ArticleBlood2015
Essential role of class II PI3K-C2α in platelet membrane morphology.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- PIK3C2B drives lung cancer progression through coordinating metabolic reprogramming and EMT-mediated metastasis.Biochemistry and biophysics reports · 2025Article
- A computational framework for the investigation of phosphoinositide regulation.PLoS computational biology · 2025Article
- Inactivation of PI3K-C2α deregulates cell death pathways and sensitizes to endotoxic shock.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Study on the Mechanism of the Adrenaline-Evoked Procoagulant Response in Human Platelets.International journal of molecular sciences · 2024Article
- Structural Basis for Highly Selective Class II Alpha Phosphoinositide-3-Kinase Inhibition.Journal of medicinal chemistry · 2023Article
- The Temporal and Spatial Changes of Autophagy and PI3K Isoforms in Different Neural Cells After Hypoxia/Reoxygenation Injury.Molecular neurobiology · 2023Article
- Beyond PI3Ks: targeting phosphoinositide kinases in disease.Nature reviews. Drug discovery · 2023Review
- Exploring the Role of PI3P in Platelets: Insights from a Novel External PI3P Pool.Biomolecules · 2023Article
- Repurposing Inhibitors of Phosphoinositide 3-kinase as Adjuvant Therapeutics for Bacterial Infections.Frontiers in antibiotics · 2023Article
- A microfluidic method to investigate platelet mechanotransduction under extensional strain.Research and practice in thrombosis and haemostasis · 2023Article
- Phosphoinositide 3-Kinases as Potential Targets for Thrombosis Prevention.International journal of molecular sciences · 2022Review
- An extensional strain sensing mechanosome drives adhesion-independent platelet activation at supraphysiological hemodynamic gradients.BMC biology · 2022Article
- Structural basis of phosphatidylinositol 3-kinase C2α function.Nature structural & molecular biology · 2022Article
- An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022Article
- PI3K Isoform Signalling in Platelets.Current topics in microbiology and immunology · 2022Article
- Insulin-like growth factor 1 promotes neurological functional recovery after spinal cord injury through inhibition of autophagy via the PI3K/Akt/mTOR signaling pathway.Experimental and therapeutic medicine · 2021Article
- Review
- Class II phosphatidylinositol 3-kinase isoforms in vesicular trafficking.Biochemical Society transactions · 2021Review
- Phosphatidylinositol 3-monophosphate: A novel actor in thrombopoiesis and thrombosis.Research and practice in thrombosis and haemostasis · 2020Review
- Transcriptomic Profiling of Circular RNA in Different Brain Regions of Parkinson's Disease in a Mouse Model.International journal of molecular sciences · 2020Article
Corrections and comments
- Commented on by
Authors and funding
11 authors.
Funding
Abstract
The physiologic roles of the class II phosphoinositide 3-kinases (PI3Ks) and their contributions to phosphatidylinositol 3-monophosphate (PI3P) and PI(3,4)P2 production remain elusive. Here we report that mice heterozygous for a constitutively kinase-dead PI3K-C2α display aberrant platelet morphology with an elevated number of barbell-shaped proplatelets, a recently discovered intermediate stage in the final process of platelet production. Platelets with heterozygous PI3K-C2α inactivation have critical defects in α-granules and membrane structure that are associated with modifications in megakaryocytes. These platelets are more rigid and unable to form filopodia after stimulation. Heterozygous PI3K-C2α inactivation in platelets led to a significant reduction in the basal pool of PI3P and a mislocalization of several membrane skeleton proteins known to control the interactions between the plasma membrane and cytoskeleton. These alterations had repercussions on the performance of platelet responses with delay in the time of arterial occlusion in an in vivo model of thrombosis and defect in thrombus formation in an ex vivo blood flow system. These data uncover a key role for PI3K-C2α activity in the generation of a basal housekeeping PI3P pool and in the control of membrane remodeling, critical for megakaryocytopoiesis and normal platelet production and function.
Indexed as
Identifiers
26109204What 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.