Kausar Ahmed - Academia.edu (original) (raw)
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Papers by Kausar Ahmed
The Journal of biological chemistry, 2013
The mechanistic action of antitumor agent OSW-1 is not clearly understood. Results: OSW-1 trigger... more The mechanistic action of antitumor agent OSW-1 is not clearly understood. Results: OSW-1 triggers a calcium-dependent cell death through inhibition of sodium-calcium exchanger 1 (NCX1) and mitochondrial calcium overload. Conclusion: Potency and efficacy of OSW-1 in eliminating leukemia cells are dependent on homeostatic calcium disruption. Significance: New insights on the role of calcium in the mechanism of OSW-1 reveal potential in therapeutics.
Experimental Hematology, 2011
Objective. Constitutive activation of the Janus kinase 2 (JAK2) due to a somatic mutation (JAK2 V... more Objective. Constitutive activation of the Janus kinase 2 (JAK2) due to a somatic mutation (JAK2 V617F ) arising in hematopoietic stem cells plays a central role in the pathophysiology of myeloproliferative neoplasms (MPNs). To investigate the hypothesis that drugs that inhibit JAK2 have therapeutic potential, we developed a small molecule inhibitor, SGI-1252, that targets the adenosine triphosphate-binding and solvent pocket of the protein.
The Journal of biological chemistry, 2013
The mechanistic action of antitumor agent OSW-1 is not clearly understood. Results: OSW-1 trigger... more The mechanistic action of antitumor agent OSW-1 is not clearly understood. Results: OSW-1 triggers a calcium-dependent cell death through inhibition of sodium-calcium exchanger 1 (NCX1) and mitochondrial calcium overload. Conclusion: Potency and efficacy of OSW-1 in eliminating leukemia cells are dependent on homeostatic calcium disruption. Significance: New insights on the role of calcium in the mechanism of OSW-1 reveal potential in therapeutics.
Experimental Hematology, 2011
Objective. Constitutive activation of the Janus kinase 2 (JAK2) due to a somatic mutation (JAK2 V... more Objective. Constitutive activation of the Janus kinase 2 (JAK2) due to a somatic mutation (JAK2 V617F ) arising in hematopoietic stem cells plays a central role in the pathophysiology of myeloproliferative neoplasms (MPNs). To investigate the hypothesis that drugs that inhibit JAK2 have therapeutic potential, we developed a small molecule inhibitor, SGI-1252, that targets the adenosine triphosphate-binding and solvent pocket of the protein.