p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle. (Articolo in rivista)

Type

• Articolo in rivista (Classe)
• Prodotto della ricerca (Classe)

Label

• p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle. (Articolo in rivista) (literal)

Anno

• 2001-01-01T00:00:00+01:00 (literal)

Alternative label

• Ciciarello M 1, Mangiacasale R 1, Casenghi M 1, Zaira Limongi M 1, D'Angelo M 2, Soddu S 2, Lavia P 1, Cundari E 1. (2001)
  p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle.
  
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Ciciarello M 1, Mangiacasale R 1, Casenghi M 1, Zaira Limongi M 1, D'Angelo M 2, Soddu S 2, Lavia P 1, Cundari E 1. (literal)

Pagina inizio

• 19205 (literal)

Pagina fine

• 19213 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni

• This article has been published in an authoritative and internationally renowned scientific journal, the I.F. of which was in 2002 6.7 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 276 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

• Mangiacasale è borsista CNR (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto

• This article descibes two novel features of cell ploidy control: 1) a checkpoint response can be triggered also by transient mitotic impairment and 2) p53 localization plays a central role in the regulation of this response. Taking into account the strict relationship between the ploidy status and the malignancy of tumors, our work contributes to the comprehension of a crucial but still incompletely elucidated phenomenon. (literal)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• 1.CNR (C.S. Genetica Evoluzionistica). 2.Istituto Regina Elena (literal)

Titolo

• p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle. (literal)

Abstract

• Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble. Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit. We also show that p53 normally associates with centrosomes in mitotic cells, whereas nocodazole disrupts this association. Together these results suggest that the induction of spindle damage, albeit transient, interferes with the subcellular localization of p53 at specific mitotic locations, which in turn dictates cell cycle arrest in the offspring of such defective mitoses. (literal)

Prodotto di

• Institute of molecular biology and pathology (IBPM) (Istituto)

Autore CNR

• ENRICO CUNDARI (Unità di personale interno)
• PATRIZIA LAVIA (Persona)

Insieme di parole chiave

• Keywords of "p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle." (Insieme di parole chiave)

Incoming links:

Prodotto

• Institute of molecular biology and pathology (IBPM) (Istituto)

Autore CNR di

• PATRIZIA LAVIA (Persona)
• ENRICO CUNDARI (Unità di personale interno)

Insieme di parole chiave di

• Keywords of "p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle." (Insieme di parole chiave)