| First Author | Mackie EJ | Year | 1999 |
| Journal | J Cell Sci | Volume | 112 ( Pt 22) |
| Pages | 3847-53 | PubMed ID | 10547346 |
| Mgi Jnum | J:59038 | Mgi Id | MGI:1350808 |
| Doi | 10.1242/jcs.112.22.3847 | Citation | Mackie EJ, et al. (1999) The tenascin-C knockout revisited. J Cell Sci 112(Pt 22):3847-53 |
| abstractText | In the past seven years, two groups have independently produced tenascin-C-knockout mice. These mice are born alive and, originally, were described as showing no abnormalities. More recent studies, many involving pathological intervention, have shown that tenascin-C-knockout mice have several defects. The mice exhibit abnormal behaviour, as well as abnormalities in brain chemistry. They also show defects in structure and repair of neuromuscular junctions, in the ability to recover from snake-venom-induced glomerulonephritis and in chemically induced dermatitis. Healing of skin wounds is morphologically normal, but the mice exhibit defects in healing after suture injury of corneas. In both skin and corneal wounds, fibronectin expression is abnormally low in tenascin-C-knockout mice. Finally, in vitro studies indicate that haemopoietic activity is defective in bone marrow from these mice. When examined together, these studies provide evidence for precise functions for tenascin-C, as well as an explanation for why the sequence of tenascin-C is so highly phylogenetically conserved. |
