The emerging mechanisms of isoform-specific PI3K signalling
By B. Vanhaesebroeck, J. Guillermet‐Guibert, M. Graupera, B. Bilanges. Nature reviews. Molecular cell biology, 2010
1,769 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/91dcad71488dcf51118d1e6844bd4b3ea8fe1f03
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Citations in the corpus
- Phosphoinositides: tiny lipids with giant impact on cell regulation. (2013, background): “These enzymes also exist in three forms in mammalian cells: PI3KC2 , PI3KC2 , and PI3KC2 (1347, 1610).”
- PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “RTK overactivation in cancer Growth factor-mediated induction of RTKs [33] or GPCRs [34] usually initiates the canonical pathway that engenders the activation of AKT, resulting in plasma membrane localization and induction of one, or more isoforms of the class I PI3K family [35] (Fig.”
- Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer (2021, background): “PI3K, as an intracellular phosphatidylinositol kinase, encompasses p85 and p110.(117) Transmembrane growth factor receptors include epidermal growth factor receptor (EGFR), Gprotein-coupled estrogen receptor (GPER), VEGF, and insulin growth factor receptor 1, etc.”
- The PI3K pathway in human disease (2017, neutral): “Generation of mice with deletion or mutation of PI3K genes has been instrumental in delineating the unique and redundant functions of PI3K isoforms in mammalian cells and tissues (Ok-kenhaug, 2013; Vanhaesebroeck et al., 2010).”
- The PI3K/AKT pathway in obesity and type 2 diabetes (2018, background): “Meanwhile, RTKs and GPCRs also activates Ras to subsequently activates PI3K [14].”
- Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “One characteristic of GPCRs is that they recognize and respond to chemically distinct ligands to effectively activate PI3K/Akt signaling in different cells.(3,68) Moreover, GPCRs regulate cancer cell proliferation and survival, and their persistent activation affects mitotic and metabolic responses,”
- PI3K in cancer: divergent roles of isoforms, modes of activation, and therapeutic targeting (2014, background): “The myotubularin (MTM) family phosphatases MTM1 and MTMR2 remove the 3ʹ phos‐ phate from PtdIns(3)P, regulating the lipid products of class II and III PI3Ks15–18.”
- PI3K signalling: the path to discovery and understanding (2012, background): “, with Vps34–Vps15 being present in several distinct complexes (reviewed in Ref”
- Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “1), which stimulates the conversion of membrane-bound phosphatidylinositol-(4,5)bisphosphate [PtdIns(4,5)P2; PIP2] to phosphatidylinositol-(3,4,5)trisphosphate [PtdIns(3,4,5)P3; PIP3] (Vanhaesebroeck et al., 2010; Thorpe et al., 2015).”
- Targeting cancer stem cell pathways for cancer therapy (2020, background): “353 AKT is a serine/threonine kinase that is expressed as three isoforms: AKT1, AKT2, and AKT3.”