Please use this identifier to cite or link to this item: https://doi.org/10.1002/jcb.24802
DC FieldValue
dc.titleClass II HDACs and neuronal regeneration
dc.contributor.authorTang, B.L.
dc.date.accessioned2014-11-26T07:43:34Z
dc.date.available2014-11-26T07:43:34Z
dc.date.issued2014
dc.identifier.citationTang, B.L. (2014). Class II HDACs and neuronal regeneration. Journal of Cellular Biochemistry 115 (7) : 1225-1233. ScholarBank@NUS Repository. https://doi.org/10.1002/jcb.24802
dc.identifier.issn10974644
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/109245
dc.description.abstractThe vastly more superior regenerative capacity of the axons of peripheral nerves over central nervous system (CNS) neurons has been partly attributed to the former's intrinsic capacity to initiate and sustain the functionality of a new growth cone. Growth cone generation involves a myriad of processes that centers around the organization of microtubule bundles. Histone deacetylases (HDACs) modulate a wide range of key neuronal processes such as neural progenitor differentiation, learning and memory, neuronal death, and degeneration. HDAC inhibitors have been shown to be beneficial in attenuating neuronal death and promoting neurite outgrowth and axonal regeneration. Recent advances have provided insights on how manipulating HDAC activities, particularly the type II HDACs 5 and 6, which deacetylate tubulin, may benefit axonal regeneration. These advances are discussed herein. © 2014 Wiley Periodicals, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/jcb.24802
dc.sourceScopus
dc.subjectAXONAL REGENERATION
dc.subjectHDAC5
dc.subjectHDAC6
dc.subjectHISTONE DEACETYLASES (HDACs)
dc.subjectNEURITE OUTGROWTH
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1002/jcb.24802
dc.description.sourcetitleJournal of Cellular Biochemistry
dc.description.volume115
dc.description.issue7
dc.description.page1225-1233
dc.description.codenJCEBD
dc.identifier.isiut000335830100002
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