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Gene Review

F10  -  coagulation factor X

Homo sapiens

Synonyms: Coagulation factor X, FX, FXA, Stuart factor, Stuart-Prower factor
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Disease relevance of F10

  • The factor X (F10) genes of 14 unrelated individuals with factor X deficiency (12 familial and two sporadic cases) were sequenced yielding a total of 13 novel mutations [1].
  • Antibody phage display was employed to isolate two scFv antibody fragments, D8 and F10, with specificity for the VEGF165 isoform [2].
  • Immunohistochemistry with D8 and F10 on colorectal carcinoma and adenoma sections revealed positive staining similar to that shown by a polyclonal VEGF antibody [2].
  • Optimal cell viability and growth were achieved using Ham's F10 medium enriched with 20% fetal bovine serum, although cells from a patient with acromegaly also grew in serum-free, defined, hormone-containing medium [3].
  • Classical hemophilia results from a defect of the intrinsic tenase complex, the main factor X (FX) activator [4].

High impact information on F10


Chemical compound and disease context of F10


Biological context of F10

  • Family studies were performed in order to distinguish the contributions of individual mutant F10 alleles to the clinical and laboratory phenotypes [1].
  • The deletion allele of a novel hexanucleotide insertion/deletion polymorphism in the F10 gene promoter region was shown by reporter gene assay, to reduce promoter activity by approximately 20% [1].
  • The expression of a number of blood coagulation factors (F) (FX, FIX, FVIII, FVII, alpha-, beta-, gamma-fibrinogen chains, protein C, and antithrombin III [AT III]) was analyzed at RNA and protein level in 5- to 10-week-old human embryos and fetuses [12].
  • Previous studies using alanine mutagenesis have identified TF residues Lys165 and Lys166 as important for factor X (FX) activation, hypothesizing either that these residues interact with phospholipid head groups or that they directly or indirectly promote macromolecular substrate binding [13].
  • All patients were homozygous for a novel FX mutation (Gly381Asp) in the structurally conserved region of the serine protease active site [14].

Anatomical context of F10

  • Hence, it was concluded that F7, F8 and F10 caused haemagglutination and were responsible for the attachment to urinary epithelial cells, while the fimbriae antigenically termed pseudotype 1 did not induce haemagglutination and played little or no role for the attachment to this kind of epithelial cells [15].
  • Cloning and expression in COS-1 cells of a full-length cDNA encoding human coagulation factor X [16].
  • Comparison with B16/F10 melanoma, a cancer cell line that is representative of previous studies in aged mice, showed that B16/F10 tumors grew minimally in the aged mice [17].
  • P production by luteal cells obtained following delivery declined markedly during 8 days of culture in Ham's F10 medium: 10% fetal calf serum [18].
  • Using this system, no significant differences were noted between control media (Krebs' or Ham's F10) and Ham's F12, Menezo's media, or Krebs' medium exposed to small pieces of a medical-grade silicone rubber semen collection device [19].

Associations of F10 with chemical compounds

  • The previous suggestion that there is a hairpin loop involving residues Gly(12) to Val(15) in the A alpha chain of human fibrinogen is supported by the slow backbone NH exchange rates of Gly(14) and Val(15), by an unusually small NH chemical shift of Val(15), and by strong sequential NOE's involving this region in F10 [20].
  • No predominant structure was found in the chain segment from Ala(1) to Gly(6) for F10 in both H2O and dimethyl sulfoxide [20].
  • These results indicate that the association of FVIIIa and FX occurs from a salt linkage(s) formed between residues of the A1 acidic C-terminus of the cofactor (within residues 349-372) and the serine protease-forming domain of the substrate [21].
  • In Study I, where much lower hormonal levels were obtained at maximum (oestradiol median 297 pmol/l and progesterone 47 nmol/l), the same pattern was observed especially for FVII, FX, fibrinogen, plasminogen and plasmin inhibitor [22].
  • Both ligand blotting and surface plasmon resonance (SPR) showed that Pn-cleaved FX and FXa bound t-PA directly when Pn-treatment was effected in the presence of aPL and Ca(2+) [23].

