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Effect of a truncated mutant factor V on hemostatic function and embryonic development in mice
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  • Published: 12 February 2026

Effect of a truncated mutant factor V on hemostatic function and embryonic development in mice

  • Andrea Miguel-Batuecas1 na1,
  • Juan A. De Pablo-Moreno2,9 na1,
  • Néstor Porras3,
  • Pablo Bermejo-Álvarez4,
  • Leopoldo González-Brusi4,
  • Luis J. Serrano5,
  • Javier M. De Pablo-Moreno3,
  • María José Sánchez6,
  • Mariano García-Arranz5,
  • Antonio Rodríguez-Bertos3,7,
  • Bilgimol Chumappumkal Joseph8,
  • Luis Revuelta9 na2 &
  • …
  • Antonio Liras1 na2 

Scientific Reports , Article number:  (2026) Cite this article

We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Cell biology
  • Developmental biology
  • Diseases
  • Genetics
  • Medical research
  • Molecular biology

Abstract

Factor V is an essential protein in the blood clotting process and plays a central role in secondary hemostasis. Its deficiency causes a rare inherited disorder characterized by episodes of severe bleeding, some of which can be life-threatening. Although previous studies have established that factor V is essential for normal embryonic development, its specific contribution to vascular maturation remains incompletely understood, factor V is believed to contribute to blood vessel stabilization and regulate angiogenesis through its interaction with thrombin. In a recent study, a CRISPR-engineered mouse model intended to produced a mild factor V deficiency disease, unexpectedly produced a frameshift mutation in the A3 domain, resulting in a truncated protein. Factor V levels in healthy embryonic mouse tissues were assessed to investigate its role at different developmental stages. The mutation markedly impaired viability, as homozygous mice exhibited a lethal phenotype with severe bleeding and perinatal death, along with impaired coagulation function. Histopathological and immunohistochemical analyses indicated a link between factor V deficiency, thrombin and α-smooth muscle actin, potentially affecting proangiogenic signaling and embryonic vascular formation. Factor V gene expression increased during late embryogenesis, underscoring its importance in vascular development and maturation. Overall, these findings are consistent with a role for factor V in stabilizing embryonic blood vessels and modulating thrombin-dependent angiogenesis, and add further detail on the developmental impact of its deficiency and the pathogenesis of congenital bleeding disorders.

Data availability

The data generated during and/or analyzed during the current study are available from the corresponding author (Antonio Liras) on reasonable request, and in the Supplementary information file.

References

  1. Barcellona, D. & Marongiu, F. The hemostatic system: 1st Part. J. Pediatr. Neonat. Individ. Med. 9, e090106. https://doi.org/10.7363/090106 (2020).

    Google Scholar 

  2. Versteeg, H. H., Heemskerk, J. W. M., Levi, M. & Reitsma, P. H. New fundamentals in hemostasis. Physiol. Rev. 93, 327–358. https://doi.org/10.1152/physrev.00016.2011 (2013).

    Google Scholar 

  3. De Pablo-Moreno, J. A., Miguel-Batuecas, A., De Sancha, M. & Liras, A. The magic of proteases: from a procoagulant and anticoagulant factor V to an equitable treatment of its inherited deficiency. Int. J. Mol. Sci. 24, 6243. https://doi.org/10.3390/ijms24076243 (2023).

    Google Scholar 

  4. Mohapatra, A. K., Todaro, A. M. & Castoldi, E. Factor V variants in bleeding and thrombosis. Res. Pract. Thromb. Haemost. 8, 102330. https://doi.org/10.1016/j.rpth.2024.102330 (2024).

    Google Scholar 

  5. Asselta, R. & Peyvandi, F. Factor V deficiency. Semin. Thromb. Hemost. 35, 382–389. https://doi.org/10.1055/s-0029-1225760 (2009).

    Google Scholar 

  6. Huang, J. N. & Koerper, M. A. Factor V deficiency: a concise review. Haemophilia 14, 1164–1169. https://doi.org/10.1111/j.1365-2516.2008.01785.x (2008).

    Google Scholar 

  7. Tabibian, S. et al. A comprehensive overview of coagulation factor V and congenital factor V deficiency. Semin. Thromb. Hemost. 45, 523–543. https://doi.org/10.1055/s-0039-1687906 (2019).

