Pro-neurotrophins, sortilin, and nociception
Nerve growth factor (NGF) signaling is important in the development and functional maintenance of nociceptors, but it also plays a central role in initiating and sustaining heat and mechanical hyperalgesia following inflammation. NGF signaling in pain has traditionally been thought of as primarily e...
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| Format: | Online |
| Language: | English |
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BlackWell Publishing Ltd
2014
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232910/ |
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pubmed-4232910 |
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pubmed-42329102014-12-19 Pro-neurotrophins, sortilin, and nociception Lewin, Gary R Nykjaer, Anders Special Issue: Neurobiology of Pain Nerve growth factor (NGF) signaling is important in the development and functional maintenance of nociceptors, but it also plays a central role in initiating and sustaining heat and mechanical hyperalgesia following inflammation. NGF signaling in pain has traditionally been thought of as primarily engaging the classic high-affinity receptor tyrosine kinase receptor TrkA to initiate sensitization events. However, the discovery that secreted proforms of nerve NGF have biological functions distinct from the processed mature factors raised the possibility that these proneurotrophins (proNTs) may have distinct function in painful conditions. ProNTs engage a novel receptor system that is distinct from that of mature neurotrophins, consisting of sortilin, a type I membrane protein belonging to the VPS10p family, and its co-receptor, the classic low-affinity neurotrophin receptor p75NTR. Here, we review how this new receptor system may itself function with or independently of the classic TrkA system in regulating inflammatory or neuropathic pain. BlackWell Publishing Ltd 2014-02 2014-02-04 /pmc/articles/PMC4232910/ /pubmed/24494677 http://dx.doi.org/10.1111/ejn.12466 Text en Copyright © 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd http://creativecommons.org/licenses/by-nc/3.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Lewin, Gary R Nykjaer, Anders |
| spellingShingle |
Lewin, Gary R Nykjaer, Anders Pro-neurotrophins, sortilin, and nociception |
| author_facet |
Lewin, Gary R Nykjaer, Anders |
| author_sort |
Lewin, Gary R |
| title |
Pro-neurotrophins, sortilin, and nociception |
| title_short |
Pro-neurotrophins, sortilin, and nociception |
| title_full |
Pro-neurotrophins, sortilin, and nociception |
| title_fullStr |
Pro-neurotrophins, sortilin, and nociception |
| title_full_unstemmed |
Pro-neurotrophins, sortilin, and nociception |
| title_sort |
pro-neurotrophins, sortilin, and nociception |
| description |
Nerve growth factor (NGF) signaling is important in the development and functional maintenance of nociceptors, but it also plays a central role in initiating and sustaining heat and mechanical hyperalgesia following inflammation. NGF signaling in pain has traditionally been thought of as primarily engaging the classic high-affinity receptor tyrosine kinase receptor TrkA to initiate sensitization events. However, the discovery that secreted proforms of nerve NGF have biological functions distinct from the processed mature factors raised the possibility that these proneurotrophins (proNTs) may have distinct function in painful conditions. ProNTs engage a novel receptor system that is distinct from that of mature neurotrophins, consisting of sortilin, a type I membrane protein belonging to the VPS10p family, and its co-receptor, the classic low-affinity neurotrophin receptor p75NTR. Here, we review how this new receptor system may itself function with or independently of the classic TrkA system in regulating inflammatory or neuropathic pain. |
| publisher |
BlackWell Publishing Ltd |
| publishDate |
2014 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232910/ |
| _version_ |
1613157022161698816 |