M
Michael P. Scheid
Researcher at York University
Publications - 37
Citations - 5304
Michael P. Scheid is an academic researcher from York University. The author has contributed to research in topics: Protein kinase B & Phosphorylation. The author has an hindex of 26, co-authored 37 publications receiving 5141 citations. Previous affiliations of Michael P. Scheid include Ontario Institute for Cancer Research & University of British Columbia.
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PKB/AKT: functional insights from genetic models
TL;DR: The physiological relevance of some of the proposed mechanisms by which PKB/AKT mediates many of its effects has been questioned, and recent work using new reagents and approaches has revealed some cracks in understanding of this important molecule.
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Wild-type PINK1 prevents basal and induced neuronal apoptosis, a protective effect abrogated by Parkinson disease-related mutations.
Agnes Petit,Toshitaka Kawarai,Erwan Paitel,Nobuo Sanjo,Mary C. Maj,Michael P. Scheid,Fusheng Chen,Yongjun Gu,Hiroshi Hasegawa,Shabnam Salehi-Rad,Linda Wang,Ekaterina Rogaeva,Paul E. Fraser,Brian D. Robinson,Peter St George-Hyslop,Anurag Tandon +15 more
TL;DR: Results suggest that PINK1 reduces the basal neuronal pro-apoptotic activity and protects neurons from staurosporine-induced apoptosis, and loss of this protective function may underlie the degeneration of nigral dopaminergic neurons in patients with Pink1 mutations.
Minireview Unravelling the activation mechanisms of protein kinase B/Akt
TL;DR: In this article, a minireview of the mechanism of protein kinase B activation is presented, including upstream regulators and secondary binding partners, and some old concepts with new twists and highlights current out-standing questions.
Journal ArticleDOI
Unravelling the activation mechanisms of protein kinase B/Akt
TL;DR: This minireview refreshes some old concepts with new twists and highlights current outstanding questions about PKB activation, including upstream regulators and secondary binding partners.
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Regulation of Bad Phosphorylation and Association with Bcl-xL by the MAPK/Erk Kinase
TL;DR: Results demonstrate for the first time in mammalian cells the involvement of the Ras-MAPK pathway in the phosphorylation of Bad and the regulation of its function.