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Activating Smoothened mutations in sporadic basal-cell carcinoma
Findings support the role of SMO as a signalling component of the SHH–receptor complex and provide direct evidence that mutated SMO can function as an oncogene in BCCs.
Renal and neuronal abnormalities in mice lacking GDNF
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).
Characterization of a multicomponent receptor for GDNF
It is demonstrated 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 cells and binds GDNF with a high affinity, which supports the hypothesis that GDNF uses a multi-subunit receptor system in which GDN FR-α and Ret function as the ligand-binding and signalling components.
The tumour-suppressor gene patched encodes a candidate receptor for Sonic hedgehog
It is shown that Re can form a physical complex with a newly cloned vertebrate homologue of the Drosophila protein Smoothened (vSmo), and that vSmo is coexpressed with vPtc in many tissues but does not bind Shh directly.
FGF and Shh Signals Control Dopaminergic and Serotonergic Cell Fate in the Anterior Neural Plate
Evidence that intersections of Shh and FGF8 create induction sites for dopaminergic neurons in the midbrain and forebrain is provided, illustrating that cell patterning in the neural plate is a multistep process in which early inducers are replaced by multiple local organizing centers which specify distinct neuronal cell types within these compartments.
GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle.
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.
Complement and microglia mediate early synapse loss in Alzheimer mouse models
In mouse models, the complement-dependent pathway and microglia that prune excess synapses in development are inappropriately activated and mediate synapse loss in AD, which is an early feature of Alzheimer's disease and correlates with cognitive decline.
Drinks like a fish: zebra fish (Danio rerio) as a behavior genetic model to study alcohol effects
Basic behavioral tests to investigate the acute effects of alcohol on zebra fish and the strategy for generating and screening mutants will be useful for the genetic and biological analysis of acute and chronic drug effects as well as addiction.
GFRα1 Is an Essential Receptor Component for GDNF in the Developing Nervous System and Kidney
Findings support the idea that GFRalpha1 and the transmembrane tyrosine kinase Ret are both necessary receptor components for GDNF in the developing kidney and nervous system, and that GDNF and neurturin can mediate some of their activities through a second receptor.
Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System
alpha-Synuclein (alpha-Syn) is a 14 kDa protein of unknown function that has been implicated in the pathophysiology of Parkinson's disease (PD). Here, we show that alpha-Syn-/- mice are viable and