Evidence map›Paper›PMID 9636196›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Incomplete embryonic lethality and fatal neonatal hemorrhage caused by prothrombin deficiency in mice.

J Xue, Q Wu, L A Westfield, E A Tuley, D Lu, Q Zhang, K Shim, X Zheng, J E Sadler

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 168 citations in OpenAlex.

  1. Article
  2. Article
  3. Effects of Prothrombin on Podocytopathy and Proteinuria in Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Fishing for answers to hemostatic and thrombotic disease: Genome editing in zebrafish.Research and practice in thrombosis and haemostasis · 2022
    Review
  9. Factor IX(a) inhibitors: an updated patent review (2003-present).Expert opinion on therapeutic patents · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Rare congenital bleeding disorders.Annals of translational medicine · 2018
    Review
  18. Article
  19. Review
  20. Review
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

9 authors at 2 institutions in 1 country.

J XueDepartment of Medicine, Department of Biochemistry and Molecular Biophysics, Barnes-Jewish Hospital and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA.
Q Wu
L A Westfield
E A Tuley
D Lu
Q Zhang
K Shim
X Zheng
J E Sadler
Barnes-Jewish Hospital · USHoward Hughes Medical Institute · US

Funding

ENTEROKINASE--AN INTESTINAL DIGESTIVE PROTEASER01DK050053 · NIDDK · WASHINGTON UNIVERSITY · PI SADLER, J EVAN · 1995 to 2003
$580k
BIOLOGICAL FUNCTIONS OF THROMBIN AND THROMBIN RECEPTORSF32HL009500 · NHLBI · BARNES-JEWISH HOSPITAL · PI XUE, JIACHUN · 1996 to 1998
–
NHLBI NIH HHS F32 HL009500NHLBI NIH HHS F32 HL09500NIDDK NIH HHS R01 DK050053NIDDK NIH HHS R01 DK50053
6 · The paper itself

Abstract

Deficiency of blood coagulation factor V or tissue factor causes the death of mouse embryos by 10.5 days of gestation, suggesting that part of the blood coagulation system is necessary for development. This function is proposed to require either generation of the serine protease thrombin and cell signaling through protease-activated receptors or an activity of tissue factor that is distinct from blood clotting. We find that murine deficiency of prothrombin clotting factor 2 (Cf2) was associated with the death of approximately 50% of Cf2(-/-) embryos by embryonic day 10.5 (E10.5), and surviving embryos had characteristic defects in yolk sac vasculature. Most of the remaining Cf2(-/-) embryos died by E15.5, but those surviving to E18.5 appeared normal. The rare Cf2(-/-) neonates died of hemorrhage on the first postnatal day. These studies suggest that a part of the blood coagulation system is adapted to perform a developmental function. Other mouse models show that the absence of platelets or of fibrinogen does not cause fetal wastage. Therefore, the role of thrombin in development may be independent of its effects on blood coagulation and instead may involve signal transduction on cells other than platelets.

Indexed as

Embryonic and Fetal DevelopmentFetal DeathAnimalsAnimals, NewbornCloning, MolecularGene TargetingHemorrhageHypoprothrombinemiasMiceProthrombinProthrombin

Identifiers

PMID9636196
PMCPMC22696
OpenAlexW2147933999

What OpenQuestion holds

Textmetadata
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.