject.mesh |
Apoptosis |
|
|
dc.subject.mesh |
Signal Transduction |
|
|
dc.subject.mesh |
Cytokines |
|
|
dc.subject.mesh |
Mice |
|
|
dc.subject.mesh |
Mice, Inbred NOD |
|
|
dc.subject.mesh |
Phosphatidylinositol 3-Kinases |
|
|
dc.subject.mesh |
Proto-Oncogene Proteins c-akt |
|
|
dc.subject.mesh |
Diabetes Mellitus, Type 1 |
|
|
dc.subject.mesh |
Gene Expression Regulation |
|
|
dc.title |
The Parasite-Derived Peptide, FhHDM-1, Selectively Modulates miRNA Expression in β-Cells to Prevent Apoptotic Pathways Induced by Proinflammatory Cytokines. |
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dc.type |
Journal Article |
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utslib.citation.volume |
2024 |
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utslib.location.activity |
England |
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utslib.for |
1116 Medical Physiology |
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pubs.organisational-group |
University of Technology Sydney |
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|
pubs.organisational-group |
University of Technology Sydney/Faculty of Engineering and Information Technology |
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pubs.organisational-group |
University of Technology Sydney/Faculty of Science |
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pubs.organisational-group |
University of Technology Sydney/Strength - CHT - Health Technologies |
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pubs.organisational-group |
University of Technology Sydney/Faculty of Science/School of Life Sciences |
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|
pubs.organisational-group |
University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering |
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pubs.organisational-group |
University of Technology Sydney/All Manual Groups |
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|
pubs.organisational-group |
University of Technology Sydney/All Manual Groups/Centre for Health Technologies (CHT) |
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utslib.copyright.status |
open_access |
* |
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dc.rights.license |
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ |
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dc.date.updated |
2024-08-06T03:53:09Z |
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pubs.issue |
1 |
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pubs.publication-status |
Published online |
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|
pubs.volume |
2024 |
|
|
utslib.citation.issue |
1 |
|
