Michael Ho
University of Melbourne
4 Papers
101 Citations
Michael Ho is an academic researcher from University of Melbourne. The author has contributed to research in topics: Amyloid precursor protein & Presenilin. The author has an hindex of 4, co-authored 4 publications.
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Papers
Presenilins Promote the Cellular Uptake of Copper and Zinc and Maintain Copper Chaperone of SOD1-dependent Copper/Zinc Superoxide Dismutase Activity
Mark Greenough,Irene Volitakis,Irene Volitakis,Qiao-Xin Li,Katrina M. Laughton,Genevieve Evin,Michael Ho,Andrew H. Dalziel,James Camakaris,Ashley I. Bush,Ashley I. Bush +10 more
TL;DR: Data indicate that presenilins are important for cellular copper and zinc turnover, influencing SOD1 activity, and having the potential to indirectly impact β-amyloid aggregation through metal ion clearance.
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Paradoxical Condensation of Copper with Elevated β-Amyloid in Lipid Rafts under Cellular Copper Deficiency Conditions IMPLICATIONS FOR ALZHEIMER DISEASE
Ya Hui Hung,Elysia Robb,Irene Volitakis,Michael Ho,Genevieve Evin,Qiao-Xin Li,Janetta G. Culvenor,Colin L. Masters,Colin L. Masters,Robert A. Cherny,Ashley I. Bush +10 more
TL;DR: It is found that copper modulates flotillin-2 association with cholesterol-rich lipid raft domains, and consequently Aβ synthesis is attenuated via copper-mediated inhibition of APP endocytosis, so that under intracellular copper deficiency conditions, Aβ·copper complexes are more likely to form.
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Effect of Metal Chelators on γ-Secretase Indicates That Calcium and Magnesium Ions Facilitate Cleavage of Alzheimer Amyloid Precursor Substrate.
Michael Ho,David E. Hoke,David E. Hoke,Yee Jia Chua,Qiao-Xin Li,Janetta G. Culvenor,Colin L. Masters,Anthony R. White,Genevieve Evin +8 more
TL;DR: Data suggest that Ca2+ and Mg2+ stabilize γ-secretase and enhance its activity and suggest that metal ions play an important role in Aβ aggregation and metabolism, thus metal chelators and ligands represent potential therapeutic agents for AD treatment.
Decreased expression of GGA3 Protein in Alzheimer's disease frontal cortex and increased co-distribution of BACE with the amyloid precursor protein
Claudia Santosa,Stefanie Rasche,Adel Barakat,Shayne A. Bellingham,Michael Ho,Jiang-Li Tan,Andrew F. Hill,Colin L. Masters,Catriona McLean,Genevieve Evin +9 more
TL;DR: Subcellular fractionation of AD cortex with low levels of GGA proteins showed an alteration of BACE distribution and extensive co-localization with APP, suggesting that altered compartmentalization of Bace in AD promotes the amyloidogenic processing of APP.