Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity (Articolo in rivista)

Type

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

Label

• Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity (Articolo in rivista) (literal)

Anno

• 2008-01-01T00:00:00+01:00 (literal)

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

• 10.1038/onc.2008.252 (literal)

Alternative label

• De Luca M, Brunetto L, Asteriti IA, Giubettini M, Lavia P, Guarguaglini G (2008)
  Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity
  in Oncogene (Basingstoke)
  (literal)

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

• De Luca M, Brunetto L, Asteriti IA, Giubettini M, Lavia P, Guarguaglini G (literal)

Pagina inizio

• 6539 (literal)

Pagina fine

• 6549 (literal)

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

• 27 (literal)

Rivista

• Oncogene (Rivista)

Note

• ISI Web of Science (WOS) (literal)

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

• Institute of Molecular Biology and Pathology, CNR (literal)

Titolo

• Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity (literal)

Abstract

• Mitotic spindle assembly is a highly regulated process, crucial to ensure the correct segregation of duplicated chromosomes in daughter cells and to avoid aneuploidy, a common feature of tumors. Among the most important spindle regulators is Aurora-A, a mitotic centrosomal kinase frequently overexpressed in tumors. Here, we investigated the role of Aurora-A in spindle pole organization in human cells. We show that RNA interference-mediated Aurora-A inactivation causes peri-centriolar material fragmentation in prometaphase, yield-ing the formation of spindles with supernumerary poles. This fragmentation does not necessarily involve centrioles and requires microtubules (MTs). Aurora-A-depleted prometaphases mislocalize the MT-stabilizing protein colonic hepatic tumor-overexpressed gene (ch-TOG), which abnormally accumulates at spindle poles, as well as the mitotic centromere-associated kinesin (MCAK), the major functional antagonist of ch-TOG, which delocalizes from poles. ch-TOG is required for extrapole formation in prometaphases lacking Aurora-A, because co-depletion of Aurora-A and ch-TOG mitigates the fragmented pole phenotype. These results indicate a novel function of Aurora-A, the regulation of ch-TOG and MCAK localization, and highlight a common pathway involving the three factors in control of spindle pole integrity. (literal)

Prodotto di

• Meccanismi molecolari del ciclo cellulare e della mitosi (SV.P15.011.001) (Modulo)
• Institute of molecular biology and pathology (IBPM) (Istituto)

Autore CNR

• PATRIZIA LAVIA (Persona)
• GIULIA GUARGUAGLINI (Persona)

Incoming links:

Autore CNR di

• GIULIA GUARGUAGLINI (Persona)
• PATRIZIA LAVIA (Persona)

Prodotto

• Institute of molecular biology and pathology (IBPM) (Istituto)
• Meccanismi molecolari del ciclo cellulare e della mitosi (SV.P15.011.001) (Modulo)

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

• Oncogene (Rivista)