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Toshiyuki Araki

Researcher at New York University

Publications -  143
Citations -  12322

Toshiyuki Araki is an academic researcher from New York University. The author has contributed to research in topics: Noonan syndrome & Phosphorylation. The author has an hindex of 45, co-authored 135 publications receiving 10380 citations. Previous affiliations of Toshiyuki Araki include Harvard University & Waseda University.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration.

Toshiyuki Araki, +2 more
- 13 Aug 2004 - 
TL;DR: It is demonstrated that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein and that SIRT1, a mammalian ortholog of Sir2, is the downstream effector of increased NMNat activity that leads to axonal protection.
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Germline gain-of-function mutations in SOS1 cause Noonan syndrome

Amy E. Roberts, +10 more
- 01 Jan 2007 - 
TL;DR: SOS1 mutants are identified as a major cause of Noonan syndrome, representing the first example of activating GEF mutations associated with human disease and providing new insights into RAS-GEF regulation.
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Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRα3–RET Receptor Complex

Robert H. Baloh, +9 more
- 01 Dec 1998 - 
TL;DR: Artemin is a survival factor for sensory and sympathetic neurons in culture and its expression pattern suggests that it also influences these neurons in vivo, indicating that like GDNF and NTN, Artemin has a preferred receptor (GFRalpha3-RET) but that alternative receptor interactions also occur.
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GFRα1-Deficient Mice Have Deficits in the Enteric Nervous System and Kidneys

Hideki Enomoto, +6 more
- 01 Aug 1998 - 
TL;DR: While stringent physiologic pairing exists between GFRalpha1 and GDNF in renal and enteric nervous system development, significant cross-talk between GDNF and other GFR alpha coreceptors must occur in other neuronal populations.