ArticleEMBO reports2009
Regulation of PI(3)K/Akt signalling and cellular transformation by inositol polyphosphate 4-phosphatase-1.
Article in EMBO reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed.
- Targeting the Akt-EphA2 axis and cell-cell adhesion enhances anoikis sensitivity in cancer cells.Scientific reports · 2026Article
- Elucidating the clinical and genetic spectrum of inositol polyphosphate phosphatase INPP4A-related neurodevelopmental disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2025Article
- CD226 implicated in Akt-dependent apoptosis of CD4Cell death & disease · 2024Article
- Plausible role of INPP4A dysregulation in idiopathic pulmonary fibrosis.Physiological reports · 2024Article
- Enhanced oxidative phosphorylation, re-organized intracellular signaling, and epigenetic de-silencing as revealed by oligodendrocyte translatome analysis after contusive spinal cord injury.Scientific reports · 2023Article
- Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023Review
- Article
- Targeting SHIP1 and SHIP2 in Cancer.Cancers · 2021Review
- Adult-Onset Myopathy with Constitutive Activation of Akt following the Loss of hnRNP-U.iScience · 2020Article
- Excitable networks controlling cell migration during development and disease.Seminars in cell & developmental biology · 2020Review
- TGFβ receptor endocytosis and Smad signaling require synaptojanin1, PI3K-C2α-, and INPP4B-mediated phosphoinositide conversions.Molecular biology of the cell · 2020Article
- Investigating the duality ofOncotarget · 2019Article
- Lipid-dependent Akt-ivity: where, when, and how.Biochemical Society transactions · 2019Review
- Secretory Inositol Polyphosphate 4-Phosphatase Protects against Airway Inflammation and Remodeling.American journal of respiratory cell and molecular biology · 2019Article
- TAPPing into PIPs: A new reporter reveals the origin of plasma membrane PI(3,4)PThe Journal of cell biology · 2019Article
- Getting the Akt Together: Guiding Intracellular Akt Activity by PI3K.Biomolecules · 2019Review
- Understanding phosphoinositides: rare, dynamic, and essential membrane phospholipids.The Biochemical journal · 2019Review
- Loss of lipid phosphatase SHIP1 promotes macrophage differentiation through suppression of dendritic cell differentiation.Cancer biology & therapy · 2019Article
- Phosphatidylinositol Kinases and Phosphatases inFrontiers in cellular and infection microbiology · 2019Review
- MicroRNA-940 Targets INPP4A or GSK3β and Activates the Wnt/β-Catenin Pathway to Regulate the Malignant Behavior of Bladder Cancer Cells.Oncology research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Akt is a crucial phosphoinositide 3-kinase (PI(3)K) effector that regulates cell proliferation and survival. PI(3)K-generated signals, PtdIns(3,4,5)P(3) and PtdIns(3,4)P(2), direct Akt plasma membrane engagement. Pathological Akt plasma membrane association promotes oncogenesis. PtdIns(3,4)P(2) is degraded by inositol polyphosphate 4-phosphatase-1 (4-ptase-1) forming PtdIns(3)P; however, the role of 4-ptase-1 in regulating the activation and function of Akt is unclear. In mouse embryonic fibroblasts lacking 4-ptase-1 ((-/-)MEFs), the Akt-pleckstrin homology (PH) domain was constitutively membrane-associated both in serum-starved and agonist-stimulated cells, in contrast to (+/+)MEFs, in which it was detected only at the plasma membrane following serum stimulation. Epidermal growth factor (EGF) stimulation resulted in increased Ser(473) and Thr(308)-Akt phosphorylation and activation of Akt-dependent signalling in (-/-)MEFs, relative to (+/+)MEFs. Significantly, loss of 4-ptase-1 resulted in increased cell proliferation and decreased apoptosis. SV40-transformed (-/-)MEFs showed increased anchorage-independent cell growth and formed tumours in nude mice. This study provides the first evidence, to our knowledge, that 4-ptase-1 controls the activation of Akt and thereby cell proliferation, survival and tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.