Analysis of TAp73-Dependent Signaling via Omics Technologies (Articolo in rivista)

Type
Label
  • Analysis of TAp73-Dependent Signaling via Omics Technologies (Articolo in rivista) (literal)
Anno
  • 2013-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1021/pr4005508 (literal)
Alternative label
  • D'Alessandro Angelo1; Marrocco Cristina1; Rinalducci Sara1; Peschiaroli Angelo2; Timperio Anna Maria1; Bongiorno-Borbone Lucilla3; Finazzi Agrò Alessandro3; Melino Gerry3-4; Zolla Lello1 (2013)
    Analysis of TAp73-Dependent Signaling via Omics Technologies
    in Journal of proteome research (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • D'Alessandro Angelo1; Marrocco Cristina1; Rinalducci Sara1; Peschiaroli Angelo2; Timperio Anna Maria1; Bongiorno-Borbone Lucilla3; Finazzi Agrò Alessandro3; Melino Gerry3-4; Zolla Lello1 (literal)
Pagina inizio
  • 4207 (literal)
Pagina fine
  • 4220 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
  • Epub 2013 Aug 22 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 12 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 9 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 Department of Ecological and Biological Sciences, University of Tuscia, Largo dell'Università, snc, 01100 Viterbo, Italy. 2 Institute of Cellular Biology and Neurobiology, CNR, Rome, Italy. 3 Department of Experimental Medicine and Biochemical Sciences, University of Rome \"Tor Vergata\", Via Montpellier 1, 00133 Rome, Italy. 4 Medical Research Council, Toxicology Unit, Hodgkin Building, Leicester University, Lancaster Road, P.O. Box 138, Leicester LE1 9HN, U.K. (literal)
Titolo
  • Analysis of TAp73-Dependent Signaling via Omics Technologies (literal)
Abstract
  • Transactivation-proficient (TA) p73 is a transcription factor belonging to the p53 family, which regulates a variety of biological processes, including neurogenesis, differentiation, apoptosis, and DNA damage checkpoint response. In the present study, we adopted multiple Omics approaches, based upon the simultaneous application of metabolomics, lipidomics, and proteomics, in order to dissect the intracellular pathways activated by p73. As cellular model, we utilized a clone of the human osteosarcoma SAOS-2 cell line that allows the expression of TAp73alpha in an inducible manner. We found that TAp73alpha promoted mitochondrial activity (accumulation of metabolic intermediates and up-regulation of proteins related to the Krebs cycle), boosted glutathione homeostasis, increased arginine-citrulline-NO metabolism, altered purine synthesis, and promoted the pentose phosphate pathway toward NADPH accumulation for reducing and biosynthetic purposes. Indeed, lipid metabolism was driven toward the accumulation and oxidation of long-chain fatty acids with pro-apoptotic potential. In parallel, the expression of TAp73alpha was accompanied by the dephosphorylation of key proteins of the mitotic spindle assembly checkpoint. In conclusion, the obtained results confirm existing evidence from transcriptomics analyses and suggest a role for TAp73alpha in the regulation of cellular metabolism, cell survival, and cell growth. (literal)
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