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Article: GLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation

TitleGLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation
Authors
KeywordsGLS2
p53 family
Neuronal differentiation
p73
Metabolism
Neurotransmitter
Apoptosis
Issue Date2013
Citation
Cell Cycle, 2013, v. 12, n. 22, p. 3564-3573 How to Cite?
AbstractThe amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). Two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53. Here, we show that the p53 family member TAp73 also drives the expression of GLS2. Specifically, we demonstrate that TAp73 regulates GLS2 during retinoic acid-induced terminal neuronal differentiation of neuroblastoma cells, and overexpression or inhibition of GLS2 modulates neuronal differentiation and intracellular levels of ATP . Moreover, inhibition of GLS activity, by removing Glutamine from the growth medium, impairs in vitro differentiation of cortical neurons. Finally, expression of GLS2 increases during mouse cerebellar development. Although, p73 is dispensable for the in vivo expression of GLS2, TAp73 loss affects GABA and Glutamate levels in cortical neurons. Together, these findings suggest a role for GLS2 acting, at least in part, downstream of p73 in neuronal differentiation and highlight a possible role of p73 in regulating neurotransmitter synthesis. © 2013 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/292793
ISSN
2023 Impact Factor: 3.4
2023 SCImago Journal Rankings: 0.947
PubMed Central ID
ISI Accession Number ID
Errata

 

DC FieldValueLanguage
dc.contributor.authorVelletri, Tania-
dc.contributor.authorRomeo, Francesco-
dc.contributor.authorTucci, Paola-
dc.contributor.authorPeschiaroli, Angelo-
dc.contributor.authorAnnicchiarico-Petruzzelli, Margherita-
dc.contributor.authorNiklison-Chirou, Maria Victoria-
dc.contributor.authorAmelio, Ivano-
dc.contributor.authorKnight, Richard A.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorMelino, Gerry-
dc.contributor.authorAgostini, Massimiliano-
dc.date.accessioned2020-11-17T14:57:13Z-
dc.date.available2020-11-17T14:57:13Z-
dc.date.issued2013-
dc.identifier.citationCell Cycle, 2013, v. 12, n. 22, p. 3564-3573-
dc.identifier.issn1538-4101-
dc.identifier.urihttp://hdl.handle.net/10722/292793-
dc.description.abstractThe amino acid Glutamine is converted into Glutamate by a deamidation reaction catalyzed by the enzyme Glutaminase (GLS). Two isoforms of this enzyme have been described, and the GLS2 isoform is regulated by the tumor suppressor gene p53. Here, we show that the p53 family member TAp73 also drives the expression of GLS2. Specifically, we demonstrate that TAp73 regulates GLS2 during retinoic acid-induced terminal neuronal differentiation of neuroblastoma cells, and overexpression or inhibition of GLS2 modulates neuronal differentiation and intracellular levels of ATP . Moreover, inhibition of GLS activity, by removing Glutamine from the growth medium, impairs in vitro differentiation of cortical neurons. Finally, expression of GLS2 increases during mouse cerebellar development. Although, p73 is dispensable for the in vivo expression of GLS2, TAp73 loss affects GABA and Glutamate levels in cortical neurons. Together, these findings suggest a role for GLS2 acting, at least in part, downstream of p73 in neuronal differentiation and highlight a possible role of p73 in regulating neurotransmitter synthesis. © 2013 Landes Bioscience.-
dc.languageeng-
dc.relation.ispartofCell Cycle-
dc.subjectGLS2-
dc.subjectp53 family-
dc.subjectNeuronal differentiation-
dc.subjectp73-
dc.subjectMetabolism-
dc.subjectNeurotransmitter-
dc.subjectApoptosis-
dc.titleGLS2 is transcriptionally regulated by p73 and contributes to neuronal differentiation-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4161/cc.26771-
dc.identifier.pmid24121663-
dc.identifier.pmcidPMC3906342-
dc.identifier.scopuseid_2-s2.0-84890403623-
dc.identifier.volume12-
dc.identifier.issue22-
dc.identifier.spage3564-
dc.identifier.epage3573-
dc.identifier.eissn1551-4005-
dc.identifier.isiWOS:000330526200019-
dc.relation.erratumdoi:10.1080/15384101.2015.1035968-
dc.relation.erratumeid:eid_2-s2.0-84943736179-
dc.identifier.issnl1551-4005-

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