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Bradley W. Doble

Researcher at McMaster University

Publications -  67
Citations -  10383

Bradley W. Doble is an academic researcher from McMaster University. The author has contributed to research in topics: GSK-3 & Wnt signaling pathway. The author has an hindex of 32, co-authored 62 publications receiving 9615 citations. Previous affiliations of Bradley W. Doble include Ontario Institute for Cancer Research & University of Manitoba.

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The ground state of embryonic stem cell self-renewal

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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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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Functional redundancy of GSK-3α and GSK-3β in wnt/β-catenin signaling shown by using an allelic series of embryonic stem cell lines

TL;DR: The generation of an allelic series of mouse embryonic stem cell (ESC) lines with 0-4 functional GSK-3 alleles is described and Gsk-3-isoform function in Wnt/beta-catenin signaling is examined to highlight the importance of considering the contributions of both homologs when studying G SK-3 functions in mammalian systems.
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Phosphorylation by p38 MAPK as an Alternative Pathway for GSK3β Inactivation

TL;DR: It is shown that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3β by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of β-catenin.
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GSK-3 is a master regulator of neural progenitor homeostasis.

TL;DR: The results indicate that GSK-3 signaling is an essential mediator of homeostatic controls that regulate neural progenitors during mammalian brain development.