Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis
Rac1 is a major player of the Rho family of small GTPases that controls multiple cell signaling pathways, such as the organization of cytoskeleton (including adhesion and motility), cell proliferation, apoptosis and activation of immune cells. In the nervous system, in particular, Rac1 GTPase plays...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2014-09-01
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Series: | Frontiers in Cellular Neuroscience |
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Online Access: | http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00279/full |
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author | Nadia eD'Ambrosi Simona eRossi Simona eRossi Valeria eGerbino Valeria eGerbino Mauro eCozzolino |
author_facet | Nadia eD'Ambrosi Simona eRossi Simona eRossi Valeria eGerbino Valeria eGerbino Mauro eCozzolino |
author_sort | Nadia eD'Ambrosi |
collection | DOAJ |
description | Rac1 is a major player of the Rho family of small GTPases that controls multiple cell signaling pathways, such as the organization of cytoskeleton (including adhesion and motility), cell proliferation, apoptosis and activation of immune cells. In the nervous system, in particular, Rac1 GTPase plays a key regulatory function of both actin and microtubule cytoskeletal dynamics and thus it is central to axonal growth and stability, as well as dendrite and spine structural plasticity. Rac1 is also a crucial regulator of NADPH-dependent membrane oxidase (NOX), a prominent source of ROS, thus having a central role in the inflammatory response and neurotoxicity mediated by microglia cells in the nervous system. As such, alterations in Rac1 activity might well be involved in the processes that give rise to Amyotrophic Lateral Sclerosis (ALS), a complex syndrome where cytoskeletal disturbances in motor neurons and redox alterations in the inflammatory compartment play pivotal and synergic roles in the final disease outcomes. Here we will discuss the genetic and mechanistic evidence indicating the relevance of Rac1 dysregulation in the pathogenesis of ALS. |
first_indexed | 2024-12-24T05:33:58Z |
format | Article |
id | doaj.art-461a8e93b72248d3973ef65741a0ff83 |
institution | Directory Open Access Journal |
issn | 1662-5102 |
language | English |
last_indexed | 2024-12-24T05:33:58Z |
publishDate | 2014-09-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cellular Neuroscience |
spelling | doaj.art-461a8e93b72248d3973ef65741a0ff832022-12-21T17:13:05ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022014-09-01810.3389/fncel.2014.00279109600Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral SclerosisNadia eD'Ambrosi0Simona eRossi1Simona eRossi2Valeria eGerbino3Valeria eGerbino4Mauro eCozzolino5Università Cattolica del Sacro CuoreNational Research CouncilFondazione Santa Lucia, IRCCSFondazione Santa Lucia, IRCCSUniversità di Roma Tor VergataNational Research CouncilRac1 is a major player of the Rho family of small GTPases that controls multiple cell signaling pathways, such as the organization of cytoskeleton (including adhesion and motility), cell proliferation, apoptosis and activation of immune cells. In the nervous system, in particular, Rac1 GTPase plays a key regulatory function of both actin and microtubule cytoskeletal dynamics and thus it is central to axonal growth and stability, as well as dendrite and spine structural plasticity. Rac1 is also a crucial regulator of NADPH-dependent membrane oxidase (NOX), a prominent source of ROS, thus having a central role in the inflammatory response and neurotoxicity mediated by microglia cells in the nervous system. As such, alterations in Rac1 activity might well be involved in the processes that give rise to Amyotrophic Lateral Sclerosis (ALS), a complex syndrome where cytoskeletal disturbances in motor neurons and redox alterations in the inflammatory compartment play pivotal and synergic roles in the final disease outcomes. Here we will discuss the genetic and mechanistic evidence indicating the relevance of Rac1 dysregulation in the pathogenesis of ALS.http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00279/fullMicrogliaMotor Neuronsrac1 GTP-Binding ProteinReactive Oxygen SpeciesNeuroinflammationNOX |
spellingShingle | Nadia eD'Ambrosi Simona eRossi Simona eRossi Valeria eGerbino Valeria eGerbino Mauro eCozzolino Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis Frontiers in Cellular Neuroscience Microglia Motor Neurons rac1 GTP-Binding Protein Reactive Oxygen Species Neuroinflammation NOX |
title | Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis |
title_full | Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis |
title_fullStr | Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis |
title_full_unstemmed | Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis |
title_short | Rac1 at the crossroad of actin dynamics and neuroinflammation in Amyotrophic Lateral Sclerosis |
title_sort | rac1 at the crossroad of actin dynamics and neuroinflammation in amyotrophic lateral sclerosis |
topic | Microglia Motor Neurons rac1 GTP-Binding Protein Reactive Oxygen Species Neuroinflammation NOX |
url | http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00279/full |
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