The nuts and bolts of AGC protein kinases

By Laura R. Pearce, D. Komander, D. Alessi. Nature reviews. Molecular cell biology, 2010

1,350 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a541646dbdf2c022982cb1ca1e91f0c2c35d8cbd

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Citations in the corpus

Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, neutral): “(491)] and, thus, while phosphorylated by PDK1 downstream of PI3K, can be recruited to lipid rafts in a TC10dependent manner by Par3 (partitioning-defective) and Par6 proteins (331).”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Once localized at the PM, AKT is phosphorylated at T308 and S473.”
Nutrient sensing and TOR signaling in yeast and mammals (2017, neutral): “Growth factors stimulate lysosomal RHEB through the PI3K-PDK1-AKT pathway (reviewed in Pearce et al , 2010; Dibble & Cantley, 2015).”
Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing (2012, background): “A 19 exon duplication was uncovered in ROCK1, which is a serine/threonine kinase that acts as an effector of Rho signaling (Pearce et al., 2010).”
Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “AGC kinase family members share similar structure and mechanisms of activation via phosphorylation of two serine and threonine residues (Pearce et al. 2010).”
Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “The activation/levels of two other IRS kinases, ROCK1 and G protein-coupled receptor kinase 2 (GRK2), is mechanistically independent of IRS [20] but is clearly influenced by insulin and altered in type 2 diabetes [88–90].”
FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. (2011, background): “In this regard, the binding of AKT has not been thoroughly investigated to any of its numerous targets [38,49,50].”
Redox regulation of FoxO transcription factors (2015, neutral): “AGC [306] Akt T24, S256, S319 [307,308] T32, S253, S315 [309] T28, S193, S258 [310,311] T26, S184”
Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control (2011, background): “Kuranda, K., V. Leberre, S. Sokol, G. Palamarczyk, and J. Francois, 2006 Investigating the caffeine effects in the yeast Saccharomyces cerevisiae brings new insights into the connection between TOR, PKC and Ras/cAMP signalling pathways.”
A systems study reveals concurrent activation of AMPK and mTOR by amino acids (2016, background): “Akt and p70-S6K are both AGC kinases that need to be phosphorylated twice for full activation: by PDK1 within the so-called T-loop, and by a phosphoinositide-dependent protein kinase 2 (PDK2) within the hydrophobic motif 28 .”
The Ras-ERK and PI3K-mTOR Pathways: Cross-talk and Compensation (2011, background): “However, when AKT is inhibited by an S6K-mediated negative feedback loop, S6K phosphorylates GSK3β Ser9 [18].”
hERG K(+) channels: structure, function, and clinical significance. (2012, background): “Kinases in this superfamily share a high degree of homology in their protein sequences especially within the catalytic kinase domain (480).”
The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “There are also the following subfamilies of protein kinases: AGC, CaMK, CK1, CMGC, STE, TK and TKL (19-27) (Table I).”