ArticleThe Journal of biological chemistry2009
Role of phosphoinositide 3-kinase beta in glycoprotein VI-mediated Akt activation in platelets.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 126 citations in OpenAlex.
- Article
- Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential.Cell communication and signaling : CCS · 2026Review
- Costunolide, a Sesquiterpene Lactone, Protects Against Platelet Activation and Thrombus Formation.Cells · 2026Article
- Hemostasis-Sparing Antiplatelet Therapy: Current Concepts and Emerging Targets in Arterial Thrombosis.Biomolecules & therapeutics · 2026Review
- Article
- Inverse relationship between platelet Akt activity and hippocampal atrophy: A pilot case-control study in patients with diabetes mellitus.World journal of clinical cases · 2024Article
- The Function of ASK1 in Sepsis and Stress-Induced Disorders.International journal of molecular sciences · 2023Review
- The NMDA receptor regulates integrin activation, ATP release and arterial thrombosis through store-operated CaFrontiers in cardiovascular medicine · 2023Article
- The role of phosphoinositide 3-kinases in immune-inflammatory responses: potential therapeutic targets for abdominal aortic aneurysm.Cell cycle (Georgetown, Tex.) · 2022Review
- GPVI expression is linked to platelet size, age, and reactivity.Blood advances · 2022Article
- PI3K Isoform Signalling in Platelets.Current topics in microbiology and immunology · 2022Article
- Effect of Evodiamine on Collagen-Induced Platelet Activation and Thrombosis.BioMed research international · 2022Article
- A novel naphthalimide derivative reduces platelet activation and thrombus formation via suppressing GPVI.Journal of cellular and molecular medicine · 2021Article
- Influence of Vincristine, Clinically Used in Cancer Therapy and Immune Thrombocytopenia, on the Function of Human Platelets.Molecules (Basel, Switzerland) · 2021Article
- Pharmacologic targeting of Cdc42 GTPase by a small molecule Cdc42 activity-specific inhibitor prevents platelet activation and thrombosis.Scientific reports · 2021Article
- Pimpinellin Inhibits Collagen-induced Platelet Aggregation and Activation Through Inhibiting Granule Secretion and PI3K/Akt Pathway.Frontiers in pharmacology · 2021Article
- cAMP- and cGMP-elevating agents inhibit GPIbα-mediated aggregation but not GPIbα-stimulated Syk activation in human platelets.Cell communication and signaling : CCS · 2019Article
- The role of PI3K/Akt signaling pathway in non-physiological shear stress-induced platelet activation.Artificial organs · 2019Article
- p110γ deficiency protects against pancreatic carcinogenesis yet predisposes to diet-induced hepatotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- PI3Kβ-A Versatile Transducer for GPCR, RTK, and Small GTPase Signaling.Endocrinology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Glycoprotein (GP) VI is a critical platelet collagen receptor. Phosphoinositide 3-kinase (PI3K) plays an important role in GPVI-mediated platelet activation, yet the major PI3K isoforms involved in this process have not been identified. In addition, stimulation of GPVI results in the activation of Akt, a downstream effector of PI3K. Thus, we investigated the contribution of PI3K isoforms to GPVI-mediated platelet activation and Akt activation. A protein kinase C inhibitor GF 109203X or a P2Y(12) receptor antagonist AR-C69931MX partly reduced GPVI-induced Akt phosphorylation. Platelets from mice dosed with clopidogrel also showed partial Akt phosphorylation, indicating that GPVI-mediated Akt phosphorylation is regulated by both secretion-dependent and -independent pathways. In addition, GPVI-induced Akt phosphorylation in the presence of ADP antagonists was completely inhibited by PI3K inhibitor LY294002 and PI3Kbeta inhibitor TGX-221 indicating an essential role of PI3Kbeta in Akt activation directly downstream of GPVI. Moreover, GPVI-mediated platelet aggregation, secretion, and intracellular Ca(2+) mobilization were significantly inhibited by TGX-221, and less strongly inhibited by PI3Kalpha inhibitor PIK75, but were not affected by PI3Kgamma inhibitor AS252424 and PI3Kdelta inhibitor IC87114. Consistently, GPVI-induced integrin alpha(IIb)beta(3) activation of PI3Kgamma(-/-) and PI3Kdelta(-/-) platelets also showed no significant difference compared with wild-type platelets. These results demonstrate that GPVI-induced Akt activation in platelets is dependent in part on G(i) stimulation through P2Y(12) receptor activation by secreted ADP. In addition, a significant portion of GPVI-dependent, ADP-independent Akt activation also exists, and PI3Kbeta plays an essential role in GPVI-mediated platelet aggregation and Akt activation.
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.