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Thrombophilia in mice expressing a tissue factor variant lacking its transmembrane and cytosolic domain.

Authors: Melis, E  Moons, L  Arnout, J  Hoylaerts, MF  Collen, D  Carmeliet, P  Dewerchin, M 
Citation: Melis E, etal., Biochem Biophys Res Commun. 2005 Jul 29;333(2):488-95.
Pubmed: (View Article at PubMed) PMID:15961065
DOI: Full-text: DOI:10.1016/j.bbrc.2005.05.144

Mice with a targeted truncation in the gene encoding tissue factor of blood coagulation (TF) to eliminate the cytosolic domain and carrying a neo(R) cassette in intron 5 unexpectedly displayed severe spontaneous thrombosis in various vascular beds. Thrombosis was observed in heterozygous TF(+/neo) mice, causing death of over 50% of adults within 36 weeks of birth, and fulminantly exacerbating in pregnant females. Homozygous TF(neo/neo) mice were more severely affected and died within 7 weeks after birth. These TF(neo) mice primarily synthesized a mutant mRNA aberrantly spliced from exon 5 to neo(R), encoding an apparently non-vesicle-binding soluble TF lacking both the transmembrane and cytosolic domain, but still capable of blood coagulation induction. This severe thrombotic phenotype associated with the presence of a non-anchored soluble TF variant underscores the recently recognized significance of circulating TF for thrombus formation and development.


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CRRD Object Information
CRRD ID: 11341696
Created: 2016-06-30
Species: All species
Last Modified: 2016-06-30
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.