ArticleMolecular and cellular biology2014
Cell activation-induced phosphoinositide 3-kinase alpha/beta dimerization regulates PTEN activity.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Structures of the PI3Kα/KRas complex on lipid bilayers reveal molecular mechanisms of PI3Kα activation.Molecular cell · 2026Article
- BAP1 dysregulation impairs trophoblast differentiation and contributes to placental dysfunction in preeclampsia.Cell death & disease · 2026Article
- Reduced Levels of miR-145-3p Drive Cell Cycle Progression in Advanced High-Grade Serous Ovarian Cancer.Cells · 2024Article
- The GPI-anchor biosynthesis pathway is critical for syncytiotrophoblast differentiation and placental development.Cellular and molecular life sciences : CMLS · 2024Article
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- The imprinted Igf2-Igf2r axis is critical for matching placental microvasculature expansion to fetal growth.Developmental cell · 2022Article
- Ablation of PI3K-p110alpha Impairs Maternal Metabolic Adaptations to Pregnancy.Frontiers in cell and developmental biology · 2022Article
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- Assembly and Molecular Architecture of the Phosphoinositide 3-Kinase p85α Homodimer.The Journal of biological chemistry · 2015Article
- Uncovering the PI3Ksome: phosphoinositide 3-kinases and counteracting PTEN form a signaling complex with intrinsic regulatory properties.Molecular and cellular biology · 2014Article
- PI-3 kinase p110β: a therapeutic target in advanced prostate cancers.American journal of clinical and experimental urology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphoinositide 3-kinase (PI3K)/PTEN (phosphatase and tensin homolog) pathway is one of the central routes that enhances cell survival, division, and migration, and it is frequently deregulated in cancer. PI3K catalyzes formation of phosphatidylinositol 3,4,5-triphosphate [PI(3,4,5)P3] after cell activation; PTEN subsequently reduces these lipids to basal levels. Activation of the ubiquitous p110α isoform precedes that of p110β at several points during the cell cycle. We studied the potential connections between p110α and p110β activation, and we show that cell stimulation promotes p110α and p110β association, demonstrating oligomerization of PI3K catalytic subunits within cells. Cell stimulation also promoted PTEN incorporation into this complex, which was necessary for PTEN activation. Our results show that PI3Ks dimerize in vivo and that PI3K and PTEN activities modulate each other in a complex that controls cell PI(3,4,5)P3 levels.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.