Evidence map›Paper›PMID 18036190›Full record

ArticleJournal of thrombosis and haemostasis : JTH2008

A viable mouse model of factor X deficiency provides evidence for maternal transfer of factor X.

S J Tai, R W Herzog, P Margaritis, V R Arruda, K Chu, J A Golden, P A Labosky, K A High

Abstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Hepato-entrained B220EMBO molecular medicine · 2018
    Article
  7. Factor X Friuli Coagulation Disorder: Almost 50 Years Later.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
    Review
  8. Article
  9. A case of factor X deficiency in a Chihuahua dog.The Canadian veterinary journal = La revue veterinaire canadienne · 2016
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Does plasmin have anticoagulant activity?Vascular health and risk management · 2010
    Article
  15. Article
  16. Article
  17. Bleeding hearts.Blood · 2009
    Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

S J TaiDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
R W Herzog
P Margaritis
V R Arruda
K Chu
J A Golden
P A Labosky
K A High
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

Structural Correlates of Protease and Cofactor FunctionP01HL074124 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI KRISHNASWAMY, SRIRAM · 2003 to 2013
$17.6M
NHLBI NIH HHS P01 HL074124
6 · The paper itself

Abstract

backgroundActivated factor X (FXa) is a vitamin K-dependent serine protease that plays a pivotal role in blood coagulation by converting prothrombin to thrombin. There are no reports of humans with complete deficiency of FX, and knockout of murine F10 is embryonic or perinatal lethal.

objectiveWe sought to generate a viable mouse model of FX deficiency.

methodsWe used a socket-targeting construct to generate F10-knockout mice by eliminating F10 exon 8 (knockout allele termed F10(tm1Ccmt), abbreviated as '-'; wild-type '+'), and a plug-targeting construct to generate mice expressing a FX variant with normal antigen levels but low levels of FX activity [4-9% normal in humans carrying the defect, Pro343-->Ser, termed FX Friuli (mutant allele termed F10(tm2Ccmt), abbreviated as F)].

resultsF10 knockout mice exhibited embryonic or perinatal lethality. In contrast, homozygous Friuli mice [F10 (F/F)] had FX activity levels of approximately 5.5% (sufficient to rescue both embryonic and perinatal lethality), but developed age-dependent iron deposition and cardiac fibrosis. Interestingly, F10 (-/F) mice with FX activity levels of 1-3% also showed complete rescue of lethality. Further study of this model provides evidence supporting a role of maternal FX transfer in the embryonic survival.

conclusionsWe demonstrate that, while complete absence of FX is incompatible with murine survival, minimal FX activity as low as 1-3% is sufficient to rescue the lethal phenotype. This viable low-FX mouse model will facilitate the development of FX-directed therapies as well as investigation of the FX role in embryonic development.

Indexed as

Models, AnimalAmino Acid SubstitutionAnimalsCardiomyopathiesExonsFactor XFactor X DeficiencyFemaleFetal DeathFibrosisGenes, LethalGene TargetingGenetic Complementation TestGenomic ImprintingGenotypeHemosiderosisFactor Xfactor X Friuli

Identifiers

PMID18036190
PMCPMC2471867
OpenAlexW1978320492

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.