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Article: Neuronal differentiation by TAp73 is mediated by microRNA-34a regulation of synaptic protein targets

TitleNeuronal differentiation by TAp73 is mediated by microRNA-34a regulation of synaptic protein targets
Authors
KeywordsCell death
Neurodegeneration
Alzheimer disease
Issue Date2011
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2011, v. 108, n. 52, p. 21093-21098 How to Cite?
AbstractThe p53-family member TAp73 is a transcription factor that plays a key role in many biological processes. Here, we show that p73 drives the expression of microRNA (miR)-34a, but not miR-34b and -c, by acting on specific binding sites on the miR-34a promoter. Expression of miR-34a is modulated in parallel with that of TAp73 during in vitro differentiation of neuroblastoma cells and cortical neurons. Retinoid-driven neuroblastoma differentiation is inhibited by knockdown of either p73 or miR-34a. Transcript expression of miR-34a is significantly reduced in vivo both in the cortex and hippocampus of p73 -/- mice; miR-34a and TAp73 expression also increase during postnatal development of the brain and cerebellum when synaptogenesis occurs. Accordingly, overexpression or silencing of miR-34a inversely modulates expression of synaptic targets, including synaptotagmin-1 and syntaxin-1A. Notably, the axis TAp73/miR-34a/synaptotagmin-1 is conserved in brains from Alzheimer's patients. These data reinforce a role for TAp73 in neuronal development.
Persistent Identifierhttp://hdl.handle.net/10722/292682
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAgostini, Massimiliano-
dc.contributor.authorTucci, Paola-
dc.contributor.authorKillick, Richard-
dc.contributor.authorCandi, Eleonora-
dc.contributor.authorSayan, Berna S.-
dc.contributor.authorDi Val Cervo, Pia Rivetti-
dc.contributor.authorNicoterad, Pierluigi-
dc.contributor.authorMcKeon, Frank-
dc.contributor.authorKnight, Richard A.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorMelino, Gerry-
dc.date.accessioned2020-11-17T14:57:00Z-
dc.date.available2020-11-17T14:57:00Z-
dc.date.issued2011-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2011, v. 108, n. 52, p. 21093-21098-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/292682-
dc.description.abstractThe p53-family member TAp73 is a transcription factor that plays a key role in many biological processes. Here, we show that p73 drives the expression of microRNA (miR)-34a, but not miR-34b and -c, by acting on specific binding sites on the miR-34a promoter. Expression of miR-34a is modulated in parallel with that of TAp73 during in vitro differentiation of neuroblastoma cells and cortical neurons. Retinoid-driven neuroblastoma differentiation is inhibited by knockdown of either p73 or miR-34a. Transcript expression of miR-34a is significantly reduced in vivo both in the cortex and hippocampus of p73 -/- mice; miR-34a and TAp73 expression also increase during postnatal development of the brain and cerebellum when synaptogenesis occurs. Accordingly, overexpression or silencing of miR-34a inversely modulates expression of synaptic targets, including synaptotagmin-1 and syntaxin-1A. Notably, the axis TAp73/miR-34a/synaptotagmin-1 is conserved in brains from Alzheimer's patients. These data reinforce a role for TAp73 in neuronal development.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.subjectCell death-
dc.subjectNeurodegeneration-
dc.subjectAlzheimer disease-
dc.titleNeuronal differentiation by TAp73 is mediated by microRNA-34a regulation of synaptic protein targets-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1112061109-
dc.identifier.pmid22160687-
dc.identifier.pmcidPMC3248477-
dc.identifier.scopuseid_2-s2.0-84855490109-
dc.identifier.volume108-
dc.identifier.issue52-
dc.identifier.spage21093-
dc.identifier.epage21098-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000298479900048-
dc.identifier.issnl0027-8424-

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