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F3  -  coagulation factor III (thromboplastin,...

Bos taurus

 
 
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Disease relevance of F3

  • Parts of bovine F3 protein were overproduced in Escherichia coli [1].
  • Two monoclonal antibodies that recognize bovine tissue factor (coagulation factor III) have been obtained following the fusion of hyperimmune mouse spleen cells with NS-1 plasmacytoma cells [2].
  • CONCLUSION: Intra-alveolar fibrin deposition and activation of coagulation in cattle with pneumonic pasteurellosis is, at least in part, mediated by TF [3].
  • Pertussis toxin had a significant (P < 0.0319) inhibitory effect on TF expression when cells were stimulated by LPS alone [4].
  • OBJECTIVE: To determine the role of tissue factor (TF) in the coagulation events leading to intra-alveolar fibrin deposition and intravascular thrombosis associated with pneumonic pasteurellosis in cattle [3].
 

High impact information on F3

  • Treatment of VIIa with (p-amidinophenyl)methanesulfonyl fluoride also enhanced its affinity for soluble TF, whereas treatment with 4-(2-aminoethyl)benzenesulfonyl fluoride, phenylmethylsulfonyl fluoride, or diisopropyl fluorophosphate had a slight effect on the affinity [5].
  • Therefore, one of the binding sites of VII with TF is probably located in the Gla-EGF1 region [6].
  • Acetylation or carbamylation of the alpha-amino group of the NH2-terminal Ile-153 of VIIa resulted in the loss of binding affinity for TF; such modifications convert VIIa into a zymogen-like inactive form by destroying the salt bridge between Ile-153 and Asp-343 in VIIa [6].
  • On the other hand, a dansyl-Glu-Gly-Arg chloromethyl ketone-treated Gla-domainless VIIa (Ki = 0.7 x 10(-7) M) showed a high affinity for TF, whereas the corresponding Gla-domainless VII similarly treated showed no binding potential, thereby indicating that binding site(s) other than in the Gla-EGF1 region are present in VIIa but not in VII [6].
  • Initiation of the extrinsic blood coagulation pathway is mediated by a complex formed between plasma-derived factor VII/VIIa and cell-derived tissue factor (TF) [6].
 

Biological context of F3

  • The increase in FVIII and TF was abolished when the nuclear transport is blocked [7].
  • Transient transfection studies with TF-promoter plasmids revealed that both, NF-kappa B and AP-1 dependent TF expression, were reduced by curcumin action [8].
  • Glycer-AGE significantly upregulated TF mRNA expression in both cells, and the upregulation was more prominent in BBMECs than in BAECs [9].
 

Anatomical context of F3

  • The aim of this study was to investigate whether AGEs have a significant effect on tissue factor (TF) expression in brain microvascular endothelial cells compared with that in other arterial endothelial cells [9].
  • OBJECTIVE: To investigate receptor-mediated intracellular events in bovine alveolar macrophages (AM) stimulated by bacterial lipopolysaccharide (LPS), using tissue factor (TF) expression as the measurable functional endpoint [4].
 

Associations of F3 with chemical compounds

  • Bovine F3, similar to those of chicken and human, was devoid of two aa residues (Ile-Thr) in the sixth immunoglobulin type C2-like domain, as compared with the mouse homolog [1].
  • We found that the VIIa-light chain (Ki = 3.5 x 10(-7) M) and its fragment consisting of the gamma-carboxyglutamic acid (Gla)-domain and the first epidermal growth factor (EGF)-like domain (Gla-EGF1 peptide; Ki = 1.0 x 10(-6) M) have an affinity for TF [6].
  • Edaravone significantly attenuated the AGE-induced upregulation of TF mRNA expression, protein expression, and activity [9].
  • Participation of reactive oxygen species (ROS) in the effect of glycer-AGE on TF expression was investigated by treatment with a free radical scavenger, edaravone, and intracellular ROS measurements with dihydroethidium (DHE) [9].
  • Treatment with all 3 PKC inhibitors caused marked reduction in TF expression of cells stimulated with LPS alone or with phorbol myristate acetate [4].
 

Other interactions of F3

 

Analytical, diagnostic and therapeutic context of F3

References

  1. Cloning of the cDNA encoding neural adhesion molecule F3 from bovine brain. Watanabe, K., Shimazaki, K., Hosoya, H., Fukamauchi, F., Takenawa, T. Gene (1995) [Pubmed]
  2. Monoclonal antibodies against bovine tissue factor, which block interaction with factor VIIa. Carson, S.D., Bach, R., Carson, S.M. Blood (1985) [Pubmed]
  3. Role of tissue factor in intra-alveolar fibrin deposition and coagulopathy associated with pneumonic pasteurellosis in cattle. Rashid, J., Weiss, D.J., Bach, R., Murtaugh, M. Am. J. Vet. Res. (1997) [Pubmed]
  4. Signaling pathways for tissue factor expression in lipopolysaccharide-stimulated bovine alveolar macrophages. Dean, D.F., Bochsler, P.N., Carroll, R.C., Olchowy, T.W., Neilsen, N.R., Slauson, D.O. Am. J. Vet. Res. (1998) [Pubmed]
  5. Molecular mechanism of tissue factor-mediated acceleration of factor VIIa activity. Higashi, S., Matsumoto, N., Iwanaga, S. J. Biol. Chem. (1996) [Pubmed]
  6. Identification of regions of bovine factor VII essential for binding to tissue factor. Higashi, S., Nishimura, H., Aita, K., Iwanaga, S. J. Biol. Chem. (1994) [Pubmed]
  7. VEGF nuclear accumulation correlates with phenotypical changes in endothelial cells. Li, W., Keller, G. J. Cell. Sci. (2000) [Pubmed]
  8. The dietary pigment curcumin reduces endothelial tissue factor gene expression by inhibiting binding of AP-1 to the DNA and activation of NF-kappa B. Bierhaus, A., Zhang, Y., Quehenberger, P., Luther, T., Haase, M., Müller, M., Mackman, N., Ziegler, R., Nawroth, P.P. Thromb. Haemost. (1997) [Pubmed]
  9. Susceptibility of brain microvascular endothelial cells to advanced glycation end products-induced tissue factor upregulation is associated with intracellular reactive oxygen species. Niiya, Y., Abumiya, T., Shichinohe, H., Kuroda, S., Kikuchi, S., Ieko, M., Yamagishi, S., Takeuchi, M., Sato, T., Iwasaki, Y. Brain Res. (2006) [Pubmed]
  10. Tissue factor (coagulation factor III) inhibition by apolipoprotein A-II. Carson, S.D. J. Biol. Chem. (1987) [Pubmed]
  11. Modulation of the effect of vascular endothelial growth factor on endothelial cells by heparin: critical role of nitric oxide-mediated mechanisms. Yagüe, S., Alvarez Arroyo, V., Castilla, A., González Pacheco, F.R., Llamas, P., Caramelo, C. J. Nephrol. (2005) [Pubmed]
 
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