Fahd A. Kuriri
RMIT University
ReceptorChemistryIntegrinTyrosineGlycoprotein IIb/IIIaTyrosine-kinase inhibitorIbrutinibGPVIProstaglandinPlatelet Glycoprotein GPIIb-IIIa ComplexPlatelet Glycoprotein GPIb-IX ComplexPlatelet activationCancer researchAmino acidNitric oxidePlateletBruton's tyrosine kinaseCell biology
2Publications
2H-index
19Citations
Publications 3
Newest
#1Fahd A. Kuriri (Shaqra University)H-Index: 2
#2Genia F. Burchall (RMIT: RMIT University)H-Index: 4
Last. Denise E. Jackson (RMIT: RMIT University)H-Index: 24
view all 7 authors...
The immunoglobulin (Ig)–immunoreceptor tyrosine–based inhibitory motif (ITIM) bearing receptors, PECAM-1 and CEACAM1 have been shown net negative regulators of platelet-collagen interactions and hemi-ITAM signalling pathways. null In this study, a double knockout (DKO) mouse null was developed with deleted PECAM-1 and CEACAM1 to study their combined contribution in platelet activation by glycoprotein VI, C-type lectin-like receptor 2 (CLEC-2), protease activated receptor PAR-4, ADP purinergic re...
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#1Gasim Dobie (RMIT: RMIT University)H-Index: 2
#2Fahd A. Kuriri (RMIT: RMIT University)H-Index: 2
Last. Denise E. Jackson (RMIT: RMIT University)H-Index: 24
view all 10 authors...
The Bruton's tyrosine kinase (Btk) inhibitor ibrutinib has proven to be efficacious in the treatment of B-cell chronic lymphocytic leukemia (B-CLL) and related diseases. However, a major adverse side effect of ibrutinib is bleeding, including major hemorrhages. The bleeding associated with ibrutinib use is thought to be due to a combination of on-target irreversible Btk inhibition, as well as off-target inhibition of other kinases, including EGFR, ITK, JAK3, and Tec kinase. In this study, we inv...
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#1Fahd A. Kuriri (RMIT: RMIT University)H-Index: 2
#2Cindy J. O’Malley (RMIT: RMIT University)H-Index: 14
Last. Denise E. Jackson (RMIT: RMIT University)H-Index: 24
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Abstract Background The main role of platelets is to control haemostasis when there is a blood vessel injury in order to minimise blood loss at the injury site. Under normal circumstances, platelets flow freely within blood vessels as the endothelial cells provide a non-adhesion surface. Naturally, bioactive mediators are released from endothelial cells to prevent and control platelet activation. However, when the vascular endothelium is ruptured, the local concentration of nitric oxide and pros...
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