A GPI-linked protein that interacts with RET to form a candidate neurturin receptor
Article Abstract:
Sensory, sympathetic and central nervous system neurons rely on the structurally-related neurturin (NTN) and glial-cell-line-derived (GDNF) to survive. The mechanism by which GDNF mediates its actions is well understood, but little is known about the actions that transmit the NTN signal. Research has identified a GPI-linked protein, designated NTNR-a, that combines with the trans-membrane tyrosine kinase Ret to form signalling and ligand-binding components of a receptor for NTN. Results show the presence of a family of multicomponent receptors consisting of Ret, receptor-specific ligand-binding subunits and a signalling subunit.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
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Mesencephalic dopaminergic neurons protected by GDNF from axotomy-induced degeneration in the adult brain
Article Abstract:
The trophic effect of glial-cell-line-derived neurotrophic factor (GDNF) on dopaminergic neurons in the brain is investigated using a newly developed rat model. The investigation involves the degeneration of the neurons by transection of the axons in the medial forebrain bundle. The degeneration causes a loss in the tyrosine hydroxylase-expressing neurons in the nigra region. The injection of GDNF eliminated the loss of these neurons, indicating that GDNF can be used for treating Parkinson's disease.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1995
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Protection and repair of the nigrostriatal dopaminergic system by GDNF in vivo
Article Abstract:
The influence of glial-cell-line-derived neurotrophic factor (GDNF) on the nigrostriatal dopamine system in C57 Bl mice is determined by using dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. The GDNF is a transforming growth factor-beta superfamily and enhances the cultured fetal mesencephalic dopamine neurons survival. The GDNF protects the dopamine system when injected into the body by restoring the fiber densities.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1995
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