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Article

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

Blood - 3 Aug 2017

Hu Zhilian, Liu Yang, Huarng Michael C, Menegatti Marzia, Reyon Deepak, Rost Megan S, Norris Zachary G, Richter Catherine E, Stapleton Alexandra N, Chi Neil C, Peyvandi Flora, Joung J Keith, Shavit Jordan A

Abstract excerpt

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...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 28576875
DOI: 10.1182/blood-2017-02-765206
PMCID: PMC5542852

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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