Class I PI3K in oncogenic cellular transformation
By Li Zhao, P. Vogt. Oncogene, 2008
616 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/9dc17b8593a64effe4b956e8b9376cb9a0e0e184
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In Genetics
In Molecular Biology
In Oncology
Citations in the corpus
- Regulation of ligands for the NKG2D activating receptor (2013, background): “Among the most common alterations in cancer cells are those that activate the PI3K pathway, which promotes survival and proliferation (42, 43).”
- The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Although these two mutations may have different impacts on PI3K targets, both drive transformation in vitro (reviewed in Zhao and Vogt, 2008).”
- The emerging mechanisms of isoform-specific PI3K signalling (2010, background): “Accumulating evidence suggests that the different mutations can induce gain-of-function of p110α through distinct molecular mechanisms, such as altering the position and mobility of the activation loop or increasing the positive surface charge of p110α and therefore enhancing its recruitment to cell”
- PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “PI3K mutation and amplification in cancer Among the numerous types of PI3K, only class I can exert lipid phosphorylation following growth stimulation [50].”