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Anthony O. Fedele
Researcher at South Australia Pathology
Publications - 12
Citations - 654
Anthony O. Fedele is an academic researcher from South Australia Pathology. The author has contributed to research in topics: Transactivation & Lysosome. The author has an hindex of 9, co-authored 12 publications receiving 543 citations. Previous affiliations of Anthony O. Fedele include University of Adelaide & Australian Research Council.
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Journal ArticleDOI
Lysosomal fusion and SNARE function are impaired by cholesterol accumulation in lysosomal storage disorders.
Alessandro Fraldi,Fabio Annunziata,Alessia Lombardi,Hermann-Josef Kaiser,Diego L. Medina,Carmine Spampanato,Anthony O. Fedele,Roman S. Polishchuk,Nicolina Cristina Sorrentino,Kai Simons,Andrea Ballabio +10 more
TL;DR: The results support a model by which cholesterol abnormalities determine lysosomal dysfunction and endocytic traffic jam in LSDs by impairing the membrane fusion machinery, thus suggesting new therapeutic targets for the treatment of these disorders.
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Cell-specific regulation of hypoxia-inducible factor (HIF)-1α and HIF-2α stabilization and transactivation in a graded oxygen environment
Cameron P. Bracken,Anthony O. Fedele,Sarah Linke,Wiltiana Balrak,Karolina Lisy,Murray L. Whitelaw,Daniel J. Peet +6 more
TL;DR: A conserved amino acid substitution between Hif-1α and HIF-2α is characterized that contributes to the intrinsically higher FIH-1-mediated asparaginyl hydroxylation of H IF-1 α and, hence, lower HIF -1α activity.
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Regulation of gene expression by the hypoxia-inducible factors.
TL;DR: In hypoxia, the O2 required for prolyl and asparaginyl hydroxylation is limiting, and HIF-alpha is thus stabilized and competent for transcription, and its mediators are attractive therapeutic targets.
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Chloroquine and bafilomycin A mimic lysosomal storage disorders and impair mTORC1 signalling
TL;DR: The data imply that widely used agents that alkalinise intralysosomal pH are mimetics of acute lysosome storage disorders (LSDs) and emphasise the importance of considering the result of CQ and BafA on mTORC1 signalling when interpreting the effects of these agents on cellular physiology.
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Functional analysis of the HGSNAT gene in patients with mucopolysaccharidosis IIIC (Sanfilippo C Syndrome).
TL;DR: It is suggested that these may function together to abolish HGSNAT activity, which has only been sequenced in alleles also possessing c.1209G>T (p.A615T), which independently has a negligible effect on HGS NAT expression.