All Outputs (4)

Prostacyclin reverses platelet stress fibre formation causing platelet aggregate instability (2017)
Journal Article
Yusuf, M. Z., Raslan, Z., Atkinson, L., Aburima, A., Thomas, S. G., Naseem, K. M., & Calaminus, S. D. (2017). Prostacyclin reverses platelet stress fibre formation causing platelet aggregate instability. Scientific reports, 7(1), Article ARTN 5582. https://doi.org/10.1038/s41598-017-05817-9

Prostacyclin (PGI2) modulates platelet activation to regulate haemostasis. Evidence has emerged to suggest that thrombi are dynamic structures with distinct areas of differing platelet activation. It was hypothesised that PGI2 could reverse platelet... Read More about Prostacyclin reverses platelet stress fibre formation causing platelet aggregate instability.

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., McNeil, C., Wheatcroft, S., Yuldasheva, N., Febbriao, M., Kearney, M., & 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.

cAMP signaling regulates platelet myosin light chain (MLC) phosphorylation and shape change through targeting the RhoA-Rho kinase-MLC phosphatase signaling pathway (2013)
Journal Article
Aburima, A., Wraith, K. S., Raslan, Z., Law, R., Magwenzi, S., & Naseem, K. M. (2013). cAMP signaling regulates platelet myosin light chain (MLC) phosphorylation and shape change through targeting the RhoA-Rho kinase-MLC phosphatase signaling pathway. Blood, 122(20), 3533-3545. https://doi.org/10.1182/blood-2013-03-487850

Cyclic adenosine monophosphate (cAMP)-dependent signaling modulates platelet shape change through unknown mechanisms. We examined the effects of cAMP signaling on platelet contractile machinery. Prostaglandin E1 (PGE1)-mediated inhibition of thrombin... Read More about cAMP signaling regulates platelet myosin light chain (MLC) phosphorylation and shape change through targeting the RhoA-Rho kinase-MLC phosphatase signaling pathway.