Claspin inhibition leads to fragile site expression. (Articolo in rivista)

Type
Label
  • Claspin inhibition leads to fragile site expression. (Articolo in rivista) (literal)
Anno
  • 2009-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1002/gcc.20710 (literal)
Alternative label
  • Focarelli ML, Soza S, Mannini L, Paulis M, Montecucco A, Musio A. (2009)
    Claspin inhibition leads to fragile site expression.
    in Genes chromosomes & cancer (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Focarelli ML, Soza S, Mannini L, Paulis M, Montecucco A, Musio A. (literal)
Pagina inizio
  • 1083 (literal)
Pagina fine
  • 1090 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 48 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Istituto di Genetica Molecolare, Consiglio Nazionale della Ricerche, via Abbiategrasso 207, 27100 Pavia, Italy - Istituto di Tecnologie Biomediche, CNR Segrate (MI), Italy - Istituto Clinico Humanitas, Rozzano (MI) Italy - ITB CNR, Pisa, Italy - Istituto Toscano Tumori, Firenze, Italy (literal)
Titolo
  • Claspin inhibition leads to fragile site expression. (literal)
Abstract
  • Fragile sites are hot spots for sister chromatid exchanges, translocations, deletions, complex rearrangements, and gene amplification. It has been hypothesized that rearrangements at fragile sites derive from unreplicated regions resulting from stalled forks that escape the ATR replication checkpoint. In the present study, we investigated the role of the Claspin (CLSPN) gene, which codes for an adaptor protein in the ATR pathway, during DNA replication stress in human cells. We show that the inhibition of the CLSPN gene leads to both genome instability and fragile site expression. Following aphidicolin treatment, we found a transient increase of Claspin synthesis due to its requirement to checkpoint activation. However, Claspin synthesis decreased after a prolonged aphidicolin treatment. We propose that CLSPN modulation, following an extreme replication block, allows rare cells to escape checkpoint mechanisms and enter mitosis with a defect in genome assembly. Our observations provide the basis for a better understanding of cell cycle checkpoints deregulation in cancer. (c) 2009 Wiley-Liss, Inc. (literal)
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