Targeted deletion of the cytosolic domain of tissue factor in mice does not affect development

Biochem Biophys Res Commun. 2001 Aug 24;286(3):580-6. doi: 10.1006/bbrc.2001.5425.

Abstract

The role of the cytosolic domain of tissue factor (TF) in signal transduction and gene regulation was studied in mice with a targeted deletion of the 18 carboxy-terminal intracellular amino acids. This deletion was introduced in exon 6 along with a floxed neo(R) selection cassette in intron 5 using homologous recombination in embryonic stem cells. Removal of the floxed neo(R) cassette by in vivo Cre-mediated loxP recombination yielded TF(+/deltaCT) and TF(deltaCT/deltaCT) mice. In contrast to TF(-/-) mice, TF(+/deltaCT) and TF(deltaCT/deltaCT) mice displayed normal embryonic development, survival, fertility, and blood coagulation. Factor VIIa or factor Xa stimulation produced similar p44/42 MAPK activation in TF(+/+) and TF(deltaCT/deltaCT) fibroblasts. These data, based on expression of a TF(deltaCT) molecule from the endogenous TF locus, provide conclusive proof that the cytosolic domain of TF is not essential for signal transduction in embryogenesis and in physiological postnatal processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Embryo, Mammalian / blood supply
  • Embryonic and Fetal Development*
  • Factor VIIa / pharmacology
  • Factor Xa / pharmacology
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Gene Deletion
  • Gene Targeting
  • Hemostasis
  • Mice
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism
  • Neovascularization, Physiologic
  • Protein Structure, Tertiary
  • Thromboplastin / chemistry
  • Thromboplastin / genetics*
  • Thromboplastin / physiology*
  • Thrombosis / etiology

Substances

  • Thromboplastin
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • Factor VIIa
  • Factor Xa