    Google Scholar 

  8. The Human Gene Mutation Database at the Institute of Medical Genetics in Cardiff (HGMD). The human gene mutation database at the Institute of Medical Genetics in Cardiff http://www.hgmd.cf.ac.uk/ac/index.php (2025)

  9. Moret, A. et al. Next generation sequencing in bleeding disorders: two novel variants in the F5 gene (Valencia-1 and Valencia-2) associated with mild factor V deficiency. J. Thromb. Thrombolysis 48, 674–678. https://doi.org/10.1007/s11239-019-01911-z (2019).

    Google Scholar 

  10. Caudill, J. S. et al. Severe coagulation factor V deficiency associated with an interstitial deletion of chromosome 1q. J. Thromb. Haemost. 5, 626–628. https://doi.org/10.1111/j.1538-7836.2007.02363.x (2007).

    Google Scholar 

  11. Guasch, J. F. et al. Severe coagulation factor V deficiency caused by a 4 bp deletion in the factor V gene. Br. J. Haematol. 101, 32–39. https://doi.org/10.1046/j.1365-2141.1998.00664.x (1998).

    Google Scholar 

  12. Holmberg, L., Henriksson, P., Ekelund, H. & Åstedt, B. Coagulation in the human fetus. J. Pediatr. 85, 860–864. https://doi.org/10.1016/S0022-3476(74)80361-6 (1974).

    Google Scholar 

  13. Poralla, C. et al. The coagulation system of extremely preterm infants: influence of perinatal risk factors on coagulation. J. Perinatol. 32, 869–873. https://doi.org/10.1038/jp.2011.182 (2012).

    Google Scholar 

  14. Terwiel, JPh., Veltkamp, J. J., Bertina, R. M. & Muller, H. P. Coagulation factors in the human fetus of about 20 weeks of gestational age. Br. J. Haematol. 45, 641–650. https://doi.org/10.1111/j.1365-2141.1980.tb07187.x (1980).

    Google Scholar 

  15. Terwiel, J. P., Veltkamp, J. J., Bertina, R. M., van der Linden, I. K. & van Tilburg, N. H. Coagulation factors in the premature infant born after about 32 weeks of gestation. Neonatology 47, 9–18. https://doi.org/10.1159/000242085 (1985).

    Google Scholar 

  16. Andrew, M. et al. Development of the human coagulation system in the full-term infant. Blood 70, 165–172 (1987).

    Google Scholar 

  17. Andrew, M. et al. Development of the human coagulation system in the healthy premature infant. Blood 72, 1651–1657 (1988).

    Google Scholar 

  18. Reverdiau-Moalic, P., Delahousse, B., Body, G., Bardos, P. & Leroy, J. Evolution of blood coagulation activators and inhibitors in the healthy human fetus. Blood 88, 900–906 (1996).

    Google Scholar 

  19. Heikinheimo, R. Coagulation studies with fetal blood. Neonatology 7, 319–327. https://doi.org/10.1159/000239936 (1964).

    Google Scholar 

  20. Hsi, B.-L., Page Faulk, W., Yeh, C.-J.G. & Mcintyre, J. A. Immunohistology of clotting factor V in human extraembryonic membranes. Placenta 8, 529–535. https://doi.org/10.1016/0143-4004(87)90081-6 (1987).

    Google Scholar 

  21. Yang, T. L. et al. The structure and function of murine factor V and its inactivation by protein C. Blood 91, 4593–4599 (1998).

    Google Scholar 

  22. Yang, T. L., Pipe, S. W., Yang, A. & Ginsburg, D. Biosynthetic origin and functional significance of murine platelet factor V. Blood 102, 2851–2855. https://doi.org/10.1182/blood-2003-04-1224 (2003).

    Google Scholar 

  23. De Pablo-Moreno, J. A., Liras, A. & Revuelta, L. Standardization of coagulation factor V reference intervals, prothrombin time, and activated partial thromboplastin time in mice for use in factor V deficiency pathological models. Front. Vet. Sci. 9, 846216. https://doi.org/10.3389/fvets.2022.846216 (2022).

    Google Scholar 

  24. Cui, J., O’Shea, K. S., Purkayastha, A., Saunders, T. L. & Ginsburg, D. Fatal haemorrhage and incomplete block to embryogenesis in mice lacking coagulation factor V. Nature 384, 66–68. https://doi.org/10.1038/384066a0 (1996).

