RET is a tyrosine kinase receptor that induces cell survival, proliferation and migration. When bound by its ligand, GDNF (glial derived neurotrophic factor) and its co-receptor, GFRalpha-1 (GDNF family receptor alpha-1), tyrosine residues in the intracellular domain of the receptor are phosphorylated as part of signal transduction. In the kidney, RET is required for branching of the ureteric bud and it also regulates the maturation of the ureter in the urinary tract. Although it is well established in mice that the absence or overexpression of RET leads to severe kidney abnormalities, the cellular basis for these defects remains unexplored. To determine whether the overexpression of RET affected the development of the urinary tract, HoxB7/RET mice were tested for the presence of vesico-ureteric reflux (VUR) in which urine flows retrogradely from the bladder back up the ureter. To further understand how the urinary tract is formed, we looked for the presence of VUR in HoxB7/RET and wildtype mice at E17. These results provide a new understanding of how combined kidney and urinary tract malformations occur in humans.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.79207 |
| Date | January 2002 |
| Creators | Yu, Hoi Yun Oriana, 1978- |
| Contributors | Gupta, Indra R. (advisor) |
| Publisher | McGill University |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Format | application/pdf |
| Coverage | Master of Science (Department of Human Genetics.) |
| Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
| Relation | alephsysno: 001974446, proquestno: AAIMQ88332, Theses scanned by UMI/ProQuest. |
Page generated in 0.0016 seconds