“…Impaired platelet aggregation and platelet spreading on fibrinogen, delayed kinetics of clot retraction, restricted cytoskeletal reorganization. Increased bleeding time and volume and rebleeding, but without spontaneous bleeding complications[150, 156, 157] | CEACAM-1 | Null | Enhanced aggregation, enhanced platelet adhesion on type I collagen but not fibrinogen, elevated granule secretion, larger and more stable thrombi | [137] |
CIB1 | Normal soluble fibrinogen binding | Normal aggregation and α-granule secretion, increased tail bleeding time and rebleeding, formation of unstable thrombi, impaired spreading on immobilized fibrinogen, reduced tyrosine phosphorylation of the integrin β3 tail | [93, 101] |
cPLA2α | Impaired fibrinogen binding in response to CRP or the lower concentration of PAR4 peptide | Impaired collagen-induced aggregation, spreading on fibrinogen, platelet aggregation. Prolonged bleeding time | [224, 225] |
Dab2 | Impaired soluble fibrinogen binding | Selectively defective in thrombin-induced aggregation, platelet spreading on fibrinogen and clot retraction. |
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