about
The GSK-3 family as therapeutic target for myocardial diseasesFunctional characterization of antibodies against heparin-platelet factor 4 complex in heparin-induced thrombocytopenia patients in Asian-Indians: relevance to inflammatory markers.Relative contributions of stromal interaction molecule 1 and CalDAG-GEFI to calcium-dependent platelet activation and thrombosis.Cardiomyocyte-specific deletion of Gsk3α mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure.Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.Human genome-wide association and mouse knockout approaches identify platelet supervillin as an inhibitor of thrombus formation under shear stressGSK-3α is a central regulator of age-related pathologies in mice.Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy.Response by Zhou et al to Letter Regarding Article, "Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy".Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.Impact of thrombogenic mutations on clinical phenotypes of von Willebrand disease.Inherited platelet function disorders versus other inherited bleeding disorders: an Indian overview.Germline de novo mutations and linkage markers vs. DNA sequencing for carrier detection in von Willebrand disease.Glanzmann's thrombasthenia in North Indians: sub classification and carrier detection by flow cytometry.Role of RFLP using TspRI for carrier detection in Glanzmann's thrombasthenia: a report on two families.Impact of 789Ala/Ala genotype on quantitative type of von Willebrand disease.Gene tracking in a family of novel identical twins affected by severe type-III von Willebrand Disease (vWD).Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model.Chronic Neuregulin-1β Treatment Mitigates the Progression of Postmyocardial Infarction Heart Failure in the Setting of Type 1 Diabetes Mellitus by Suppressing Myocardial Apoptosis, Fibrosis, and Key Oxidant-Producing Enzymes.Modulation of clinical phenotype of Glanzmann's thrombasthenia by thrombogenic mutations.Phenotypic and molecular characterisation of type 3 von Willebrand disease in a cohort of Indian patients.Characterization of VWF gene conversions causing von Willebrand diseaseTxA Receptor-Based Vaccination: A Novel Potential Therapeutic Approach to Limit ThrombosisTroponin I-Interacting Protein KinaseCharacterisation of mutations and molecular studies of type 2 von Willebrand diseaseCoinheritance of Severe von Willebrand Disease With Glanzmann ThrombastheniaAcquired Glanzmann’s thrombasthenia associated with Hairy cell leukaemiaMolecular defects in ITGA2B and ITGB3 genes in patients with Glanzmann thrombastheniaCarrier Detection in Glanzmann ThrombastheniaEvidence for non-HFE linked hemochromatosis in Asian IndiansPlatelet activation markers in evaluation of thrombotic risk factors in various clinical settingsCardiomyocyte-GSK-3α promotes mPTP opening and heart failure in mice with chronic pressure overload
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P50
description
researcher ORCID ID = 0000-0001-6530-6068
@en
wetenschapper
@nl
name
Firdos Ahmad
@ast
Firdos Ahmad
@en
Firdos Ahmad
@es
Firdos Ahmad
@nl
type
label
Firdos Ahmad
@ast
Firdos Ahmad
@en
Firdos Ahmad
@es
Firdos Ahmad
@nl
prefLabel
Firdos Ahmad
@ast
Firdos Ahmad
@en
Firdos Ahmad
@es
Firdos Ahmad
@nl
P106
P1153
55545862620
P21
P31
P496
0000-0001-6530-6068