The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism

By J. Engelman, Ji Luo, Lewis C. Cantley. Nature reviews genetics, 2006

3,342 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9153cf9b582d9d3c686ae014fb8130a20d94a898

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. T. Yuan
2. Lewis C. Cantley
3. J. Engelman
4. Padinjat Raghu
5. M. Wymann
6. J. Clarke
7. Amit Gupta
8. B. Manning

In Molecular Biology

1. J. Engelman
2. P. Pandolfi
3. T. Franke
4. Arkaitz Carracedo
5. B. Manning
6. Lewis C. Cantley
7. Carlos L. Arteaga
8. Jingxiang Huang

Citations in the corpus

• PI3K pathway alterations in cancer: variations on a theme (2008, positive): “AKT Amplifications in multiple AKT isoforms have been reported in pancreatic, ovarian, and head and neck cancers (Engelman et al., 2006).”
• Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “cerevisiae [12], has significantly contributed to the elucidation of the function of members of the PI3K family [13].”
• Signal transduction in cancer. (2015, neutral): “Regulation of glucose transport and hexokinase by Akt promotes glycolysis, leading to generation of nucleotides and amino acids necessary for cell growth (Engelman et al. 2006).”
• The Lin28/let-7 axis regulates glucose metabolism (2011, background): “…toward glyco- lytic metabolism can increase a cancer cell’s ability to generate biomass, a phenomenon termed the ‘‘Warburg Effect’’ (Denko, 2008; Engelman et al., 2006; Gao et al., 2009; Guertin and Sabatini, 2007; Laplante and Sabatini, 2009; Vander Heiden et al., 2009; Yun et al.,…”
• Cellular response to hyperosmotic stresses. (2007, background): “Class IA (PI3K-IA), which generates phosphatidylinositol 3,4,5-trisphosphate (PIP3) from phosphatidylinositol 4,5-bisphosphate (PIP2), is involved in activation of TonEBP/OREBP (78).”
• The PI3K pathway in human disease (2017, background): “…with a role in cytoskeletal remodeling that is mediated through interaction with ARP2/3 (Moniz et al., 2017). p110a mediates most tissue responses to insulin and IGF1, driving tissue growth and maintaining glucose homeostasis throughout development (Engelman et al., 2006; Foukas et al., 2006).”
• Phosphatidylinositol 5-phosphate 4-kinase (PIP4K) regulates TOR signaling and cell growth during Drosophila development (2013, methodology): “In vitro, PIP4K enzymes can phosphorylate both PI5P and PI3P to produce PI(4,5)P2 and PI(3,4)P2, respectively (8, 9).”
• Cardiovascular actions of insulin. (2007, background): “Multiple isoforms of p85 and p110 exist and consist of p110 , p110 , and p110 catalytic subunit isoforms that bind to the major regulator p85 isoforms, p85 , p55 , and p50 (11).”
• The RAS/RAF/MEK/ERK and the PI3K/AKT signalling pathways: role in cancer pathogenesis and implications for therapeutic approaches (2012, background): “9% 9% [12] [12] [12] [31] [12] PIK3R1 Mutation Glioma Colon 4 % 3 % [23] [23] AKT1 Mutation Colon Breast Ovarian Lung 1 % 4 % 1 % 0 % [23] [23] [23] [23] Amplification Gastric Breast 20% 1% [4] [35] AKT2 Mutation Colon Breast 1% 0 % [34] [23] Amplification Pancreas Ovarian Breast 20% 14.”
• The PI3K pathway as drug target in human cancer. (2010, background): “AKT promotes cell survival by inhibiting proapoptotic Bcl-2 family members BAD and BAX.5,18 AKT also impedes negative regulation of the transcription factor NF- B, leading to increased transcription of antiapoptotic and prosurvival genes.22 Phosphorylation of Mdm2 by AKT antagonizes p53-mediated apo”