Characterization of a multicomponent receptor for GDNF

@article{Treanor1996CharacterizationOA,
  title={Characterization of a multicomponent receptor for GDNF},
  author={James J. S. Treanor and Laurie J. Goodman and Frederic j. de Sauvage and Donna M. Stone and Kris T. Poulsen and C D Beck and Christa L. Gray and Mark P. Armanini and Richard A. Pollock and Franz F. Hefti and Heidi Phillips and A Goddard and Mark W. Moore and Anna Buj-Bello and Alun M. Davies and Naoya Asai and Masahide Takahashi and Richard A. Vandlen and Christopher E. Henderson and Arnon Rosenthal},
  journal={Nature},
  year={1996},
  volume={382},
  pages={80-83}
}
GLIAL-CELL-LINE-DERIVED neurotrophic factor (GDNF)1 is a potent survival factor for central and peripheral neurons2–6, and is essential for the development of kidneys and the enteric nervous system7–9. Despite the potential clinical and physiological importance of GDNF, its mechanism of action is unknown. Here we show that physiological responses to GDNF require the presence of a novel glycosyl-phosphatidylinositol (GPI)-linked protein (designated GDNFR-α) that is expressed on GDNF-responsive… 
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Comparison of the expression patterns of GFRα-3 and Ret suggests that these molecules could form a receptor pair and interact with GDNF family members to play unique roles in development.
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Since GDNF and NTN are expected as therapeutic agents in neurodegenerative disorders such as Parkinson's disease and amyotrophic lateral sclerosis, the studies on the mechanisms of their biological actions through Ret would contribute to the development of new therapeutic strategies for these diseases.
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In vivo differences in localization of the GDNF family members, its coreceptors and Ret suggest this ligand/receptor interaction has extensive and multiple functions in the CNS as well as in peripheral tissues.
GDNF: a novel factor with therapeutic potential for neurodegenerative disorders.
TLDR
In vivo differences in localization of the GDNF family members, its coreceptors and Ret suggest this ligand/receptor interaction has extensive and multiple functions in the CNS as well as in peripheral tissues.
GDNF synthesis, signaling, and retrograde transport in motor neurons
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The neuroprotective effects of GDNF may be used to develop treatments and therapies to ameliorate neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS).
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References

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TLDR
In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake and did not increase total neuron or astrocyte numbers or transmitter uptake.
Defects in enteric innervation and kidney development in mice lacking GDNF
TLDR
It is demonstrated that GDNF induces ureter bud formation and branching during metanephros development, and is essential for proper innervation of the gastrointestinal tract.
Protection and repair of the nigrostriatal dopaminergic system by GDNF in vivo
TLDR
It is concluded that intracerebral GDNF administration exerts both protective and reparative effects on the nigrostriatal dopamine system, which may have implications for the development of new treatment strategies for Parkinson's disease.
Renal and neuronal abnormalities in mice lacking GDNF
TLDR
It is shown that at postnatal day 0 (P0), GDNF-deficient mice have deficits in dorsal root ganglion, sympathetic and nodose neurons, but not in hindbrain noradrenergic or midbrain dopaminergic neurons, and GDNF is important for the development and/or survival of enteric, sympathetic, and sensory neurons and the renal system, but is not essential for catecholaminergic neuron in the central nervous system (CNS).
Renal agenesis and the absence of enteric neurons in mice lacking GDNF
TLDR
Mice defective in GDNF expression are generated by using homologous recombination in embryonic stem cells to delete each of its two coding exons, and ablation of the GDNF gene does not affect the differentiation and survival of dopamine neurons, at least during embryonic development.
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TLDR
Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture and to be a good candidate for treatment of motoneuron disease.
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TLDR
It is shown that mice homozygous for a targeted mutation in c-ret develop to term, but die soon after birth, showing renal agenesis or severe dysgenesis, and lacking enteric neurons throughout the digestive tract, indicating an essential component of a signalling pathway required for renal organogenesis and enteric neurogenesis.
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TLDR
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