Gene amplification in human cells knocked down for RAD54. (Articolo in rivista)

Type

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

Label

• Gene amplification in human cells knocked down for RAD54. (Articolo in rivista) (literal)

Anno

• 2011-01-01T00:00:00+01:00 (literal)

Alternative label

• Ruiz-Herrera A, Smirnova A, Khoriauli L, Nergadze SG, Mondello C, Giulotto E. (2011)
  Gene amplification in human cells knocked down for RAD54.
  in Genome integrity
  (literal)

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

• Ruiz-Herrera A, Smirnova A, Khoriauli L, Nergadze SG, Mondello C, Giulotto E. (literal)

Pagina inizio

• 5 (literal)

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• 2 (literal)

Rivista

• Genome integrity (Rivista)

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• Dipartimento di Genetica e Microbiologia \"Adriano Buzzati-Traverso\", Università di Pavia, Via Ferrata 1, 27100 Pavia, Italy; Istituto di Genetica Molecolare, CNR, Via Abbiategrasso 207, 27100 Pavia, Italy; Departament de Biologia Cel.lular, Fisiologia i Immunologia and Institut de Biotecnologia i Biomedicina (IBB), Universitat Autònoma de Barcelona, 08193, Campus Bellaterra, Barcelona, Spain (literal)

Titolo

• Gene amplification in human cells knocked down for RAD54. (literal)

Abstract

• ABSTRACT: BACKGROUND: In mammalian cells gene amplification is a common manifestation of genome instability promoted by DNA double-strand breaks (DSBs). The repair of DSBs mainly occurs through two mechanisms: non-homologous end-joining (NHEJ) and homologous recombination (HR). We previously showed that defects in the repair of DSBs via NHEJ could increase the frequency of gene amplification. In this paper we explored whether a single or a combined defect in DSBs repair pathways can affect gene amplification. RESULTS: We constructed human cell lines in which the expression of RAD54 and/or DNA-PKcs was constitutively knocked-down by RNA interference. We analyzed their radiosensitivity and their capacity to generate amplified DNA. Our results showed that both RAD54 and DNA-PKcs deficient cells are hypersensitive to gamma-irradiation and generate methotrexate resistant colonies at a higher frequency compared to the proficient cell lines. In addition, the analysis of the cytogenetic organization of the amplicons revealed that isochromosome formation is a prevalent mechanism responsible for copy number increase in RAD54 defective cells. CONCLUSIONS: Defects in the DSBs repair mechanisms can influence the organization of amplified DNA. The high frequency of isochromosome formation in cells deficient for RAD54 suggests that homologous recombination proteins might play a role in preventing rearrangements at the centromeres. (literal)

Prodotto di

• Institute of molecular genetics (IGM) (Istituto)
• Studio di pathway coinvolti nella progressione tumorale (ME.P05.005.002) (Modulo)

Autore CNR

• CHIARA MONDELLO (Unità di personale interno)

Incoming links:

Prodotto

• Institute of molecular genetics (IGM) (Istituto)
• Studio di pathway coinvolti nella progressione tumorale (ME.P05.005.002) (Modulo)

Autore CNR di

• CHIARA MONDELLO (Unità di personale interno)

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

• Genome integrity (Rivista)