Trk receptors: roles in neuronal signal transduction.

@article{Huang2003TrkRR,
  title={Trk receptors: roles in neuronal signal transduction.},
  author={Eric J. Huang and Louis F Reichardt},
  journal={Annual review of biochemistry},
  year={2003},
  volume={72},
  pages={
          609-42
        }
}
Trk receptors are a family of three receptor tyrosine kinases, each of which can be activated by one or more of four neurotrophins-nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophins 3 and 4 (NT3 and NT4). Neurotrophin signaling through these receptors regulates cell survival, proliferation, the fate of neural precursors, axon and dendrite growth and patterning, and the expression and activity of functionally important proteins, such as ion channels and… 
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Cell Survival through Trk Neurotrophin Receptors Is Differentially Regulated by Ubiquitination
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It is reported that the Trk receptors are multimonoubiquitinated in response to neurotrophins, and the results indicate that Trk neurotrophin receptors are differentially regulated by ubiquitination to modulate the survival of neurons.
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References

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TLDR
Three-dimensional structures of the Trk receptors, in one instance in association with a neurotrophin, have revealed the structural bases underlying specificity in neurotrophIn signaling, where key intermediates are localized to different membrane compartments.
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Adenosine acting through the A2A receptors exerts a trophic effect through the engagement of Trk receptors, providing an explanation for neuroprotective actions of adenosine through a unique signaling mechanism and raising the possibility that small molecules may be used to elicit neurotrophic effects for the treatment of neurodegenerative diseases.
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Preliminary characterization of these mutant mice has provided significant information regarding the role of these receptors in the ontogeny of the mammalian nervous system, and TrkC-deficient mice display strikingly abnormal movements consistent with loss of proprioception.
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Potential mechanisms by which adenosine can activate trophic responses through Trk tyrosine kinase receptors are discussed, including the seven transmembrane spanning Adenosine 2A (A2A) receptor.
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TLDR
Function-perturbing antibodies to the p75 low-affinity NGF receptor potentiated the NT-3 responses of both forms of TrkA in the transfected PC12nnr5 cell lines, suggesting that the low-Affinity N GF receptor suppresses the ability of TrKA to respond to NT- 3.
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TLDR
A number of novel p75NTR-interacting proteins have been identified that transmit growth, survival, and apoptotic signals.
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TLDR
It is suggested that PI3-K may be required for the signals initiated by TrkA internalization and demonstrate that specific endocytic events may distinguish ERK signaling via Rap1 and Ras.
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TLDR
The data suggest that naturally occurring truncated trkB receptors function as inhibitory modulators of neurotrophin responsiveness and the homodimerization of gp145trkB appears to be an essential step in activation of the BDNF signaling cascade.
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TLDR
PACAP can exert trophic effects through a mechanism involving Trk receptors and utilization of tyrosine kinase signaling, which may explain several neuroprotective actions of PACAP upon neuronal populations after injury, nerve lesion, or neurotrophin deprivation.
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