Sympathoadrenal Hyperplasia Causes Renal Malformations in RetMEN2B-Transgenic Mice

Volume: 155, Issue: 6, Pages: 2167 - 2179
Published: Dec 1, 1999
Abstract
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 gfrα-1, or the ligand glial cell line-derived neurotrophic factor results in renal agenesis. Transgenic embryos that express a constitutively active form of Ret (RetMEN2B) under the control of the dopamine-β-hydroxylase (DβH) promoter develop profound neuroglial hyperplasia of their sympathetic...
Paper Details
Title
Sympathoadrenal Hyperplasia Causes Renal Malformations in RetMEN2B-Transgenic Mice
Published Date
Dec 1, 1999
Volume
155
Issue
6
Pages
2167 - 2179
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