Loss of p21(CDKN1A) impairs entry to quiescence and activates a DNA damage response in normal fibroblasts induced to quiescence. (Articolo in rivista)

Type

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

Label

• Loss of p21(CDKN1A) impairs entry to quiescence and activates a DNA damage response in normal fibroblasts induced to quiescence. (Articolo in rivista) (literal)

Anno

• 2009-01-01T00:00:00+01:00 (literal)

Alternative label

• Perucca P, Cazzalini O, Madine M, Savio M, Laskey RA, Vannini V, Prosperi E, Stivala LA. (2009)
  Loss of p21(CDKN1A) impairs entry to quiescence and activates a DNA damage response in normal fibroblasts induced to quiescence.
  in Cell cycle (Georget. Tex.); Landes Bioscience, Austin (Stati Uniti d'America)
  (literal)

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

• Perucca P, Cazzalini O, Madine M, Savio M, Laskey RA, Vannini V, Prosperi E, Stivala LA. (literal)

Pagina inizio

• 105 (literal)

Pagina fine

• 114 (literal)

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

• 8 (literal)

Rivista

• Cell cycle (Rivista)

Note

• ISI Web of Science (WOS) (literal)

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

• Dipartimento di Medicina Sperimentale, sez. Patologia Generale \"C. Golgi\", Universita' di Pavia, Pavia, Italy; Hutchison/MRC Research Centre; Istituto di Genetica Molecolare del CNR (literal)

Titolo

• Loss of p21(CDKN1A) impairs entry to quiescence and activates a DNA damage response in normal fibroblasts induced to quiescence. (literal)

Abstract

• The cell cycle inhibitor p21(CDKN1A) induces cell cycle arrest under different conditions, including senescence and terminal differentiation. Still debated is its involvement in the reversible transition from proliferation to a non-dividing quiescent state (G(0)), in which a significant role has been attributed to cell cycle inhibitor p27(CDKN1B). Here we provide evidence showing that high p21 protein levels are necessary to enter and maintain the quiescence state following contact inhibition and growth factor withdrawal. In fact, entry into quiescence was impaired, both in human fibroblasts in which p21 gene has been deleted, or protein expression knocked-down by RNA interference. Importantly, in the absence of p21, human fibroblasts activate a DNA damage-like signalling pathway, as shown by phosphorylation of histone H2AX and Chk1 proteins. In addition, we show that in the absence of p21, checkpoint is activated by an unscheduled entry into S phase, with a reduced efficiency in DNA maturation, in the presence of high c-myc protein levels. These results highlight the role of p21 in counteracting inappropriate proliferation stimuli for genome stability maintenance. (literal)

Editore

• Landes Bioscience (Editore)

Prodotto di

• Institute of molecular genetics (IGM) (Istituto)
• Sviluppi metodologici in citometria e applicazioni alla sperimentazione biomedica; in vitro imaging (ME.P06.010.001) (Modulo)

Autore CNR

• ENNIO PROSPERI (Persona)

Incoming links:

Prodotto

• Institute of molecular genetics (IGM) (Istituto)
• Sviluppi metodologici in citometria e applicazioni alla sperimentazione biomedica; in vitro imaging (ME.P06.010.001) (Modulo)

Autore CNR di

• ENNIO PROSPERI (Persona)

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

• Cell cycle (Rivista)

Editore di

• Landes Bioscience (Editore)