ArticlePloS one2013
Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 25 citations in OpenAlex.
- Decompression Mechanism of Radish Seed in Prehypertension Rats through Integration of Transcriptomics and Metabolomics Methods.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022Article
- Role of PI3K/Akt signaling pathway in cardiac fibrosis.Molecular and cellular biochemistry · 2021Review
- PI3KC2β inactivation stabilizes VE-cadherin junctions and preserves vascular integrity.EMBO reports · 2021Article
- Titanium Dioxide Nanoparticles Alter the Cellular Phosphoproteome in A549 Cells.Nanomaterials (Basel, Switzerland) · 2020Article
- Downregulation of class II phosphoinositide 3-kinase PI3K-C2β delays cell division and potentiates the effect of docetaxel on cancer cell growth.Journal of experimental & clinical cancer research : CR · 2019Article
- Revisiting PI3-kinase signalling in angiogenesis.Vascular biology (Bristol, England) · 2019Review
- Novel roles for class II Phosphoinositide 3-Kinase C2β in signalling pathways involved in prostate cancer cell invasion.Scientific reports · 2016Article
- Endothelial p110γPI3K Mediates Endothelial Regeneration and Vascular Repair After Inflammatory Vascular Injury.Circulation · 2016Article
- The class II PI 3-kinase, PI3KC2α, links platelet internal membrane structure to shear-dependent adhesive function.Nature communications · 2015Article
- Development of synchronous VHL syndrome tumors reveals contingencies and constraints to tumor evolution.Genome biology · 2014Article
- Analysis of common and coding variants with cardiovascular disease in the Diabetes Heart Study.Cardiovascular diabetology · 2014Article
- Targeting p110gamma in gastrointestinal cancers: attack on multiple fronts.Frontiers in physiology · 2014Review
- PI3K at the crossroads of tumor angiogenesis signaling pathways.Molecular & cellular oncologyReview
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 at 3 institutions in 2 countries.
Funding
Abstract
The question of whether the distinct isoforms of the family of enzymes phosphoinositide 3-kinases (PI3Ks) play redundant roles within a cell or whether they control distinct cellular processes or distinct steps within the same cellular process has gained considerable importance in the recent years due to the development of inhibitors able to selectively target individual isoforms. It is important to understand whether inhibition of one PI3K can result in compensatory effect from other isoform(s) and therefore whether strategies aimed at simultaneously blocking more than one PI3K may be needed. In this study we investigated the relative contribution of distinct PI3K isoforms to endothelial cells (EC) functions specifically regulated by the sphingolipid sphingosine-1-phosphate (S1P) and by high density lipoproteins (HDL), the major carrier of S1P in human plasma. Here we show that a co-ordinated action of different PI3Ks is required to tightly regulate remodelling of EC on Matrigel, a process dependent on cell proliferation, apoptosis and migration. The contribution of each isoform to this process appears to be distinct, with the class II enzyme PI3K-C2β and the class IB isoform p110γ mainly regulating the S1P- and HDL-dependent EC migration and PI3K-C2α primarily controlling EC survival. Data further indicate that PI3K-C2β and p110γ control distinct steps involved in cell migration supporting the hypothesis that different PI3Ks regulate distinct cellular processes.
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.