AKT/PKB signaling: navigating downstream.

By B. Manning, Lewis C. Cantley. Cell, 2007

6,155 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/18fa10deedaf2138b6a696860cfaebcc0feacfe2

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Citations in the corpus

Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “PTEN-AKT signaling PTEN converts the lipid second messenger PIP3 to PIP2, thereby suppressing the activity PI3K and AKT, which are kinases that control pathways important for cell cycle progression [73], size [74], and metabolism [75].”
An emerging role of mTOR in lipid biosynthesis (2009, positive): “The binding of insulin to its cell surface receptor activates PI3K, promotes the production of phosphatidylinositol (3,4,5)-triphosphate (PIP3), and increases the recruitment and the activation of Akt at the plasma membrane (reviewed in [4]).”
Role of autophagy in cancer (2007, background): “Furthermore, constitutive activation of the PI3K pathway is one of the most common events in human cance”
PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “In addition, AKT posttranslational modification, such as lysine modifications, tyrosine phosphorylation, O-GlcNAcylation, acetylation, and sumoylation are important in retaining AKT hyperactivation in cancers, even in conditions where normal PI3K and PTEN activity persists [1, 117, 118].”
The PI3K/AKT Pathway as a Target for Cancer Treatment. (2016, background): “AKT phosphorylates a host of cellular proteins, including GSK3α, GSK3β, FoxO transcription factors, MDM2, BAD, and p27KIP1 to facilitate survival and cell cycle entry (4).”
A complex interplay between Akt, TSC2, and the two mTOR complexes (2009, background): “Once active, Akt phosphorylates a number of substrates involved in regulating cell survival, growth, proliferation, and metabolism [4].”
FKBP51 Affects Cancer Cell Response to Chemotherapy by Negatively Regulating Akt (2009, positive): “Consistent with previous studies (Brognard et al., 2007), Akt1 and Akt3 were coimmunoprecipitated with PHLPP2, whereas Akt2 and Akt3 were coimmunoprecipitated with PHLPP1 (Figures 3A and 3B).”
MicroRNA control in the immune system: basic principles. (2009, background): “…cyclin for the G1 to S transition, and (2) AKT-mediated phosphorylation of FOXO transcription factors, and their subsequent translocation to the cytoplasm from the nucleus, where they drive transcription of p21 and p27, two negative regulators of the G1 to S transition (Manning and Cantley, 2007).”
PTEN loss in the continuum of common cancers, rare syndromes and mouse models (2011, positive): “PTEN therefore negatively regulates the AKT pathway, leading to decreased phosphorylation of AKT substrates such as tuberous sclerosis 2 (TSC2) and PRAS40 (encoded by AKT1S1 ) that control mTOR activity, p27 (encoded by CDKN1B ), p21 (encoded by CDKN1A ), glycogen synthase kinase 3 (GSK3A and GSK”
The PI3K/AKT pathway in obesity and type 2 diabetes (2018, background): “AKT regulates two processes by glycolysis Glucose 6-phosphate and glycogen synthase kinase 3 (GSK3) to produce cellular energy via glycolysis and promotes glycogen production by inhibiting [30].”
Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “transcription factors of the FoxO family, and stimulates protein synthesis via the mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3b (GSK3b) [4].”