Pharmacological inhibitors of glycogen synthase kinase 3.
By L. Meijer, M. Flajolet, Paul Greengard. TIPS - Trends in Pharmacological Sciences, 2004
608 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/fd31dd477dfd6b08dbe063715558af360ec75efb
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In Molecular Biology
- J. Hayes
- B. Doble
- J. Woodgett
- Michael T. McMahon
- A. Cuadrado
- A. Dinkova-Kostova
- Masayuki Yamamoto
- Liam Baird
In Oncology
Citations in the corpus
- SCF/β-TrCP Promotes Glycogen Synthase Kinase 3-Dependent Degradation of the Nrf2 Transcription Factor in a Keap1-Independent Manner (2011, background): “Now we report that a potent and selective inhibitor of GSK-3, SB216367 (arylindolemaleimide, IC50 34 nM) (and data not shown with CT99021, aminopyrimidine IC50 10 nM (31)) as well as siRNAs against GSK-3 isoforms produce an increase in the level of Nrf2 protein.”
- Functional redundancy of GSK-3α and GSK-3β in wnt/β-catenin signaling shown by using an allelic series of embryonic stem cell lines (2007, background): “Most inhibitors of GSK-3 cannot discriminate between GSK-3α or β based on their ATPcompetitive mode of action (Meijer et al., 2004).”
- Differentiation and persistence of memory CD8+ T cells depend on T cell factor 1 (2010, methodology): “To determine whether Eomes expression is responsive to activation of Wnt signaling, we used 6-bromo-substituted indirubin-acetoxime (BIO-acetoxime), a specific inhibitor of GSK-3b, to block b-catenin phosphorylation and degradation (Meijer et al., 2004).”