ArticleGenes & development2012
The p110α and p110β isoforms of PI3K play divergent roles in mammary gland development and tumorigenesis.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 125 citations in OpenAlex.
- PTEN Loss Promotes PI3Kβ Phosphorylation and EPHA2/SRC/p-PI3KβY962 Complex Assembly to Drive Tumorigenesis.Cancer discovery · 2026Article
- Review
- Reversal of endocrine resistance via N6AMT1-NEDD4L pathway-mediated p110α degradation.Oncogene · 2025Article
- Review
- Repurposing Inhibitors of Phosphoinositide 3-kinase as Adjuvant Therapeutics for Bacterial Infections.Frontiers in antibiotics · 2023Article
- The effect of the alpha-specific PI3K inhibitor alpelisib combined with anti-HER2 therapy in HER2+/PIK3CA mutant breast cancer.Frontiers in oncology · 2023Article
- Article
- Blocking PI3K p110β Attenuates Development of PTEN-Deficient Castration-Resistant Prostate Cancer.Molecular cancer research : MCR · 2022Article
- Review
- PI3K and AKT at the Interface of Signaling and Metabolism.Current topics in microbiology and immunology · 2022Article
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- Article
- Breast Cancer Treatments: Updates and New Challenges.Journal of personalized medicine · 2021Review
- p85β alters response to EGFR inhibitor in ovarian cancer through p38 MAPK-mediated regulation of DNA repair.Neoplasia (New York, N.Y.) · 2021Article
- Dengue Virus Dysregulates Master Transcription Factors and PI3K/AKT/mTOR Signaling Pathway in Megakaryocytes.Frontiers in cellular and infection microbiology · 2021Article
- Recent Updates on the Involvement of PI3K/AKT/mTOR Molecular Cascade in the Pathogenesis of Hyperproliferative Skin Disorders.Frontiers in medicine · 2021Review
- Propolis Suppresses UV-Induced Photoaging in Human Skin through Directly Targeting Phosphoinositide 3-Kinase.Nutrients · 2020Article
- Review
- Divergent Roles of PI3K Isoforms in PTEN-Deficient Glioblastomas.Cell reports · 2020Article
- CD9 induces cellular senescence and aggravates atherosclerotic plaque formation.Cell death and differentiation · 2020Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Class Ia phosphatidylinositol 3 kinase (PI3K) is required for oncogenic receptor-mediated transformation; however, the individual roles of the two commonly expressed class Ia PI3K isoforms in oncogenic receptor signaling have not been elucidated in vivo. Here, we show that genetic ablation of p110α blocks tumor formation in both polyoma middle T antigen (MT) and HER2/Neu transgenic models of breast cancer. Surprisingly, p110β ablation results in both increased ductal branching and tumorigenesis. Biochemical analyses suggest a competition model in which the less active p110β competes with the more active p110α for receptor binding sites, thereby modulating the level of PI3K activity associated with activated receptors. Our findings demonstrate a novel p110β-based regulatory role in receptor-mediated PI3K activity and identify p110α as an important target for treatment of HER2-positive disease.
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Registered trials
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.