J
James R. Woodgett
Researcher at Lunenfeld-Tanenbaum Research Institute
Publications - 325
Citations - 53780
James R. Woodgett is an academic researcher from Lunenfeld-Tanenbaum Research Institute. The author has contributed to research in topics: GSK-3 & Protein kinase A. The author has an hindex of 113, co-authored 319 publications receiving 51191 citations. Previous affiliations of James R. Woodgett include Asahikawa Medical College & Texas A&M University.
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Journal ArticleDOI
Immunological evidence for two physiological forms of protein kinase C.
James R. Woodgett,Tony Hunter +1 more
TL;DR: The two forms were not related by either partial proteolysis or differential phosphorylation, showing that two distinct forms of this enzyme exist in mammalian cells.
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CpG Island microarray probe sequences derived from a physical library are representative of CpG Islands annotated on the human genome
Lawrence E. Heisler,Dax Torti,Paul C. Boutros,John D. Watson,Charles K. Chan,Neil Winegarden,Mark Takahashi,Patrick Yau,Tim H M Huang,Peggy J. Farnham,Igor Jurisica,James R. Woodgett,Rod Bremner,Linda Z. Penn,Sandy D. Der +14 more
TL;DR: The high representation of genomic CGI in this rich collection of clones supports the utilization of microarrays produced with this library for the study of global epigenetic mechanisms and protein–chromatin interactions.
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mTOR regulates brain morphogenesis by mediating GSK3 signaling
TL;DR: It is shown that mammalian target of rapamycin (mTOR) is required for maintaining neural progenitor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain development and that GSK3, a master regulator of neural progentitors, interacts with mTOR and controls its activity in cortical progenitors.
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Β-Catenin activation synergizes with PTEN loss to cause bladder cancer formation
Imran Ahmad,Jennifer P. Morton,Lukram Babloo Singh,Sorina Radulescu,Rachel A. Ridgway,Satish Patel,James R. Woodgett,Douglas J. Winton,M. M. Taketo,Xue-Ru Wu,Hing Y. Leung,Owen J. Sansom +11 more
TL;DR: Data show that deregulated Wnt signalling has a critical role in promoting UCC, and suggests that human UCC that have high levels of Wnt and PI3 kinase signalling may be responsive to mTOR inhibition.
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Targeting glycogen synthase kinase-3 (GSK-3) in the treatment of Type 2 diabetes.
TL;DR: Despite its pleiotropic nature, GSK-3 has significant promise as a target for diabetes due to functional partitioning of the enzyme, tissue-selectivity and acute dosage-dependency of effects of inhibition, suggesting useful therapeutic windows.