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The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Injury-Induced HDAC5 Nuclear Export Is Essential for Axon Regeneration

Open access
Cho, Yongcheol, Sloutsky, Roman, Naegle, Kristen M., Cavalli, Valeria·2013·Cell

Abstract

SUMMARY Reactivation of a silent transcriptional program is a critical step in successful axon regeneration following injury. Yet how such program is unlocked after injury remains largely unexplored. We found that axon injury in peripheral sensory neurons elicits a back-propagating calcium wave that invades the soma and causes nuclear export of HDAC5 in a PKCµ–dependent manner. Injury-induced HDAC5 nuclear export enhances histone acetylation to activate a pro-regenerative gene expression program. HDAC5 nuclear export is required for axon regeneration, since expression of a nuclear-trapped HDAC5 mutant prevents axon regeneration, whereas enhancing HDAC5 nuclear export promotes axon regeneration in vitro and in vivo. Components of this HDAC5 pathway failed to be activated in a model of central nervous system injury. These studies reveal a signaling mechanism from the axon injury site to the soma that controls neuronal growth competence and suggest a role for HDAC5 as a transcriptional switch controlling axon regeneration.

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Metadata

Authors
Cho, Y., Sloutsky, R., Naegle, K. M., & Cavalli, V.
Venue
Cell
Publisher
Elsevier BV
Published
2013-11
Volume
155
Issue
4
Pages
894-908
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2130367422
Cited by
327
References
4
FWCI
12.67
Type
journal article
Language
en
Open access
bronze

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