    Google Scholar 

  25. Weyand, A. C. et al. Analysis of factor V in zebrafish demonstrates minimal levels needed for early hemostasis. Blood Adv. 3, 1670–1680. https://doi.org/10.1182/bloodadvances.2018029066 (2019).

    Google Scholar 

  26. Yang, T. et al. Rescue of fatal neonatal hemorrhage in factor V deficient mice by low level transgene expression. Thromb. Haemost. 83, 70–77. https://doi.org/10.1055/s-0037-1613760 (2000).

    Google Scholar 

  27. De Pablo-Moreno, J. A. et al. Development of a novel and viable knock-in factor V deficiency murine model: utility for an ultra-rare disease. PLoS ONE 20, e0321864. https://doi.org/10.1371/journal.pone.0321864 (2025).

    Google Scholar 

  28. Connolly, A. J., Ishihara, H., Kahn, M. L., Farese, R. V. & Coughlin, S. R. Role of the thrombin receptor in development and evidence for a second receptor. Nature 381, 516–519. https://doi.org/10.1038/381516a0 (1996).

    Google Scholar 

  29. Griffin, C. T. A role for thrombin receptor signaling in endothelial cells during embryonic development. Science 293, 1666–1670. https://doi.org/10.1126/science.1061259 (2001).

    Google Scholar 

  30. Ong, K., Horsfall, W., Conway, E. & Schuh, A. Early embryonic expression of murine coagulation system components. Thromb. Haemost. 84, 1023–1030. https://doi.org/10.1055/s-0037-1614166 (2000).

    Google Scholar 

  31. Xue, J. et al. Incomplete embryonic lethality and fatal neonatal hemorrhage caused by prothrombin deficiency in mice. Proc. Natl Acad. Sci. USA 95, 7603–7607. https://doi.org/10.1073/pnas.95.13.7603 (1998).

    Google Scholar 

  32. Bermejo-Álvarez, P., Park, K.-E. & Telugu, B. P. Utero-tubal embryo transfer and vasectomy in the mouse model. J. Vis. Exp. https://doi.org/10.3791/51214 (2014).

    Google Scholar 

  33. Lamas-Toranzo, I. et al. Strategies to reduce genetic mosaicism following CRISPR-mediated genome edition in bovine embryos. Sci. Rep. 9, 14900. https://doi.org/10.1038/s41598-019-51366-8 (2019).

    Google Scholar 

  34. Joseph, B. C. et al. An engineered activated factor V for the prevention and treatment of acute traumatic coagulopathy and bleeding in mice. Blood Adv. 6, 959–969. https://doi.org/10.1182/bloodadvances.2021005257 (2022).

    Google Scholar 

  35. Joseph, B. C. et al. Traumatic bleeding and mortality in mice are intensified by iron deficiency anemia and can be rescued with tranexamic acid. Res. Pract. Thromb. Haemost. 8, 102543. https://doi.org/10.1016/j.rpth.2024.102543 (2024).

    Google Scholar 

  36. Cañete, A. et al. Characterization of a fetal liver cell population endowed with long-term multiorgan endothelial reconstitution potential. Stem Cells 35, 507–521. https://doi.org/10.1002/stem.2494 (2017).

    Google Scholar 

  37. Sanchez, M. et al. An SCL 3′ enhancer targets developing endothelium together with embryonic and adult haematopoietic progenitors. Development 126, 3891–3904. https://doi.org/10.1242/dev.126.17.3891 (1999).

    Google Scholar 

  38. Serrano, L. J. et al. Searching for a cell-based therapeutic tool for haemophilia A within the embryonic/foetal liver and the aorta-gonads-mesonephros region. Thromb. Haemost. 118, 1370–1381. https://doi.org/10.1055/s-0038-1661351 (2018).

    Google Scholar 

  39. Birling, M.-C., Herault, Y. & Pavlovic, G. Modeling human disease in rodents by CRISPR/Cas9 genome editing. Mamm. Genome 28, 291–301. https://doi.org/10.1007/s00335-017-9703-x (2017).

    Google Scholar 

  40. Serrano, L. J. et al. Development and characterization of a factor V-deficient CRISPR cell model for the correction of mutations. Int. J. Mol. Sci. 23, 5802. https://doi.org/10.3390/ijms23105802 (2022).

