Article
Sympathoadrenal hyperplasia causes renal malformations in Ret(MEN2B)-transgenic mice.
The American journal of pathology - 1 Dec 1999
Gestblom C, Sweetser D A, Doggett B, Kapur R P
Abstract excerpt
The tyrosine kinase receptor Ret is expressed in the ureteric bud and is required for normal renal development. Constitutive loss of Ret, its co-receptor gfralpha-1, or the ligand glial cell line-derived neurotrophic factor results in renal agenesis. Transgenic embryos that express a constitutively active form of Ret (Ret(MEN2B)) under the control of the dopamine-beta-hydroxylase (DbetaH) promoter develop...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
