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The PI3K/AKT/mTOR interactive pathway
Open accessAbstract
The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) signalling pathway is hyperactivated or altered in many cancer types and regulates a broad range of cellular processes including survival, proliferation, growth, metabolism, angiogenesis and metastasis. The PI3K/AKT/mTOR pathway is regulated by a wide-range of upstream signalling proteins and it regulates many downstream effectors by collaborating with various compensatory signalling pathways, primarily with RAF/MEK/ERK pathway. Limited clinical success of the available targeted therapeutic agents and challenges mediated by tumour heterogeneity across different cancer types emphasize the importance of alterations in the PI3K/AKT/mTOR pathway in the design of effective personalized treatment strategies. Here we report a comprehensive PI3K/AKT/mTOR network that represents the intricate crosstalk between compensatory pathways, which can be utilized to study the AKT signalling mechanism in detail and improve the personalized combinatorial therapeutic strategies.
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“PI3K inhibition, shown to increase autophagy38.”
From APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia (2024) · cites this paper as [38]
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PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers
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Metadata
- Authors
- Ersahin, T., Tuncbag, N., & Cetin-Atalay, R.
- Affiliations
- Cancer Systems Biology Laboratory, Graduate School of Informatics, ODTU a , 06800 Ankara, Turkey rengul@metu.edu.tr +90-312-210-3745 +90-312-210-7887
- Venue
- Molecular BioSystems
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-04-20
- Volume
- 11
- Issue
- 7
- Pages
- 1946-1954
- ISSN
- 1742-2051 (ISSN-L)
- 1742-206X
- OpenAlex
- W2062689336
- Cited by
- 683
- References
- 125
- Citations by year
- 2026: 62 · 2025: 110 · 2024: 119 · 2023: 96 · 2022: 82 · 2021: 71 · 2020: 56 · 2019: 43 · 2018: 30 · 2017: 8 · 2016: 5 · 2015: 1
- FWCI
- 6.37
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Molecular BioSystems (publishedVersion)
- PubMed (publishedVersion)
- OpenMETU (Middle East Technical University) (submittedVersion, cc-by-nc-nd)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- PI3K/AKT/mTOR pathway, Raf/MEK/ERK pathway, pathway crosstalk, cancer, tumor heterogeneity, precision oncology, combination therapy, targeted therapy resistance
- MeSH terms
- Humans, Phosphatidylinositol 3-Kinases, MAP Kinase Signaling System, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Protein Interaction Maps
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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