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Details on Person Under normal physiological conditions, activated protein C (...
| Class:Id | Summation:9930438 |
|---|---|
| _displayName | Under normal physiological conditions, activated protein C (... |
| _timestamp | 2024-12-12 09:42:54 |
| created | [InstanceEdit:9930429] Shamovsky, Veronica, 2024-12-03 |
| literatureReference | [LiteratureReference:9930463] Factor V Leiden Mutation [LiteratureReference:9930459] Factor v leiden and inflammation [LiteratureReference:9930475] Mechanisms of the factor V Leiden paradox [LiteratureReference:9930414] Factor V Leiden [LiteratureReference:9930447] Mutation in blood coagulation factor V associated with resistance to activated protein C [LiteratureReference:9930433] Factor V Leiden Thrombophilia [LiteratureReference:9930477] Factor V enhances the cofactor function of protein S in the APC-mediated inactivation of factor VIII: influence of the factor VR506Q mutation [LiteratureReference:9930446] Better or worse than the original [LiteratureReference:9930489] Factor V Leiden-independent activated protein C resistance: Communication from the plasma coagulation inhibitors subcommittee of the International Society on Thrombosis and Haemostasis Scientific and Standardisation Committee |
| modified | [InstanceEdit:9931718] Shamovsky, Veronica, 2024-12-12 |
| text | Under normal physiological conditions, activated protein C (APC) regulates clotting by cleaving factor Va (FVa) at R534 and R334, preventing excessive clot formation. FV R534Q (FV Leiden) and FV A540V (FV Bonn) variants are resistant to APC, impairing its ability to inactivate FVa by cleaving it at residue R534 (Bertina RM et al., 1994; van Stralen KJ et al., 2008; Pezeshkpoor B et al., 2016). The defective cleavage of these FV variants may also interfere with APC-mediated inactivation of factor VIIIa (FVIIIa), where non-activated but APC-cleaved FV functions as an APC cofactor (Váradi K et al., 1996; Pezeshkpoor B et al., 2016). In addition to APC resistance, FVa Bonn (A540V) exhibits increased affinity for factor Xa (FXa) (Pezeshkpoor B et al., 2016), which diminishes APC-mediated cleavage at R534, as FXa and APC share a common exosite on FV (reviewed by Bernardi F, 2016). These conditions may lead to prolonged FVa (and FVIII) activity, enhanced function of the prothrombinase FVa:FXa complex, and sustained thrombin generation, which may increase the risk of developing abnormal blood clots causing venous thromboembolism (VTE) in individuals carrying the FV Leiden or FV Bonn mutation (reviewed by Pastori et al., 1999; Perez-Pujol S et al., 2012; van Cott EM et al., 2016; Albagoush SA et al., 2023; Moore GW et al., 2023). |
| (summation) | [FailedReaction:9930452] F5 R534Q, A540V is not cleaved by activated protein C [Homo sapiens] |
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No pathways have been reviewed or authored by Under normal physiological conditions, activated protein C (... (9930438)