Physical interactions of F10

  • Cumulatively, our data reveal that substrates FIX and FX in addition to interacting with FVIIa (enzyme) interact with TF (cofactor) using, in part, the EGF1 domain [24].
  • The A2 domain of FVIII significantly increases the affinity and stoichiometry of FVIIIa binding to platelets and contributes to the stability of the FX-activating complex [25].
  • We next investigated whether the FX derivatives could interact with the plasmin precursor plasminogen, and we found that plasmin exposed a binding site only on proPL-bound FX [26].
  • This indicates that the N-terminal residues of the FVII Gla domain are important for the structural integrity of the peptide, and implicates the Gla domain per se in a direct interaction with phospholipid-bound FX [27].
  • The relative orientation of Gla and EGF domains in coagulation factor X is altered by Ca2+ binding to the first EGF domain. A combined NMR-small angle X-ray scattering study [28].

Enzymatic interactions of F10

  • Consistently, the antibody depressed TF/FVII-catalyzed FX activation was shown on Western blotting analysis [29].

Regulatory relationships of F10

  • The presence of EGR-FIXa and FX increases both the number and the affinity of binding sites on activated platelets for both FVIII and FVIIIa, emphasizing the validity of a three-receptor model in the assembly of the F-X-activating complex on the platelet surface [25].
  • Protease-activated receptor-2 (PAR-2) is cleaved and activated by trypsin-like proteolytic enzymes, including tryptase and activated coagulation factor X (FXa) [30].
  • Protamine significantly inhibited factor VII (FVII) activation but not the dissected FX activation [31].
  • The use of a xenogenic cell line to deliver hIL-2 stimulates a strong immunologic cytotoxic anti-tumor response that leads to significant prolongation of survival in mice challenged with the B16/F10 intracranial melanoma tumor [32].
  • None of the compounds examined altered the ability of alpha 1-antitrypsin to inhibit activated coagulation factor X (Xa) [33].

Other interactions of F10

  • Strikingly, when FX was present, low picomolar concentrations of FVIIa caused robust signaling in cells expressing TF and PAR2 [34].
  • The complex of FVIII-FX was made covalent following reaction with the zero-length cross-linking reagent 1-ethyl-3-(3dimethylaminopropyl-)carbodiimide hydrochloride (EDC) [21].
  • The study of this FX deficiency provides an "in vivo" and "in vitro" model for the investigation of Gla domain interactions [35].
  • Whale plasma contained inhibitory activities against thrombin, activated Stuart factor, activated PTA, activated Fletcher factor, and plasmin [36].
  • A 1.5-kb cDNA (FX) encoding full-length human coagulation factor X was isolated from a human fetal liver cDNA library [16].

Analytical, diagnostic and therapeutic context of F10

  • Western blot analysis of FIX, FX, and FVII in 5- to 10-week soluble liver proteins and 6- to 8-week plasma showed a low level of FIX versus a higher concentration of both FVII and FX, when compared with corresponding adult values, ie, a liver protein level of 10% versus 100% and a plasma concentration level of 10% versus 40% [12].
  • Treatment of the cells with the combination of FVIIa (10 nM) and FX (150 nM), reduced apoptosis by nearly 50% compared with untreated, control cells using an ELISA that detects histone-DNA fragments [37].
  • Sequence analysis of the FX-FVIII337-372 adduct suggested that the first 12 NH2-terminal residues of the FX and peptide do not participate in cross-link formation [21].
  • The identity of the insert in a selected phage lambda clone was confirmed to be FX by nucleotide (nt) sequence analysis and restriction mapping [16].
  • There were lower FV, FVII, FX values in the patient group compared to the control groups on admission [38].


