Protection by recombinant alpha 1-antitrypsin Ala357 Arg358 against arterial hypotension induced by factor XII fragment.

Détails

ID Serval
serval:BIB_89B0B5E9BBC1
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Protection by recombinant alpha 1-antitrypsin Ala357 Arg358 against arterial hypotension induced by factor XII fragment.
Périodique
The Journal of clinical investigation
Auteur⸱e⸱s
Schapira M., Ramus M.A., Waeber B., Brunner H.R., Jallat S., Carvallo D., Roitsch C., Courtney M.
ISSN
0021-9738 (Print)
ISSN-L
0021-9738
Statut éditorial
Publié
Date de publication
08/1987
Peer-reviewed
Oui
Volume
80
Numéro
2
Pages
582-585
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
The specificity of serpin superfamily protease inhibitors such as alpha 1-antitrypsin or C1 inhibitor is determined by the amino acid residues of the inhibitor reactive center. To obtain an inhibitor that would be specific for the plasma kallikrein-kinin system enzymes, we have constructed an antitrypsin mutant having Arg at the reactive center P1 residue (position 358) and Ala at residue P2 (position 357). These modifications were made because C1 inhibitor, the major natural inhibitor of kallikrein and Factor XIIa, contains Arg at P1 and Ala at P2. In vitro, the novel inhibitor, alpha 1-antitrypsin Ala357 Arg358, was more efficient than C1 inhibitor for inhibiting kallikrein. Furthermore, Wistar rats pretreated with alpha 1-antitrypsin Ala357 Arg358 were partially protected from the circulatory collapse caused by the administration of beta-Factor XIIa.
Mots-clé
Animals, Blood Coagulation, Complement C1 Inactivator Proteins/metabolism, Factor XII/antagonists & inhibitors, Hypotension/prevention & control, Kallikreins/metabolism, Kinetics, Prekallikrein/metabolism, Rats, Recombinant Proteins, Thrombin/metabolism, Thrombin Time, alpha 1-Antitrypsin/analogs & derivatives, alpha 1-Antitrypsin/pharmacology
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 15:27
Dernière modification de la notice
24/02/2024 7:33
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