Class II phosphatidylinositol 3-kinase isoforms in vesicular trafficking
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Phosphatidylinositol 3-kinases (PI3Ks) are critical regulators of many cellular processes including cell survival, proliferation, migration, cytoskeletal reorganization, and intracellular vesicular trafficking. They are a family of lipid kinases that phosphorylate membrane phosphoinositide lipids at the 3' position of their inositol rings, and in mammals they are divided into three classes. The role of the class III PI3K Vps34 is well-established, but recent evidence suggests the physiological significance of class II PI3K isoforms in vesicular trafficking. This review focuses on the recently discovered functions of the distinct PI3K-C2α and PI3K-C2β class II PI3K isoforms in clathrin-mediated endocytosis and consequent endosomal signaling, and discusses recently reported data on class II PI3K isoforms in different physiological contexts in comparison with class I and III isoforms.
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The PI3K/AKT/mTOR pathway is a major downstream signaling cascade of EGFR and represents an important bypass mechanism contributing to resistance to cetuximab and panitumumab.
“The phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway is a major downstream signaling cascade of EGFR and represents an important bypass mechanism contributing to resistance to cetuximab and panitumumab [40,41,42,43,44].”
From Overcoming Resistance to Anti-EGFR Therapies: Mechanisms of Cetuximab and Panitumumab Resistance and Emerging Combination Strategies (2026) · cites this paper as [42]
The ‘Cellular functions of class II PI3K isoforms’ section discusses PI3K regulation of Akt and mTORC1, but does not identify the PI3K/AKT/mTOR pathway as a major downstream cascade of EGFR. Neither that section nor the passages retrieved for cetuximab, panitumumab and resistance address a bypass mechanism for those drugs. (LLM, conf=0.72)
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Schink, K. O., Tan, K.-W., & Stenmark, H. (2016) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-111315-125349 · Cited by 283 · see citing works
Structural Basis for Regulation of Phosphoinositide Kinases and Their Involvement in Human Disease
Burke, J. E. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.08.005 · Cited by 276 · see citing works
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Henrykowska, G., Bartusik-Aebisher, D., Dynarowicz, K., Ramesh, T. S., Smolak, B., & Aebisher, D. (2026) · Pharmaceuticals · doi:10.3390/ph19071041 · Cited by 1 · see citing works
- Authors
- Yoshioka, K.
- Affiliations
- Kanazawa University (JP)
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- Yoshioka, Kazuaki
- ORCID
- Yoshioka, Kazuaki
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- Biochemical Society Transactions
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- Portland Press Ltd.
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- 2021-03-05
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- 893-901
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- 0300-5127 (ISSN-L)
- 1470-8752
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- PMC8106491
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- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- PI3K-C2α, vesicle trafficking, clathrin-mediated endocytosis, endosomal signaling, phosphoinositide 3-phosphate, Vps34, lipid kinase, membrane trafficking
- MeSH terms
- Animals, Biological Transport, Endocytosis, Humans, Isoenzymes, Endosomes, Signal Transduction, Cytoplasmic Vesicles, Intracellular Space, Class II Phosphatidylinositol 3-Kinases
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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