Recent advances in factor XII structure and function.
Journal
Current opinion in hematology
ISSN: 1531-7048
Titre abrégé: Curr Opin Hematol
Pays: United States
ID NLM: 9430802
Informations de publication
Date de publication:
01 09 2022
01 09 2022
Historique:
entrez:
2
8
2022
pubmed:
3
8
2022
medline:
5
8
2022
Statut:
ppublish
Résumé
Factor XII (FXII), the precursor of the protease FXIIa, contributes to pathologic processes including angioedema and thrombosis. Here, we review recent work on structure-function relationships for FXII based on studies using recombinant FXII variants. FXII is a homolog of pro-hepatocyte growth factor activator (Pro-HGFA). We prepared FXII in which domains are replaced by corresponding parts of Pro-HGA, and tested them in FXII activation and activity assays. In solution, FXII and prekallikrein undergo reciprocal activation to FXIIa and kallikrein. The rate of this process is restricted by the FXII fibronectin type-2 and kringle domains. Pro-HGA replacements for these domains accelerate FXII and prekallikrein activation. When FXII and prekallikrein bind to negatively charged surfaces, reciprocal activation is enhanced. The FXII EGF1 domain is required for surface binding. We propose a model in which FXII is normally maintained in a closed conformation resistant to activation by intramolecular interactions involving the fibronectin type-2 and kringle domains. These interactions are disrupted when FXII binds to a surface through EGF1, enhancing FXII activation and prekallikrein activation by FXIIa. These observations have important implications for understanding the contributions of FXII to disease, and for developing therapies to treat thrombo-inflammatory disorders.
Identifiants
pubmed: 35916558
doi: 10.1097/MOH.0000000000000727
pii: 00062752-202209000-00002
pmc: PMC9350914
mid: NIHMS1816236
doi:
Substances chimiques
Fibronectins
0
Factor XII
9001-30-3
Prekallikrein
9055-02-1
Kallikreins
EC 3.4.21.-
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
233-243Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL144113
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL140025
Pays : United States
Informations de copyright
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
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