Coagulation factor XI (FA11) (274-284) Heavy
A-[U-13C6,15N-Leu]-SGFS-[U-13C6,15N-Leu]-QS-[C(Cam)]-R-acid
Description
Application Data
Description
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Coagulation factor XI is an inactive protein precursor of the coagulation protease factor XIa, a major component of coagulation in the clotting cascade.
Application Data
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Catalogue number crb1300898 Molecular Weight 1238.6 Sequence (one letter code) A-[U-13C6,15N-Leu]-SGFS-[U-13C6,15N-Leu]-QS-[C(Cam)]-R-acid
Sequence (three letter code) H-Ala-[U-13C6,15N-Leu]-Ser-Gly-Phe-Ser-[U-13C6,15N-Leu]-Gln-Ser-[Cys(Cam)]-Arg-OH
Purity >95% Storage -20°C References Emsley et al (2010) Structure and function of factor XI. Blood. 115(13) 2569 PMID: 20110423
Smith et al (2015) How it all starts: initiation of the clotting cascade. Crit. Rev. Biochem. Mol. Biol. 50(4) 326 PMID: 26018600
Manufactured in: United Kingdom Coagulation factor XI is an inactive protein precursor of the coagulation protease factor XIa, a major component of coagulation in the clotting cascade. Structurally factor XI is a disulfide dimer in which each subunit is made up of apple domains which are 90 or 91 amino acid repeats. At the C-terminus a catalytic domain is present. Within the blood it is found to be in complex with kininogen.
Factor XI needs to be activated by either factor XIIa, α-thrombin, meizothrombin and factor XIa autoactivation through cleavage of factor XI’s Arg369-Ile370 bond. This produces active coagulation protease factor XIa, necessary for thrombin generation in the clotting cascade.
The clotting cascade occurs in response to a vascular injury to reduce the amount of blood flow to the site of injury. It can be activated through the tissue factor pathway or the contact pathway.
A deficiency in factor XI can contribute to bleeding disorders and can be the result of mutations on the FXI gene. Such mutations can include: Glu117Stop which results in the formation of a truncated protein and the missense mutation Phe283Leu effecting FXI dimer formation.