Journal article icon

Journal article

Genome editing of factor X in zebrafish reveals unexpected tolerance of severe defects in the common pathway

Abstract:

Deficiency of factor X (F10) in humans is a rare bleeding disorder with a heterogeneous phenotype and limited therapeutic options. Targeted disruption of F10 and other common pathway factors in mice results in embryonic/neonatal lethality with rapid resorption of homozygous mutants, hampering additional studies. Several of these mutants also display yolk sac vascular defects, suggesting a role for thrombin signaling in vessel development. The zebrafish is a vertebrate model that demonstrates ...

Expand abstract
Publication status:
Published
Peer review status:
Peer reviewed

Actions


Access Document


Files:
Publisher copy:
10.1182/blood-2017-02-765206

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Role:
Author
More from this funder
Name:
Bayer
Grant:
Hemophilia Awards Program (J.A.S.
More from this funder
Name:
National Hemophilia Foundation/Novo Nordisk
Grant:
Career Development Award
More from this funder
Name:
Hemophilia of Georgia
Grant:
Clinical Scientist Development Grant
More from this funder
Name:
National Institutes of Health
Grant:
National Institute of General Medical Sciences grant R01-GM088040 (J.K.J.
Publisher:
American Society of Hematology
Journal:
Blood More from this journal
Volume:
130
Issue:
5
Pages:
666-676
Publication date:
2017-08-03
Acceptance date:
2017-05-23
DOI:
EISSN:
1528-0020
ISSN:
0006-4971
Pubs id:
pubs:725027
UUID:
uuid:27a6e577-59c6-4381-bc0d-8a7f84d03544
Local pid:
pubs:725027
Source identifiers:
725027
Deposit date:
2017-09-02

Terms of use


Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP