about
Occlusive thrombi arise in mammals but not birds in response to arterial injury: evolutionary insight into human cardiovascular diseasePlatelet signalingPlatelets lacking PIP5KIγ have normal integrin activation but impaired cytoskeletal-membrane integrity and adhesionDisruption of SEMA4D ameliorates platelet hypersensitivity in dyslipidemia and confers protection against the development of atherosclerosisRGS/Gi2alpha interactions modulate platelet accumulation and thrombus formation at sites of vascular injuryDiminished contact-dependent reinforcement of Syk activation underlies impaired thrombus growth in mice lacking Semaphorin 4D.Hematopoietic lineage cell specific protein 1 (HS1) is a functionally important signaling molecule in platelet activation.Peptides derived from MARCKS block coagulation complex assembly on phosphatidylserine.Eph kinases and ephrins support thrombus growth and stability by regulating integrin outside-in signaling in platelets.Minding the gaps to promote thrombus growth and stabilityA systems approach to hemostasis: 1. The interdependence of thrombus architecture and agonist movements in the gaps between platelets.A systems approach to hemostasis: 2. Computational analysis of molecular transport in the thrombus microenvironment.Simulation of intrathrombus fluid and solute transport using in vivo clot structures with single platelet resolution.Microcirculation as a target for the anti-inflammatory properties of statins.Regulated surface expression and shedding support a dual role for semaphorin 4D in platelet responses to vascular injuryA newly identified complex of spinophilin and the tyrosine phosphatase, SHP-1, modulates platelet activation by regulating G protein-dependent signaling.JAM-A protects from thrombosis by suppressing integrin αIIbβ3-dependent outside-in signaling in platelets.Contact-dependent signaling events that promote thrombus formation.A systems approach to hemostasis: 4. How hemostatic thrombi limit the loss of plasma-borne molecules from the microvasculature.Loss of PIP5KIbeta demonstrates that PIP5KI isoform-specific PIP2 synthesis is required for IP3 formation.Novel therapeutic targets at the platelet vascular interface.Inhibition of Rho-kinase leads to rapid activation of phosphatidylinositol 3-kinase/protein kinase Akt and cardiovascular protection.Harnessing the platelet signaling network to produce an optimal hemostatic response.Spatiotemporal regulation of coagulation and platelet activation during the hemostatic response in vivo.Loss of PIKfyve in platelets causes a lysosomal disease leading to inflammation and thrombosis in mice.Minding the gaps--and the junctions, too.Phosphatidylinositol transfer protein-α in platelets is inconsequential for thrombosis yet is utilized for tumor metastasis.The calcium-dependent protease calpain causes endothelial dysfunction in type 2 diabetesPlatelets and hemostasis: a new perspective on an old subjectInterrelationships between structure and function during the hemostatic response to injuryUse of electron microscopy to study platelets and thrombi
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description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Timothy J Stalker
@nl
Timothy J Stalker
@sl
Timothy J. Stalker
@en
Timothy J. Stalker
@es
type
label
Timothy J Stalker
@nl
Timothy J Stalker
@sl
Timothy J. Stalker
@en
Timothy J. Stalker
@es
prefLabel
Timothy J Stalker
@nl
Timothy J Stalker
@sl
Timothy J. Stalker
@en
Timothy J. Stalker
@es
P106
P1153
6604080841
P21
P31
P496
0000-0002-0017-4268