Home > Publications Database > ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS. > print

001     141516
005     20240321220952.0
024 7 _ |a 10.1016/j.neuron.2019.07.007
|2 doi
024 7 _ |a pmid:31400829
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024 7 _ |a pmc:PMC6763392
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024 7 _ |a 0896-6273
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024 7 _ |a 1097-4199
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037 _ _ |a DZNE-2020-07840
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Tedeschi, Andrea
|0 P:(DE-2719)2810470
|b 0
245 _ _ |a ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS.
260 _ _ |a New York, NY
|c 2019
|b Elsevier
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2019-09-01
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Injured axons fail to regenerate in the adult CNS, which contrasts with their vigorous growth during embryonic development. We explored the potential of re-initiating axon extension after injury by reactivating the molecular mechanisms that drive morphogenetic transformation of neurons during development. Genetic loss- and gain-of-function experiments followed by time-lapse microscopy, in vivo imaging, and whole-mount analysis show that axon regeneration is fueled by elevated actin turnover. Actin depolymerizing factor (ADF)/cofilin controls actin turnover to sustain axon regeneration after spinal cord injury through its actin-severing activity. This pinpoints ADF/cofilin as a key regulator of axon growth competence, irrespective of developmental stage. These findings reveal the central role of actin dynamics regulation in this process and elucidate a core mechanism underlying axon growth after CNS trauma. Thereby, neurons maintain the capacity to stimulate developmental programs during adult life, expanding their potential for plasticity. Thus, actin turnover is a key process for future regenerative interventions.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
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542 _ _ |i 2019-09-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2020-09-25
|2 Crossref
|u http://www.elsevier.com/open-access/userlicense/1.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 2 |a Actins: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Axons: metabolism
|2 MeSH
650 _ 2 |a Axons: pathology
|2 MeSH
650 _ 2 |a Cofilin 1: genetics
|2 MeSH
650 _ 2 |a Cofilin 1: metabolism
|2 MeSH
650 _ 2 |a Cofilin 2: genetics
|2 MeSH
650 _ 2 |a Cofilin 2: metabolism
|2 MeSH
650 _ 2 |a Destrin: genetics
|2 MeSH
650 _ 2 |a Destrin: metabolism
|2 MeSH
650 _ 2 |a Growth Cones: metabolism
|2 MeSH
650 _ 2 |a Growth Cones: pathology
|2 MeSH
650 _ 2 |a Intravital Microscopy
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Microscopy, Confocal
|2 MeSH
650 _ 2 |a Nerve Regeneration: genetics
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: genetics
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: metabolism
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: pathology
|2 MeSH
650 _ 2 |a Time-Lapse Imaging
|2 MeSH
700 1 _ |a Dupraz, Sebastian
|0 P:(DE-2719)2810386
|b 1
700 1 _ |a Curcio, Michele
|0 P:(DE-2719)2811540
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700 1 _ |a Laskowski, Claudia J
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700 1 _ |a Schaffran, Barbara
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700 1 _ |a Flynn, Kevin C
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700 1 _ |a Da Silva Santos, Telma
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700 1 _ |a Stern, Sina
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700 1 _ |a Hilton, Brett J
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700 1 _ |a Larson, Molly J E
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700 1 _ |a Gurniak, Christine B
|b 10
700 1 _ |a Witke, Walter
|b 11
700 1 _ |a Bradke, Frank
|0 P:(DE-2719)2810270
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773 1 8 |a 10.1016/j.neuron.2019.07.007
|b : Elsevier BV, 2019-09-01
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|t Neuron
|v 103
|y 2019
|x 0896-6273
773 _ _ |a 10.1016/j.neuron.2019.07.007
|g Vol. 103, no. 6, p. 1073 - 1085.e6
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856 4 _ |u https://www.sciencedirect.com/science/article/pii/S0896627319306336
856 7 _ |2 Pubmed Central
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856 4 _ |u https://pub.dzne.de/record/141516/files/DZNE-2020-07840_Restricted.pdf
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913 1 _ |a DE-HGF
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Marc 21