Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/37742
Full metadata record
DC FieldValueLanguage
dc.contributor.authorAgostini, Massimiliano-
dc.contributor.authorAnnicchiarico-Petruzzelli, Margherita-
dc.contributor.authorMelino, Gerry-
dc.contributor.authorRufini, Alessandro-
dc.date.accessioned2016-06-14T10:29:30Z-
dc.date.available2016-06-14T10:29:30Z-
dc.date.issued2016-04-22-
dc.identifier.citationOncotarget, 2016, 7 (21), pp. 29881-29900en
dc.identifier.urihttp://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=8935en
dc.identifier.urihttp://hdl.handle.net/2381/37742-
dc.description.abstractReactive oxygen species are involved in both physiological and pathological processes including neurodegeneration and cancer. Therefore, cells have developed scavenging mechanisms to maintain redox homeostasis under control. Tumor suppressor genes play a critical role in the regulation of antioxidant genes. Here, we investigated whether the tumor suppressor gene TAp73 is involved in the regulation of metabolic adaptations triggered in response to oxidative stress. H2O2 treatment resulted in numerous biochemical changes in both control and TAp73 knockout (TAp73-/-) mouse embryonic fibroblasts, however the extent of these changes was more pronounced in TAp73-/- cells when compared to control cells. In particular, loss of TAp73 led to alterations in glucose, nucleotide and amino acid metabolism. In addition, H2O2 treatment resulted in increased pentose phosphate pathway (PPP) activity in null mouse embryonic fibroblasts. Overall, our results suggest that in the absence of TAp73, H2O2 treatment results in an enhanced oxidative environment, and at the same time in an increased pro-anabolic phenotype. In conclusion, the metabolic profile observed reinforces the role of TAp73 as tumor suppressor and indicates that TAp73 exerts this function, at least partially, by regulation of cellular metabolism.en
dc.language.isoenen
dc.publisherImpact Journalsen
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/27119504-
dc.rightsCopyright © 2016 Impact Journals, LLC. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0/ ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
dc.subjectROSen
dc.subjectmetabolismen
dc.subjectoxidative stressen
dc.subjectp53 familyen
dc.subjectp73en
dc.titleMetabolic pathways regulated by TAp73 in response to oxidative stressen
dc.typeJournal Articleen
dc.identifier.doi10.18632/oncotarget.8935-
dc.identifier.eissn1949-2553-
dc.identifier.pii8935-
dc.description.statusPeer-revieweden
dc.description.versionPublisher Versionen
dc.type.subtypeJOURNAL ARTICLE-
pubs.organisational-group/Organisationen
pubs.organisational-group/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGYen
pubs.organisational-group/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicineen
pubs.organisational-group/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine/Department of Cancer Studies and Molecular Medicineen
dc.dateaccepted2016-04-16-
Appears in Collections:Published Articles, Dept. of Cancer Studies and Molecular Medicine

Files in This Item:
File Description SizeFormat 
8935-135530-4-PB-2.pdfPublished (publisher PDF)4.42 MBAdobe PDFView/Open


Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.