The renaissance of GSK3

By P. Cohen, S. Frame. Nature reviews. Molecular cell biology, 2001

1,581 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/df2f44c5157d5055cadea88c8416b949b663125e

How researchers see this paper

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In Molecular Biology

1. A. Dinkova-Kostova
2. J. Hayes
3. John Calvin Reed
4. Matthias Mann
5. Jens S. Andersen
6. Lauren E Tebay
7. Wenqing Xu
8. Michael T. McMahon

In Oncology

1. Y. Ben‐Neriah
2. A. Dinkova-Kostova
3. M. Hung
4. Matthias Mann
5. James P. Allison
6. J. Hayes
7. J. Hsu
8. Dihua Yu

Citations in the corpus

• ROS and ROS-Mediated Cellular Signaling (2016, background): “The membranal PIP3, a signaling molecule, recruits and activates proteins that contain the pleckstrin homology (PH) domain such as the phosphoinositide-dependent protein kinase (PDK) and protein kinase B (Akt) serine/threonine kinases and the activation of PDK and Akt successively promotes the activ”
• Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore (2004, neutral): “22).”
• Wnt Signaling Requires the Sequestration of Glycogen Synthase Kinase 3 inside Multivesicular Endosomes (2010, positive): “This promiscuous enzyme phosphorylates serine or threonine at position À4 of sites primed by phosphorylation (S/TXXXS/T[PO 3 ]) (Cohen and Frame, 2001).”
• (Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms. (2006, background): “SGK1 further phosphorylates, and thus inhibits, glycogen synthase kinase 3 (GSK3) (276).”
• Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease (2005, background): “For example, GSK-3 is activated through the phosphorylation at Tyr216 or is inhibited when Ser9 is phosphorylated by Akt activity (Cohen and Frame, 2001).”
• PTEN and the PI3-kinase pathway in cancer. (2009, background): “AKTmediated phosphorylation inhibits the activities of some proteins such as the proapoptotic protein BAD and glycogen synthase kinase 3 (GSK3), which modulates glucose metabolism as well as cell-cycle-regulatory proteins (12).”
• Glycosylation and stabilization of programmed death ligand-1 suppresses T-cell activity (2016, positive): “Since activation of AKT by EGFR suppresses GSK3 b activity through Ser9 phosphorylation 35 , inhibition of EGF signalling in BLBC cells creates a therapeutic benefit by reducing cancer cell immune escape via PD-L1 destabilization.”
• Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, positive): “GSK-3 is a key regulator of glycogen metabolism that inhibits glycogen synthase, as well as being a regulator of insulin signaling, cell fate specification in embryo development, and cell cycle and apoptosis (reviewed in [293, 294]).”
• Synthetic Lethality of Combined Bcl-2 Inhibition and p53 Activation in AML: Mechanisms and Superior Antileukemic Efficacy (2017, background): “p53 Activation Downregulates the Ras/Raf/MEK/ERK Signaling Cascade To determine the mechanism by which p53 activation regulates GSK3 activity, we first measured the effects of p53 expression on AKT, which is widely known to phosphorylate and inactivate GSK3 (Cohen and Frame, 2001; Maurer et al., 200”