The glamour and gloom of glycogen synthase kinase-3.

By R. Jope, G. Johnson. TIBS -Trends in Biochemical Sciences. Regular ed, 2004

1,591 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a789440e887c2dc9a72c67de173933ac6b07f0cd

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In Molecular Biology

1. J. Rathmell
2. Eléonore Beurel
3. B. Doble
4. Tianyan Gao
5. S. Grieco
6. A. Newton
7. R. Jope
8. J. Wofford

Citations in the corpus

• SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. (2006, background): “It is however also possible that other AGC-type kinases such as PKC and or RSK, which have been proposed to phosphorylate GSK3 at the same inhibitory sites (Jope and Johnson, 2004), could compensate for the function of doubly phosphorylated Akt.”
• Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “However, since complete inhibition of GSK3 would have widespread consequences on many cellular functions [3], even with both mechanisms of inhibition acting together a therapeutic level of lithium does not completely inhibit GSK3 but only reduces its maximal activity.”
• PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms. (2007, background): “Some substrates, such as FoxO1, GSK-3b, and TSC2 are inactivated by both PHLPP isoforms via regulation of all three Akt isoforms. inhibited by activation of the p70S6K-mediated feedback loop.”
• Cytokine stimulation promotes glucose uptake via phosphatidylinositol-3 kinase/Akt regulation of Glut1 activity and trafficking. (2007, background): “Akt can directly phosphorylate GSK3 / on serines 21/9 to inhibit GSK3 kinase activity (Jope and Johnson, 2004) and maintain surface Glut1 levels even in the absence of IL3.”
• Wnt Signaling Requires the Sequestration of Glycogen Synthase Kinase 3 inside Multivesicular Endosomes (2010, positive): “GSK3 has many substrates in addition to b-Catenin, including Dvl, Axin, and APC (Jope and Johnson, 2004).”
• 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): “Introduction Glycogen synthase kinase-3 (GSK-3) is a widely expressed and highly conserved serine/ threonine protein kinase that is encoded by two genes in mammals, generating two related protein homologues termed GSK-3α and β (Frame and Cohen, 2001; Jope and Johnson, 2004).”
• Mechanisms underlying differential responses to FGF signaling. (2005, background): “An important molecule that could mediate the integration of Wnt and FGF signaling is GSK-3ß, which can also be phosphorylated by AKT [44].”
• LTP inhibits LTD in the hippocampus via regulation of GSK3beta. (2007, positive): “For example, in the canonical wnt pathway GSK3β-binding proteins control access of β-catenin (Jope and Johnson, 2004).”
• Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “Among the many transcription factors regulated by GSK3 are Fos/Jun AP-1, CREB, heat shock factor 1, nuclear factor of activated T cells (NFAT), myc, C/EBP, NF-κB, p53, signal transducer and activator of transcription-3 (STAT3), as well as many others that have been reviewed previously (Grimes and Jo”