Population
GP V-null mice, wild-type mice, and human platelets
Comparison
Proteolytically inactive thrombin and active… vs Wild-type vs GP V null genotypes
Design
Preclinical
Authors
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No immediate clinical implications; leaves open proteolytic-independent thrombin signaling in human thrombosis.
The study identifies a novel thrombin signaling mechanism where the GP Ib-IX-V complex acts as a thrombin receptor after GP V cleavage, leading to platelet activation.
Ramakrishnan et al. (2001) studied this question.
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