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Article: TAp73 acts via the bHLH Hey2 to promote long-term maintenance of neural precursors

TitleTAp73 acts via the bHLH Hey2 to promote long-term maintenance of neural precursors
Authors
Issue Date2010
Citation
Current Biology, 2010, v. 20, n. 22, p. 2058-2065 How to Cite?
AbstractIncreasing evidence suggests that deficits in adult stem cell maintenance cause aberrant tissue repair and premature aging [1]. While the mechanisms regulating stem cell longevity are largely unknown, recent studies have implicated p53 and its family member p63. Both proteins regulate organismal aging [2-4] as well as survival and self-renewal of tissue stem cells [5-9]. Intriguingly, haploinsufficiency for a third family member, p73, causes age-related neurodegeneration [10]. While this phenotype is at least partially due to loss of the ΔNp73 isoform, a potent neuronal prosurvival protein [11-16], a recent study showed that mice lacking the other p73 isoform, TAp73, have perturbations in the hippocampal dentate gyrus [17], a major neurogenic site in the adult brain. These findings, and the link between the p53 family, stem cells, and aging, suggest that TAp73 might play a previously unanticipated role in maintenance of neural stem cells. Here, we have tested this hypothesis and show that TAp73 ensures normal adult neurogenesis by promoting the long-term maintenance of neural stem cells. Moreover, we show that TAp73 does this by transcriptionally regulating the bHLH Hey2, which itself promotes neural precursor maintenance by preventing premature differentiation. © 2010 Elsevier Ltd All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/291998
ISSN
2023 Impact Factor: 8.1
2023 SCImago Journal Rankings: 2.982
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFujitani, Masashi-
dc.contributor.authorCancino, Gonzalo I.-
dc.contributor.authorDugani, Chandrasagar B.-
dc.contributor.authorWeaver, Ian C.G.-
dc.contributor.authorGauthier-Fisher, Andrée-
dc.contributor.authorPaquin, Annie-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorWojtowicz, Martin J.-
dc.contributor.authorMiller, Freda D.-
dc.contributor.authorKaplan, David R.-
dc.date.accessioned2020-11-17T14:55:33Z-
dc.date.available2020-11-17T14:55:33Z-
dc.date.issued2010-
dc.identifier.citationCurrent Biology, 2010, v. 20, n. 22, p. 2058-2065-
dc.identifier.issn0960-9822-
dc.identifier.urihttp://hdl.handle.net/10722/291998-
dc.description.abstractIncreasing evidence suggests that deficits in adult stem cell maintenance cause aberrant tissue repair and premature aging [1]. While the mechanisms regulating stem cell longevity are largely unknown, recent studies have implicated p53 and its family member p63. Both proteins regulate organismal aging [2-4] as well as survival and self-renewal of tissue stem cells [5-9]. Intriguingly, haploinsufficiency for a third family member, p73, causes age-related neurodegeneration [10]. While this phenotype is at least partially due to loss of the ΔNp73 isoform, a potent neuronal prosurvival protein [11-16], a recent study showed that mice lacking the other p73 isoform, TAp73, have perturbations in the hippocampal dentate gyrus [17], a major neurogenic site in the adult brain. These findings, and the link between the p53 family, stem cells, and aging, suggest that TAp73 might play a previously unanticipated role in maintenance of neural stem cells. Here, we have tested this hypothesis and show that TAp73 ensures normal adult neurogenesis by promoting the long-term maintenance of neural stem cells. Moreover, we show that TAp73 does this by transcriptionally regulating the bHLH Hey2, which itself promotes neural precursor maintenance by preventing premature differentiation. © 2010 Elsevier Ltd All rights reserved.-
dc.languageeng-
dc.relation.ispartofCurrent Biology-
dc.titleTAp73 acts via the bHLH Hey2 to promote long-term maintenance of neural precursors-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.cub.2010.10.029-
dc.identifier.pmid21074438-
dc.identifier.scopuseid_2-s2.0-78649331805-
dc.identifier.volume20-
dc.identifier.issue22-
dc.identifier.spage2058-
dc.identifier.epage2065-
dc.identifier.isiWOS:000284923700033-
dc.identifier.issnl0960-9822-

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