Platelet Disorders and Treatments

This study uses molecular dynamics simulations to compare the physical stability and binding energy of VWF-GPIb and FXI-GPIb bonds, finding VWF-GPIb more stable with higher binding energy.

This study shows that glucocorticoid receptor activation increases TSP-1 expression through p38 MAPK and AGO-2 phosphorylation, and microRNA-1-3p inhibition in endothelial cells and platelets.

This study shows that RUNX1 haploinsufficiency reduces megakaryocyte-biased hematopoietic progenitor cells and identifies drug targets to correct this defect.

This study shows that Cdk2 is required for platelet activation by inhibiting PP1 phosphatase activity and promoting Erk activation through phosphorylation of PPP1R12a.

The paper uses a mathematical model to analyze megakaryopoiesis in TPO receptor-deficient and overexpressed mice, identifying strain-dependent parameters and suggesting an unknown control mechanism.

The paper identifies four proteins causally linked to platelet traits using genomic, epidemiological, and experimental data.

The paper shows that platelet receptor signaling differs between healthy men and women and changes after myocardial infarction, with implications for sex-specific anti-platelet therapy.

The paper develops a computational model of CLEC-2 signaling and validates its predictions experimentally, revealing temperature-dependent activation and lipid raft involvement.

The paper reports a diagnostic HTS test for bleeding, thrombotic, and platelet disorders, identifying molecular diagnoses in 897 out of 2,390 patients.

This study identifies altered miRNA expression during platelet storage and links them to functional changes and storage lesions.

The paper simulates the structural impact of missense SNPs in the thrombopoietin receptor C-MPL and maps their geographical distribution across populations.

The paper reports a new clinical syndrome linked to ACTB mutations, characterized by thrombocytopenia, microcephaly, and developmental disability, and identifies altered cytoskeletal interactions in affected cells.