All Outputs (4)

Atherogenic lipid stress induces platelet hyperactivity through CD36-mediated hyposensitivity to prostacyclin-; the role of phosphodiesterase 3A. (2019)
Journal Article
Berger, M., Raslan, Z., Aburima, A., Magwenzi, S., Wraith, K. S., Spurgeon, B. E., …Naseem, K. M. (2020). Atherogenic lipid stress induces platelet hyperactivity through CD36-mediated hyposensitivity to prostacyclin-; the role of phosphodiesterase 3A. Haematologica, 105(3), 808-819. https://doi.org/10.3324/haematol.2018.213348

©2020 Ferrata Storti Foundation Prostacyclin (PGI2) controls platelet activation and thrombosis through a cyclic adenosine monophosphate (cAMP) signaling cascade. However, in patients with cardiovascular diseases this protective mechanism fails for r... Read More about Atherogenic lipid stress induces platelet hyperactivity through CD36-mediated hyposensitivity to prostacyclin-; the role of phosphodiesterase 3A..

Targeting of type I protein kinase A to lipid rafts is required for platelet inhibition by the 3′,5′-cyclic adenosine monophosphate-signaling pathway (2015)
Journal Article
Raslan, Z., Magwenzi, S., Aburima, A., Taskén, K., & Naseem, K. M. (2015). Targeting of type I protein kinase A to lipid rafts is required for platelet inhibition by the 3′,5′-cyclic adenosine monophosphate-signaling pathway. Journal of thrombosis and haemostasis : JTH, 13(9), 1721-1734. https://doi.org/10.1111/jth.13042

Background Platelet adhesion to von Willebrand factor (VWF) is modulated by 3′,5′-cyclic adenosine monophosphate (cAMP) signaling through protein kinase A (PKA)-mediated phosphorylation of glycoprotein (GP)Ibβ. A-kinase anchoring proteins (AKAPs) are... Read More about Targeting of type I protein kinase A to lipid rafts is required for platelet inhibition by the 3′,5′-cyclic adenosine monophosphate-signaling pathway.

Oxidized LDL activates blood platelets through CD36/NOX2–mediated inhibition of the cGMP/protein kinase G signaling cascade (2015)
Journal Article
Magwenzi, S., Woodward, C., Wraith, K. S., Aburima, A., Raslan, Z., Jones, H., …Naseem, K. M. (2015). Oxidized LDL activates blood platelets through CD36/NOX2–mediated inhibition of the cGMP/protein kinase G signaling cascade. Blood, 125(17), 2693-2703. https://doi.org/10.1182/blood-2014-05-574491

Oxidized low-density lipoprotein (oxLDL) promotes unregulated platelet activation in dyslipidemic disorders. Although oxLDL stimulates activatory signaling, it is unclear how these events drive accelerated thrombosis. Here, we describe a mechanism fo... Read More about Oxidized LDL activates blood platelets through CD36/NOX2–mediated inhibition of the cGMP/protein kinase G signaling cascade.

Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade (2010)
Journal Article
Roberts, W., Magwenzi, S., Aburima, A., & Naseem, K. (2010). Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade. Blood, 116(20), 4297-4306. https://doi.org/10.1182/blood-2010-01-265561

Cyclic adenosine monophosphate (cAMP)-dependent signaling modulates platelet function at sites of vascular injury. Here we show that thrombospondin-1 (TSP-1) prevents cAMP/protein kinase A (PKA) signaling through a CD36-dependent mechanism. Prostagla... Read More about Thrombospondin-1 induces platelet activation through CD36-dependent inhibition of the cAMP/protein kinase A signaling cascade.