    Google Scholar 

  41. Cardiero, G., Musollino, G., Prezioso, R. & Lacerra, G. mRNA analysis of frameshift mutations with stop codon in the last exon: the case of hemoglobins Campania [α1 cod95 (−C)] and Sciacca [α1 cod109 (−C)]. Biomedicines 9, 1390. https://doi.org/10.3390/biomedicines9101390 (2021).

    Google Scholar 

  42. Iengar, P. An analysis of substitution, deletion and insertion mutations in cancer genes. Nucleic Acids Res. 40, 6401–6413. https://doi.org/10.1093/nar/gks290 (2012).

    Google Scholar 

  43. Hart, D. P. FVIII immunogenicity—bioinformatic approaches to evaluate inhibitor risk in non-severe hemophilia A. Front. Immunol. 11, 1498. https://doi.org/10.3389/fimmu.2020.01498 (2020).

    Google Scholar 

  44. Natalia, R., Jayne, L., Shawn, T., Paula, J. & David, L. The Canadian “National Program for hemophilia mutation testing” database: a ten-year review. Am. J. Hematol. 88, 1030–1034. https://doi.org/10.1002/ajh.23557 (2013).

    Google Scholar 

  45. Peters, L. L. et al. Large-scale, high-throughput screening for coagulation and hematologic phenotypes in mice. Physiol. Genomics 11, 185–193. https://doi.org/10.1152/physiolgenomics.00077.2002 (2002).

    Google Scholar 

  46. Delev, D., Pavlova, A., Heinz, S., Seifried, E. & Oldenburg, J. Factor 5 mutation profile in German patients with homozygous and heterozygous factor V deficiency. Haemophilia 15, 1143–1153. https://doi.org/10.1111/j.1365-2516.2009.02048.x (2009).

    Google Scholar 

  47. Bernal, S. et al. High mutational heterogeneity, and new mutations in the human coagulation factor V gene: Future perspectives for factor V deficiency using recombinant and advanced therapies. Int. J. Mol. Sci. 22, 9705. https://doi.org/10.3390/ijms22189705 (2021).

    Google Scholar 

  48. Schreuder, M., Reitsma, P. H. & Bos, M. H. A. Blood coagulation factor Va’s key interactive residues and regions for prothrombinase assembly and prothrombin binding. J. Thromb. Haemost. 17, 1229–1239. https://doi.org/10.1111/jth.14487 (2019).

    Google Scholar 

  49. Brooks, J. W. Postmortem changes in animal carcasses and estimation of the postmortem interval. Vet. Pathol. 53, 929–940. https://doi.org/10.1177/0300985816629720 (2016).

    Google Scholar 

  50. Lippi, G. et al. Inherited and acquired factor V deficiency. Blood Coagul. Fibrinolysis 22, 160–166. https://doi.org/10.1097/MBC.0b013e3283424883 (2011).

    Google Scholar 

  51. Hassan, H. J. et al. Blood coagulation factors in human embryonic-fetal development: preferential expression of the FVII/tissue factor pathway. Blood 76, 1158–1164 (1990).

    Google Scholar 

  52. Kashif, M. & Isermann, B. Role of the coagulation system in development. Thromb. Res. 131, S14–S17. https://doi.org/10.1016/S0049-3848(13)70012-4 (2013).

    Google Scholar 

  53. Naderi, M., Tabibian, S., Shamsizadeh, M. & Dorgalaleh, A. Miscarriage and recurrent miscarriage in patients with congenital factor V deficiency: a report of six cases in Iran. Int. J. Hematol. 103, 673–675. https://doi.org/10.1007/s12185-016-1981-7 (2016).

    Google Scholar 

  54. Shibata, M., Makihara, N. & Iwasawa, A. The yolk sac’s essential role in embryonic development. Reprod. Med. Biol. 11, 243–258. https://doi.org/10.7831/ras.11.0_243 (2023).

    Google Scholar 

  55. Goh, I. et al. Yolk sac cell atlas reveals multiorgan functions during human early development. Science 381, eadd7564. https://doi.org/10.1126/science.add7564 (2023).