  1. Molecular analysis of the genotype-phenotype relationship in factor X deficiency. Millar, D.S., Elliston, L., Deex, P., Krawczak, M., Wacey, A.I., Reynaud, J., Nieuwenhuis, H.K., Bolton-Maggs, P., Mannucci, P.M., Reverter, J.C., Cachia, P., Pasi, K.J., Layton, D.M., Cooper, D.N. Hum. Genet. (2000) [Pubmed]
  2. Isolation and characterisation of vascular endothelial growth factor-165 specific scFv fragments by phage display. Smith, K.A., Kirkpatrick, N., Madden, L.A., Topping, K.P., Monson, J.R., Greenman, J. Int. J. Oncol. (2003) [Pubmed]
  3. Establishment of functional human pituitary tumor cell cultures. Melmed, S., Odenheimer, D., Carlson, H.E., Hershman, J.M. In vitro. (1982) [Pubmed]
  4. Thrombin-activable factor X re-establishes an intrinsic amplification in tenase-deficient plasmas. Louvain-Quintard, V.B., Bianchini, E.P., Calmel-Tareau, C., Tagzirt, M., Le Bonniec, B.F. J. Biol. Chem. (2005) [Pubmed]
  5. Alternatively spliced human tissue factor: a circulating, soluble, thrombogenic protein. Bogdanov, V.Y., Balasubramanian, V., Hathcock, J., Vele, O., Lieb, M., Nemerson, Y. Nat. Med. (2003) [Pubmed]
  6. Prostacyclin stimulation of the activation of blood coagulation factor X by platelets. Dutta-Roy, A.K., Ray, T.K., Sinha, A.K. Science (1986) [Pubmed]
  7. A role for heterologous gap junctions between melanoma and endothelial cells in metastasis. Ito, A., Katoh, F., Kataoka, T.R., Okada, M., Tsubota, N., Asada, H., Yoshikawa, K., Maeda, S., Kitamura, Y., Yamasaki, H., Nojima, H. J. Clin. Invest. (2000) [Pubmed]
  8. Herpes simplex virus type 1-encoded glycoprotein C contributes to direct coagulation factor X-virus binding. Livingston, J.R., Sutherland, M.R., Friedman, H.M., Pryzdial, E.L. Biochem. J. (2006) [Pubmed]
  9. Activation of blood coagulation factor X by arginine-specific cysteine proteinases (gingipain-Rs) from Porphyromonas gingivalis. Imamura, T., Potempa, J., Tanase, S., Travis, J. J. Biol. Chem. (1997) [Pubmed]
  10. gamma-Glutamyl transpeptidase overexpression increases metastatic growth of B16 melanoma cells in the mouse liver. Obrador, E., Carretero, J., Ortega, A., Medina, I., Rodilla, V., Pellicer, J.A., Estrela, J.M. Hepatology (2002) [Pubmed]
  11. Molecular basis for thymidine modulation of the efficacy and toxicity of alkylating agents. Hwu, W.J., Mozdziesz, D.E. Pharmacol. Ther. (1997) [Pubmed]
  12. Blood coagulation factors in human embryonic-fetal development: preferential expression of the FVII/tissue factor pathway. Hassan, H.J., Leonardi, A., Chelucci, C., Mattia, G., Macioce, G., Guerriero, R., Russo, G., Mannucci, P.M., Peschle, C. Blood (1990) [Pubmed]
  13. Substrate recognition by tissue factor-factor VIIa. Evidence for interaction of residues Lys165 and Lys166 of tissue factor with the 4-carboxyglutamate-rich domain of factor X. Huang, Q., Neuenschwander, P.F., Rezaie, A.R., Morrissey, J.H. J. Biol. Chem. (1996) [Pubmed]
  14. Impaired prothrombinase activity of factor X Gly381Asp results in severe familial CRM+ FX deficiency. Pinotti, M., Camire, R.M., Baroni, M., Rajab, A., Marchetti, G., Bernardi, F. Thromb. Haemost. (2003) [Pubmed]
  15. O, K, H and fimbrial antigens in Escherichia coli serotypes associated with pyelonephritis and cystitis. Orskov, I., Orskov, F., Birch-Andersen, A., Kanamori, M., Svanborg-Edén, C. Scandinavian journal of infectious diseases. Supplementum. (1982) [Pubmed]
  16. Cloning and expression in COS-1 cells of a full-length cDNA encoding human coagulation factor X. Messier, T.L., Pittman, D.D., Long, G.L., Kaufman, R.J., Church, W.R. Gene (1991) [Pubmed]
  17. The effects of aging on tumor growth and angiogenesis are tumor-cell dependent. Reed, M.J., Karres, N., Eyman, D., Cruz, A., Brekken, R.A., Plymate, S. Int. J. Cancer (2007) [Pubmed]
  18. Progesterone production by luteal cells isolated from cynomolgus monkeys: effects of gonadotropin and prolactin during acute incubation and cell culture. Stouffer, R.L., Coensgen, J.L., Hodgen, G.D. Steroids (1980) [Pubmed]
  19. Mouse embryo culture for screening in human IVF. Ackerman, S.B., Taylor, S.P., Swanson, R.J., Laurell, L.H. Arch. Androl. (1984) [Pubmed]
