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
The ground state of embryonic stem cell self-renewal
Qi-Long Ying,Jason Wray,Jennifer Nichols,Laura Batlle-Morera,Bradley W. Doble,James R. Woodgett,Philip Cohen,Austin Smith +7 more
TL;DR: It is shown that extrinsic stimuli are dispensable for the derivation, propagation and pluripotency of ES cells and reveal that ES cells have an innate programme for self-replication that does not require extrinsics instruction.
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The stress-activated protein kinase subfamily of c-Jun kinases.
John M. Kyriakis,Papia Banerjee,Eleni Nikolakaki,Eleni Nikolakaki,Tianang Dai,Elizabeth A. Rubie,M. F. Ahmad,Joseph Avruch,James R. Woodgett +8 more
TL;DR: The kinase p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-α, hence they are designated stress-activated protein kinases, or SAPKs.
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GSK-3: tricks of the trade for a multi-tasking kinase.
TL;DR: Since increased GSK-3 activity may be linked to pathology in diseases such as Alzheimer's disease and non-insulin-dependent diabetes mellitus, several new G SKS-3 inhibitors, such as the aloisines, the paullones and the maleimides, have been developed and hold promise as therapeutic agents.
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Phosphorylation of c- jun mediated by MAP kinases
TL;DR: Evidence is presented that mitogen-activated protein-serine (MAP) kinases (pp54 and pp42/44) specifically phosphorylate these sites and that their phosphorylation positively regulates the transacting activity of c-jun.
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Requirement for glycogen synthase kinase-3β in cell survival and NF-κB activation
TL;DR: It is shown that disruption of the murine GSK-3β gene results in embryonic lethality caused by severe liver degeneration during mid-gestation, a phenotype consistent with excessive tumour necrosis factor (TNF) toxicity, as observed in mice lacking genes involved in the activation of the transcription factor activation NF-κB.