Resistance to thromboembolism in PI3Kgamma-deficient mice.
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, ISSN: 0892-6638, Vol: 15, Issue: 11, Page: 2019-2021
2001
- 208Citations
- 55Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations208
- Citation Indexes208
- 208
- CrossRef160
- Captures55
- Readers55
- 55
Article Description
Platelet aggregation and subsequent thrombosis are the major cause of ischemic diseases such as heart attack and stroke. ADP, acting via G protein-coupled receptors (GPCRs), is an important signal in thrombus formation and involves activation of phosphoinositide 3-kinases (PI3K). When platelets from mice lacking the G protein-activated PI3Kgamma isoform were stimulated with ADP, aggregation was impaired. Collagen or thrombin, however, evoked a normal response. ADP stimulation of PI3Kgamma-deficient platelets resulted in decreased PKB/Akt phosphorylation and alpha(IIb)beta(3) fibrinogen receptor activation. These effects did not influence bleeding time but protected PI3Kgamma-null mice from death caused by ADP-induced platelet-dependent thromboembolic vascular occlusion. This result demonstrates an unsuspected, well-defined role for PI3Kgamma downstream of ADP and suggests that pharmacological targeting of PI3Kgamma has a potential use as antithrombotic therapy.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0035464192&origin=inward; http://dx.doi.org/10.1096/fj.00-0810fje; http://www.ncbi.nlm.nih.gov/pubmed/11511514; https://onlinelibrary.wiley.com/doi/10.1096/fj.00-0810fje; https://dx.doi.org/10.1096/fj.00-0810fje; https://faseb.onlinelibrary.wiley.com/doi/10.1096/fj.00-0810fje
Wiley
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