Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases?
The c-Abl tyrosine kinase is implicated in diverse cellular activities including growth factor signaling, cell adhesion, oxidative stress, and DNA damage response. Studies in mouse models have shown that the kinases of the c-Abl family play a role in the development of the central nervous system. Re...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2012/683097 |
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| author | Stefania Gonfloni Emiliano Maiani Claudia Di Bartolomeo Marc Diederich Gianni Cesareni |
| author_facet | Stefania Gonfloni Emiliano Maiani Claudia Di Bartolomeo Marc Diederich Gianni Cesareni |
| author_sort | Stefania Gonfloni |
| collection | DOAJ |
| description | The c-Abl tyrosine kinase is implicated in diverse cellular activities including growth factor signaling, cell adhesion, oxidative stress, and DNA damage response. Studies in mouse models have shown that the kinases of the c-Abl family play a role in the development of the central nervous system. Recent reports show that aberrant c-Abl activation causes neuroinflammation and neuronal loss in the forebrain of transgenic adult mice. In line with these observations, an increased c-Abl activation is reported in human neurodegenerative pathologies, such as Parkinson’s, and Alzheimer’s diseases. This suggests that aberrant nonspecific posttranslational modifications induced by c-Abl may contribute to fuel the recurrent phenotypes/features linked to neurodegenerative disorders, such as an impaired mitochondrial function, oxidative stress, and accumulation of protein aggregates. Herein, we review some reports on c-Abl function in neuronal cells and we propose that modulation of different aspects of c-Abl signaling may contribute to mediate the molecular events at the interface between stress signaling, metabolic regulation, and DNA damage. Finally, we propose that this may have an impact in the development of new therapeutic strategies. |
| format | Article |
| id | doaj-art-c10e53257a924b2c8b20c1b2188f7dfb |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-c10e53257a924b2c8b20c1b2188f7dfb2025-02-03T05:53:55ZengWileyInternational Journal of Cell Biology1687-88761687-88842012-01-01201210.1155/2012/683097683097Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases?Stefania Gonfloni0Emiliano Maiani1Claudia Di Bartolomeo2Marc Diederich3Gianni Cesareni4Department of Biology, University of Rome “Tor Vergata,” Via della Ricerca Scientifica, 00133 Rome, ItalyDepartment of Biology, University of Rome “Tor Vergata,” Via della Ricerca Scientifica, 00133 Rome, ItalyDepartment of Biology, University of Rome “Tor Vergata,” Via della Ricerca Scientifica, 00133 Rome, ItalyLaboratoire de Biologie Moléculaire et Cellulaire du Cancer, Fondation de Recherche Cancer et Sang, Hôpital Kirchberg, 9 Rue Edward Steichen, 2540 Luxembourg, LuxembourgDepartment of Biology, University of Rome “Tor Vergata,” Via della Ricerca Scientifica, 00133 Rome, ItalyThe c-Abl tyrosine kinase is implicated in diverse cellular activities including growth factor signaling, cell adhesion, oxidative stress, and DNA damage response. Studies in mouse models have shown that the kinases of the c-Abl family play a role in the development of the central nervous system. Recent reports show that aberrant c-Abl activation causes neuroinflammation and neuronal loss in the forebrain of transgenic adult mice. In line with these observations, an increased c-Abl activation is reported in human neurodegenerative pathologies, such as Parkinson’s, and Alzheimer’s diseases. This suggests that aberrant nonspecific posttranslational modifications induced by c-Abl may contribute to fuel the recurrent phenotypes/features linked to neurodegenerative disorders, such as an impaired mitochondrial function, oxidative stress, and accumulation of protein aggregates. Herein, we review some reports on c-Abl function in neuronal cells and we propose that modulation of different aspects of c-Abl signaling may contribute to mediate the molecular events at the interface between stress signaling, metabolic regulation, and DNA damage. Finally, we propose that this may have an impact in the development of new therapeutic strategies.http://dx.doi.org/10.1155/2012/683097 |
| spellingShingle | Stefania Gonfloni Emiliano Maiani Claudia Di Bartolomeo Marc Diederich Gianni Cesareni Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? International Journal of Cell Biology |
| title | Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? |
| title_full | Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? |
| title_fullStr | Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? |
| title_full_unstemmed | Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? |
| title_short | Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? |
| title_sort | oxidative stress dna damage and c abl signaling at the crossroad in neurodegenerative diseases |
| url | http://dx.doi.org/10.1155/2012/683097 |
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