  20. High-resolution NMR studies of fibrinogen-like peptides in solution: resonance assignments and conformational analysis of residues 1-23 of the A alpha chain of human fibrinogen. Ni, F., Scheraga, H.A., Lord, S.T. Biochemistry (1988) [Pubmed]
  21. Interaction of the A1 subunit of factor VIIIa and the serine protease domain of factor X identified by zero-length cross-linking. Lapan, K.A., Fay, P.J. Thromb. Haemost. (1998) [Pubmed]
  22. Prediction of changes in levels of haemostatic variables during natural menstrual cycle and ovarian hyperstimulation. Andersson, O., Blombäck, M., Bremme, K., Wramsby, H. Thromb. Haemost. (1997) [Pubmed]
  23. Binding of plasminogen and tissue plasminogen activator to plasmin-modulated factor X and factor Xa. Grundy, J.E., Lavigne, N., Hirama, T., MacKenzie, C.R., Pryzdial, E.L. Biochemistry (2001) [Pubmed]
  24. The N-terminal epidermal growth factor-like domain in factor IX and factor X represents an important recognition motif for binding to tissue factor. Zhong, D., Bajaj, M.S., Schmidt, A.E., Bajaj, S.P. J. Biol. Chem. (2002) [Pubmed]
  25. Structural and functional characterization of platelet receptor-mediated factor VIII binding. Ahmad, S.S., Scandura, J.M., Walsh, P.N. J. Biol. Chem. (2000) [Pubmed]
  26. Plasmin converts factor X from coagulation zymogen to fibrinolysis cofactor. Pryzdial, E.L., Lavigne, N., Dupuis, N., Kessler, G.E. J. Biol. Chem. (1999) [Pubmed]
  27. Synthesis and characterization of wild-type and variant gamma-carboxyglutamic acid-containing domains of factor VII. Martin, D.M., O'Brien, D.P., Tuddenham, E.G., Byfield, P.G. Biochemistry (1993) [Pubmed]
  28. The relative orientation of Gla and EGF domains in coagulation factor X is altered by Ca2+ binding to the first EGF domain. A combined NMR-small angle X-ray scattering study. Sunnerhagen, M., Olah, G.A., Stenflo, J., Forsén, S., Drakenberg, T., Trewhella, J. Biochemistry (1996) [Pubmed]
  29. Anticoagulant potential of an antibody against factor VII. Chu, A.J., Mathews, S.T. J. Surg. Res. (2003) [Pubmed]
  30. Protease-activated receptor-2 expression in IgA nephropathy: a potential role in the pathogenesis of interstitial fibrosis. Grandaliano, G., Pontrelli, P., Cerullo, G., Monno, R., Ranieri, E., Ursi, M., Loverre, A., Gesualdo, L., Schena, F.P. J. Am. Soc. Nephrol. (2003) [Pubmed]
  31. Protamine inhibits tissue factor-initiated extrinsic coagulation. Chu, A.J., Wang, Z.G., Raicu, M., Beydoun, S., Ramos, N. Br. J. Haematol. (2001) [Pubmed]
  32. Gene therapy for experimental brain tumors using a xenogenic cell line engineered to secrete hIL-2. Lesniak, M.S., Tyler, B.M., Pardoll, D.M., Brem, H. J. Neurooncol. (2003) [Pubmed]
  33. Effect of sulphated polysaccharides on the alpha 1-antitrypsin inhibition of amidolysis catalysed by coagulation cascade proteinases. Long, W.F., Williamson, F.B. Br. J. Pharmacol. (1981) [Pubmed]
  34. Tissue factor- and factor X-dependent activation of protease-activated receptor 2 by factor VIIa. Camerer, E., Huang, W., Coughlin, S.R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  35. Reduced activation of the Gla19Ala FX variant via the extrinsic coagulation pathway results in symptomatic CRMred FX deficiency. Pinotti, M., Marchetti, G., Baroni, M., Cinotti, F., Morfini, M., Bernardi, F. Thromb. Haemost. (2002) [Pubmed]
  36. Studies on the blood clotting and fibrinolytic system in the plasma from a sei (baleen) whale. Saito, H., Poon, M., Goldsmith, G.H., Ratnoff, O.D., Arnason, U. Proc. Soc. Exp. Biol. Med. (1976) [Pubmed]
  37. Formation of tissue factor-factor VIIa-factor Xa complex prevents apoptosis in human breast cancer cells. Jiang, X., Guo, Y.L., Bromberg, M.E. Thromb. Haemost. (2006) [Pubmed]
  38. Effects of high-dose methylprednisolone therapy on coagulation factors in patients with acute immune thrombocytopenic purpura. Oner, A.F., Bay, A., Kuru, M., Uner, A., Arslan, S., Caksen, H. Clin. Appl. Thromb. Hemost. (2005) [Pubmed]
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