Signal transduction for clinicians: Why should we care?
ABSTRACT Neurons must respond to a bewildering array of external and internal stimuli and must distinguish among them to generate an appropriate response or change in metabolic or electrical activity. Furthermore, the response of a cell to a given stimulus must depend on what else is happening inside and outside the cell at the time of arrival of that stimulus. The process of signal transduction is what gives the cell and organism the flexibility and "knowledge base" to carry out these functions. Conversely, aberrations of signal transduction underlie an increasing array of developmental, genetic, and acquired diseases and conditions of the nervous system. Pharmacological modulation of signal transduction pathways and their effectors holds great promise for the remediation of these neurologic disorders.
SourceAvailable from: Nina F Schor[Show abstract] [Hide abstract]
ABSTRACT: Neuroblastoma is, at once, the most common and deadly extracranial solid tumor of childhood. Efforts aimed at targeting the neural characteristics of these tumors have taught us much about neural crest cell biology, apoptosis induction in the nervous system, and neurotrophin receptor signaling and intracellular processing. But neuroblastoma remains a formidable enemy to the oncologist and an enigmatic target to the neuroscientist.Journal of child neurology 04/2013; 28(6). DOI:10.1177/0883073813483173 · 1.59 Impact Factor
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ABSTRACT: Necdin is a protein known to interact with the neurotrophin receptors, neurotrophic tyrosine kinase receptor type 1 (TrkA) and 75 kD low-affinity neurotrophin receptor (p75NTR). TrkA and p75NTR play roles in development and disease of the nervous system and chemoresistance of nervous system tumors. Necdin deletion is associated with Prader-Willi syndrome. The present studies demonstrate that the effects of necdin on the susceptibility of neuroblastoma cells to oxidant stress are dependent on the ratio of p75NTR to TrkA in the cell. In low p75NTR:TrkA ratio cells, necdin down-regulation decreases sensitivity to oxidant stress and expression of and signaling through TrkA. In high p75NTR:TrkA cells, necdin down-regulation is without effect. The effects of necdin deletion on the developing nervous system may depend on the relative expression of p75NTR and TrkA in the cells of particular regions of the nervous system.Pediatric Research 12/2010; 69(4):279-84. DOI:10.1203/PDR.0b013e31820a5773 · 2.84 Impact Factor
European Journal of Paediatric Neurology 02/2003; 7(5):211-5. DOI:10.1016/S1090-3798(03)00102-8 · 1.93 Impact Factor