A transforming mutation in the pleckstrin homology domain of AKT1 in cancer

By J. Carpten, Andrew L. Faber, Candice L. Horn, Gregory P. Donoho, S. Briggs, C. Robbins, G. Hostetter, S. Boguslawski, T. Moses, S. Savage and 14 more. Nature, 2007

1,319 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a3f587b0972091c9e32e117aaa9dae33e08ca2d0

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Citations in the corpus

The Roles of Post-translational Modifications in the Context of Protein Interaction Networks (2015, neutral): “RAC-alpha serine/ threonine-protein kinase ENSP00000270202 Breast cancer (BC) [MIM:114480]; Colorectal cancer (CRC) [MIM:114500] [72]; Proteus syndrome (PROTEUSS) [MIM:176920] [73]”
PI3K pathway alterations in cancer: variations on a theme (2008, neutral): “The PH domain mutation results in constitutive association with the plasma membrane and prolonged AKT activation that is sufficient to transform cells in culture (Carpten et al., 2007).”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Furthermore, the gain-of-function E17K somatic mutation of AKT1 occurs in breast, colorectal, and ovarian cancers [268].”
PTEN and the PI3-kinase pathway in cancer. (2009, background): “(41) identified a transforming E17K PH-domain mutation in AKT1 in breast (8%), colorectal (6%), and ovarian (2%) cancers.”
Network-based global inference of human disease genes (2008, methodology): “The protein kinase AKT1, ranked at 27, is a novel oncogene, and recently a transformingmutationwas identified in human breast, colorectal, and ovarian cancers (Carpten et al, 2007).”
PI3K/Akt: getting it right matters (2008, background): “Philip Tsichlis’ group identified v-akt as the gene transduced by the rodent retrovirus AKT8 (Bellacosa et al., 1991), and subsequently showed that its cellular homolog, then named c-akt, encoded the cytoplasmic serine-threonine protein kinase Akt in mice (Bellacosa et al., 1993).”
The RAS/RAF/MEK/ERK and the PI3K/AKT signalling pathways: role in cancer pathogenesis and implications for therapeutic approaches (2012, background): “The AKT1 mutation was found to be mutually exclusive with PIK3CA mutations and complete loss of PTEN protein expression in breast, colorectal and ovarian cancers, suggesting that AKT1 mutations are sufficient for complete activation of the PI3K pathway [32].”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “But recently, the group of Thomas reported a novel point mutation in the lipid-binding pocket of AKT1 in breast, colorectal and ovarian cancer patients that leads to AKT1 targeting to plasma membrane and activation of downstream effectors (Carpten et al., 2007).”