G
Garth J. S. Cooper
Researcher at University of Auckland
Publications - 309
Citations - 17579
Garth J. S. Cooper is an academic researcher from University of Auckland. The author has contributed to research in topics: Amylin & Insulin. The author has an hindex of 63, co-authored 299 publications receiving 16490 citations. Previous affiliations of Garth J. S. Cooper include Manchester Academic Health Science Centre & University of Manchester.
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Journal ArticleDOI
Characterization of proteomic changes in cardiac mitochondria in streptozotocin-diabetic rats using iTRAQ™ isobaric tags
Mia Jüllig,Anthony J. R. Hickey,Martin Middleditch,David J. Crossman,Stanley Chun-Wei Lee,Garth J. S. Cooper +5 more
TL;DR: Proteomic changes in diabetic rat heart mitochondria following 120 days of streptozotocin‐diabetes are reported using the recently developed iTRAQ™ labeling method, which permits quantification of proteins directly from complex mixtures, bypassing the limitations associated with gel‐based methods such as 2‐DE.
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Calcitonin gene-related peptide and somatostatin inhibit insulin release from individual rat B cells.
TL;DR: Somatostatin and calcitonin gene-related peptide, fragment 28-37 were shown to inhibit glucose-stimulated insulin release as assessed by the size of individual plaques and the number of recruited B cells, and hence to reduce the total area of plaques formed, suggesting that these peptides which can be immunolocalised in islet cells may have a role in the regulation of insulin secretion.
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Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington’s Disease
Stefano Patassini,Stefano Patassini,Stefano Patassini,Paul Begley,Jingshu Xu,Stephanie J. Church,Nina Kureishy,Suzanne J. Reid,Henry J. Waldvogel,Richard L.M. Faull,Russell G. Snell,Richard D. Unwin,Garth J. S. Cooper +12 more
TL;DR: C cerebral pantothenate deficiency is a newly-identified metabolic defect in human HD that could potentially impair neuronal CoA biosynthesis; stimulate polyol-pathway activity; impair glycolysis and tricarboxylic acid cycle activity; and modify brain-urea metabolism.
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Role of Ca2+ in apoptosis evoked by human amylin in pancreatic islet beta-cells.
TL;DR: The results suggest that, whereas alterations in cytosolic Ca(2+) homoeostasis do have a significant role in certain forms of beta-cell death, they do not contribute to the pathway of apoptosis evoked by hA in islet beta-cells.
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Proteins associated with immunopurified granules from a model pancreatic islet beta-cell system: proteomic snapshot of an endocrine secretory granule.
Anthony J. R. Hickey,Joshua Bradley,Gretchen L. Skea,Martin Middleditch,Christina M. Buchanan,Anthony R. J. Phillips,Garth J. S. Cooper,Garth J. S. Cooper +7 more
TL;DR: Proteins present in purified granules from the INS-1E beta-cell model identified by LC-MS/MS may increase understanding of granule secretion and the processes leading to protein aggregation and beta- cell death in type-2 diabetes.