    Google Scholar 

  56. Segers, K., Dahlbäck, B. & Nicolaes, G. Coagulation factor V and thrombophilia: background and mechanisms. Thromb. Haemost. 98, 530–542. https://doi.org/10.1160/TH07-02-0150 (2007).

    Google Scholar 

  57. Liebman, H. A., Furie, B. C. & Furie, B. Hepatic vitamin K–dependent carboxylation of blood-clotting proteins. Hepatology 2, 488S-494S. https://doi.org/10.1002/hep.1840020416 (1982).

    Google Scholar 

  58. Tatsumi, K. et al. Hepatocyte is a sole cell type responsible for the production of coagulation factor IX in vivo. Cell Med. 3, 25–31. https://doi.org/10.3727/215517912X639496 (2012).

    Google Scholar 

  59. Jensen, A.H.-B., Josso, F., Zamet, P., Monset-Couchard, M. & Minkowski, A. Evolution of blood clotting factor levels in premature infants during the first 10 days of life: a study of 96 cases with comparison between clinical status and blood clotting factor levels. Pediatr. Res. 7, 638–644. https://doi.org/10.1203/00006450-197307000-00007 (1973).

    Google Scholar 

  60. Huang, X. et al. Frame-shifted proteins of a given gene retain the same function. Nucleic Acids Res. 48, 4396–4404. https://doi.org/10.1093/nar/gkaa169 (2020).

    Google Scholar 

  61. Shi, G.-D. et al. iTRAQ-based proteomics profiling of Schwann cells before and after peripheral nerve injury. Iran. J. Basic Med. Sci. https://doi.org/10.22038/ijbms.2018.26944.6588 (2018).

    Google Scholar 

  62. Dai, Y., Kretz, C. A., Kim, P. Y. & Gross, P. L. A specific fluorescence resonance energy quenching-based biosensor for measuring thrombin activity in whole blood. J. Thromb. Haemost. 22, 1627–1639. https://doi.org/10.1016/j.jtha.2024.02.007 (2024).

    Google Scholar 

  63. Krenzlin, H., Lorenz, V., Danckwardt, S., Kempski, O. & Alessandri, B. The importance of thrombin in cerebral injury and disease. Int. J. Mol. Sci. 17, 84. https://doi.org/10.3390/ijms17010084 (2016).

    Google Scholar 

  64. Bhat, V. et al. Vascular remodeling underlies rebleeding in hemophilic arthropathy. Am. J. Hematol. 90, 1027–1035. https://doi.org/10.1002/ajh.24133 (2015).

    Google Scholar 

  65. Wang, J., Zohar, R. & McCulloch, C. A. Multiple roles of α-smooth muscle actin in mechanotransduction. Exp. Cell Res. 312, 205–214. https://doi.org/10.1016/j.yexcr.2005.11.004 (2006).

    Google Scholar 

  66. Ito, K. et al. An immunohistochemical analysis of tissue thrombin expression in the human atria. PLoS ONE 8, e65817. https://doi.org/10.1371/journal.pone.0065817 (2013).

    Google Scholar 

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Acknowledgements

The authors would like to thank Benedicto Jerónimo, supervisor of the animal facility, for his care for the safety and welfare of the animals. We thank the technical staff at CABD, Tamara Garcia-Leal, Ana Franco, and Candida Mateos, for their support with embryo collection and animal husbandry. We would also like to thank the genomics unit, CAI of biological techniques, of the Complutense University of Madrid, for their work on the Sanger sequencing of the samples.

Funding

This research was funded by the Association for Research and Cure of Factor V deficiency (ASDEFAV), grant number ASDEFAV/2021–25; the Complutense University of Madrid and Banco Santander, grant number CT63/19-CT64/19; the Spanish Ministry of Science and Innovation, grant number PID2020-117501RB-I00; the Community of Madrid, grant number CT85/23; MJS work was supported by a Spanish María de Maeztu Unit excellence grant CEX-2020-001088-M to the CABD, and by Regional Government of Andalusia, Department of Innovation (PAI-BIO-295).

