Neurotrophins To Cleave or Not to Cleave

  title={Neurotrophins To Cleave or Not to Cleave},
  author={Moses V Chao and Mark A. Bothwell},

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The yin and yang of neurotrophin action
The proteolytic cleavage of proneurotrophins represents a mechanism that controls the direction of action of neurotrophins and has profound implications for the understanding of the role of neurotrophic molecules in a wide range of cellular processes.
Jekyll–Hyde neurotrophins: the story of proNGF
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  • 2002
Selectivity in neurotrophin signaling: theme and variations.
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    Annual review of neuroscience
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Variations in neurotrophin signaling have revealed variations in the Ras/MAP kinase, PI3 kinases, and phospholipase C pathways, which transmit spatial and temporal information, which may represent a general mechanism eliciting specificity in growth factor responses.
Growth Factors: To Cleave or not to Cleave
The recent advance in understanding of the importance of growth factors processing by the proprotein convertases on the malignant phenotypes of tumor cells, tumorigenesis and angiogenesis is reviewed and the potential use of their maturation blockade/activation as a new potential therapeutic strategy is reviewed.
The p75 neurotrophin receptor.
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The critical roles of neurotrophins in the regulation of neuronal survival and apoptosis are summarized.
Neurotrophin survival signaling mechanisms.
Difficulties in administering trophic factors have led to the consideration of using small molecules, such as G protein-coupled receptor (GPCR) ligands, which can participate in transactivation events.
Neurotrophins and the immune system
Results from studies to date support the idea that neurotrophins may regulate some immune functions, and play an important role in the development of the thymus and in the survival of thymocytes.
Contrasting effects of overexpressing the neurotrophin receptors TrkA and TrkB during development
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Neurotrophins as synaptic modulators
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  • Biology
    Nature Reviews Neuroscience
  • 2001
By this account, neurotrophins may participate in activity-dependent synaptic plasticity, linking synaptic activity with long-term functional and structural modification of synaptic connections.
Regulation of Cell Survival by Secreted Proneurotrophins
It is shown that the proforms of nerve growth factor (NGF) and the pro forms of brain derived neurotrophic factor (BDNF) are secreted and cleaved extracellularly by the serine protease plasmin and by selective matrix metalloproteinases (MMPs).
Neuronal life and death decisions: functional antagonism between the Trk and p75 neurotrophin receptors
Biochemical and functional interactions between the neurotrophin receptors trk and p75NTR
A close proximity of the two neurotrophin receptors within cell membranes is indicated, and it is suggested that the signalling pathways they initiate may interact soon after their activation.
Two Peptides Derived from the Nerve Growth Factor Precursor Are Biologically Active
Both propeptides induced rapid tyrosine phosphorylation of the Trk protein in both prostatic adenocarcinoma cells and PC12 cells, thus implicating trk in their mechanism of action, and support the hypothesis that two peptides within the NGF precursor protein are biologically active.
Cellular processing of the nerve growth factor precursor by the mammalian pro-protein convertases.
This comparative study shows that the three candidate mammalian subtilisin/kexin-like convertases identified process proNGF into NGF and that the nature of the final processed products is dependent on the intracellular environment.
The Neurotrophin Receptor p75 Binds Neurotrophin-3 on Sympathetic Neurons with High Affinity and Specificity
It is concluded that p75NTR can exist in neurons in a confirmation conferring hitherto unrecognized properties to this receptor, as well as other receptors identified on nerve growth factor-dependent sympathetic neurons.
Competitive Signaling Between TrkA and p75 Nerve Growth Factor Receptors Determines Cell Survival
Results indicate that TrkA-mediated rescue involves not only activation of survival signals but also simultaneous suppression of a death signal by p75, a novel mechanism that achieves alternative cellular responses by merging signals from different ligand–receptor systems.
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