18 results on '"Kim, KyungHo"'
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2. Signaling-mediated cooperativity between glycoprotein Ib-IX and protease-activated receptors in thrombin-induced platelet activation
3. Hydroxyurea with AKT2 inhibition decreases vaso-occlusive events in sickle cell disease mice
4. NOX2 is critical for heterotypic neutrophil-platelet interactions during vascular inflammation
5. Platelet ERO1α Is Crucial for Ca2+ Mobilization and Platelet Activation in Atherothrombosis
6. Agonist-induced platelet procoagulant activity requires shear and a Rac1-dependent signaling mechanism
7. G protein–dependent basal and evoked endothelial cell vWF secretion
8. Platelet protein disulfide isomerase is required for thrombus formation but not for hemostasis in mice
9. Extracellular protein disulfide isomerase regulates ligand-binding activity of αMβ2 integrin and neutrophil recruitment during vascular inflammation
10. Specific Inhibition of AKT with ARQ 092, an Orally-Available Selective AKT Inhibitor, Attenuates Acute Vaso-Occlusive Events in Sickle Cell Disease
11. Co-Administration of Hydroxyurea and a Specific AKT2 Inhibitor Has Beneficial Effects on Acute Vaso-Occlusive Events and Survival in Sickle Cell Disease Mice
12. Platelet Surface PDI Controls the Ligand-Binding Function of Glycoprotein Ibalpha and Platelet-Neutrophil Interactions Under Thromboinflammatory Conditions
13. Neutrophil DREAM Is a Novel Regulator for Beta2 Integrin Function through NF-Kappab Signaling and Modulates Neutrophil Recruitment during Vascular Inflammation
14. DREAM, a Transcription Repressor, Is Critical for Calcium Signaling and Platelet Thrombus Formation Independently of Its Transcriptional Activity
15. NADPH Oxidase 2 Is Critical for Heterotypic Neutrophil-Platelet Interactions during Vascular Inflammation
16. Platelet ERO1α Is Crucial for Ca2+Mobilization and Platelet Activation in Atherothrombosis
17. Neutrophil Akt2 Plays a Critical Role In Heterotypic Neutrophil-Platelet Interactions During Vascular Inflammation
18. A Mechanism For Switch Of Integrin Signaling Direction and a New Anti-Thrombotic Strategy Through Selective Outside-In Signaling Inhibition
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