Author information

Author notes

  1. These authors contributed equally: Andrea Miguel-Batuecas and Juan A. De Pablo-Moreno.

  2. These authors jointly supervised this work: Luis Revuelta and Antonio Liras.

Authors and Affiliations

  1. Department of Genetics, Physiology and Microbiology, School of Biological Sciences, Complutense University, Madrid, Spain

    Andrea Miguel-Batuecas & Antonio Liras

  2. Department of Veterinary Sciences, Faculty of Biomedical and Health Sciences, Universidad Europea de Madrid, Villaviciosa de Odón, Madrid, Spain

    Juan A. De Pablo-Moreno

  3. VISAVET Health Surveillance Centre, Complutense University, Madrid, Spain

    Néstor Porras, Javier M. De Pablo-Moreno & Antonio Rodríguez-Bertos

  4. Animal Reproduction Department, INIA, CSIC, Madrid, Spain

    Pablo Bermejo-Álvarez & Leopoldo González-Brusi

  5. Fundación Jiménez Díaz University Hospital Health Research Institute, Fundación Jiménez Díaz University Hospital, and Department of Surgery, Autonomous University, Madrid, Spain

    Luis J. Serrano & Mariano García-Arranz

  6. Centro Andaluz de Biología del Desarrollo (CABD), Consejo Superior de Investigaciones Científicas (CSIC), Junta de Andalucía (JA), Pablo de Olavide University (UPO), Sevilla, Spain

    María José Sánchez

  7. Department of Internal Medicine and Animal Surgery, School of Veterinary Medicine, Complutense University, Madrid, Spain

    Antonio Rodríguez-Bertos

  8. Division of Hematology/Oncology, Department of Medicine, University of California San Diego, La Jolla, CA, USA

    Bilgimol Chumappumkal Joseph

  9. Department of Physiology, School of Veterinary Medicine, Complutense University, Madrid, Spain

    Juan A. De Pablo-Moreno & Luis Revuelta

Authors
  1. Andrea Miguel-Batuecas
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  2. Juan A. De Pablo-Moreno
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Contributions

A.L. project administration and coordination, A.L., P.B.A., L.R. supervision, A.L., J.A.D.P.M., N.P., P.B.A., L.J.S. conceptualization, A.L., P.B.A., M.J.S., M.G.A., L.R. resources, A.L., P.B.A., M.G.A., A.R.B., L.R. funding acquisition, A.L., A.M.B., J.A.D.P.M., N.P., P.B.A., L.J.S., J.M.D.P.M., M.G.A., A.R.B. methodology, A.L., A.M.B., J.A.D.P.M., P.B.A., L.G.B., L.J.S., J.M.D.P.M., M.J.S., M.G.A., A.R.B., L.R., B.C.J. investigation, A.L., A.M.B., J.A.D.P.M., M.G.A., B.C.J. formal analysis and data curation and interpretation, A.L., A.M.B., J.A.D.P.M., N.P., P.B.A., L.G.B., B.C.J. writing—Original draft, A.L., A.M.B., J.A.D.P.M., N.P., P.B.A., M.G.A., L.R., B.C.J. writing—Review & Editing.

Corresponding author

Correspondence to Antonio Liras.

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Competing interests

The authors declare that they have no competing interests. AL, JADPM, LR, AMB, PBA, and LGB, have a mouse model, deficient infactor V, protected by Spanish patent (Ref. ES2948817B2). Holders: Complutense University of Madrid, and Superior Council for Scientific Research. Spain. Official Bulletin of Industrial Property (21-02-2024) Volume 2: Inventions. p. 8. Available in: https://sede.oepm.gob.es/bopiweb/descargaPublicaciones/formBusqueda.action

Ethics approval

The study was conducted in compliance with Royal Decree 53/2013 and Directive 2010/63/EU. All procedures used were approved by the School of Veterinary Medicine of the Complutense University of Madrid, the Ethics Committees on Animal Experimentation of the Complutense University, and the Madrid Regional Government (PROEX 040/17 and PROEX 358.4/21).

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Miguel-Batuecas, A., De Pablo-Moreno, J.A., Porras, N. et al. Effect of a truncated mutant factor V on hemostatic function and embryonic development in mice. Sci Rep (2026). https://doi.org/10.1038/s41598-026-38387-w

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  • Received: 09 September 2025

  • Accepted: 29 January 2026

  • Published: 12 February 2026

  • DOI: https://doi.org/10.1038/s41598-026-38387-w

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Keywords

  • Factor V
  • Factor V deficiency
  • Embryogenesis
  • Truncated mouse model
  • CRISPR/Cas9
  • Thrombin
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