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While in the present analyze, we generated a different knockin (KI) transgenic mouse design where by the Pro32Pro33 isoform is expressed within the endogenous integrin β
These details reveal that various signaling pathways downstream from PAR4 activation, beyond Src, modify platelet attachment within the context of the Pro32Pro33 mutation.
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, 2013). These polymorphisms vary from our KI design mainly because they Exhibit greater fibrinogen binding/affinity and represent a constitutively Energetic receptor. The Pro32Pro33 integrin β
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locus, changing the endogenous Ser32Gln33. Pro32Pro33 mice have altered adhesion and enhanced velocity in aggregation, leading to a proaggregatory phenotype observed in tail bleeding and nonfatal thromboembolism.