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Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration

The poor or lack of injured adult central nervous system (CNS) axon regeneration results in devastating consequences and poor functional recovery. The interplay between the intrinsic and extrinsic factors contributes to robust inhibition of axon regeneration of injured CNS neurons. The insufficient...

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Detalles Bibliográficos
Autores principales: Vigneswara, Vasanthy, Kundi, Sarina, Ahmed, Zubair
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405719/
https://www.ncbi.nlm.nih.gov/pubmed/22848811
http://dx.doi.org/10.1155/2012/361721
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author Vigneswara, Vasanthy
Kundi, Sarina
Ahmed, Zubair
author_facet Vigneswara, Vasanthy
Kundi, Sarina
Ahmed, Zubair
author_sort Vigneswara, Vasanthy
collection PubMed
description The poor or lack of injured adult central nervous system (CNS) axon regeneration results in devastating consequences and poor functional recovery. The interplay between the intrinsic and extrinsic factors contributes to robust inhibition of axon regeneration of injured CNS neurons. The insufficient or lack of trophic support for injured neurons is considered as one of the major obstacles contributing to their failure to survive and regrow their axons after injury. In the CNS, many of the signalling pathways associated with neuronal survival and axon regeneration are regulated by several classes of receptor tyrosine kinases (RTK) that respond to a variety of ligands. This paper highlights and summarises the most relevant recent findings pertinent to different classes of the RTK family of molecules, with a particular focus on elucidating their role in CNS axon regeneration.
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spelling pubmed-34057192012-07-30 Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration Vigneswara, Vasanthy Kundi, Sarina Ahmed, Zubair J Signal Transduct Review Article The poor or lack of injured adult central nervous system (CNS) axon regeneration results in devastating consequences and poor functional recovery. The interplay between the intrinsic and extrinsic factors contributes to robust inhibition of axon regeneration of injured CNS neurons. The insufficient or lack of trophic support for injured neurons is considered as one of the major obstacles contributing to their failure to survive and regrow their axons after injury. In the CNS, many of the signalling pathways associated with neuronal survival and axon regeneration are regulated by several classes of receptor tyrosine kinases (RTK) that respond to a variety of ligands. This paper highlights and summarises the most relevant recent findings pertinent to different classes of the RTK family of molecules, with a particular focus on elucidating their role in CNS axon regeneration. Hindawi Publishing Corporation 2012 2012-07-16 /pmc/articles/PMC3405719/ /pubmed/22848811 http://dx.doi.org/10.1155/2012/361721 Text en Copyright © 2012 Vasanthy Vigneswara et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Vigneswara, Vasanthy
Kundi, Sarina
Ahmed, Zubair
Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title_full Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title_fullStr Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title_full_unstemmed Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title_short Receptor Tyrosine Kinases: Molecular Switches Regulating CNS Axon Regeneration
title_sort receptor tyrosine kinases: molecular switches regulating cns axon regeneration
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405719/
https://www.ncbi.nlm.nih.gov/pubmed/22848811
http://dx.doi.org/10.1155/2012/361721
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