http://www.cnr.it/ontology/cnr/individuo/prodotto/ID182470
Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development (Articolo in rivista)
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- Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.ccr.2007.01.014 (literal)
- Alternative label
Vecchione, Andrea; Baldassarre, Gustavo; Ishii, Hideshi; Nicoloso, Milena S.; Belletti, Barbara; Petrocca, Fabio; Zanesi, Nicola; Fong, Louise Y. Y.; Battista, Sabrina; Guarnieri, Daniela; Baffa, Raffaele; Alder, Hansjuerg; Farber, John L.; Donovan, Peter J.; Croce, Carlo M. (2007)
Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development
in Cancer cell (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Vecchione, Andrea; Baldassarre, Gustavo; Ishii, Hideshi; Nicoloso, Milena S.; Belletti, Barbara; Petrocca, Fabio; Zanesi, Nicola; Fong, Louise Y. Y.; Battista, Sabrina; Guarnieri, Daniela; Baffa, Raffaele; Alder, Hansjuerg; Farber, John L.; Donovan, Peter J.; Croce, Carlo M. (literal)
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- Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA
Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA
Univ Roma La Sapienza, Osped Santo Andrea, Fac MEd 2, Div Pathol, I-00185 Rome, Italy
IRCCS, CRO 2, Div Expt Oncol, I-33081 Aviano, Italy
Jichi Med Sch, Ctr Mol Med, Toxhigi 3290498, Japan
Univ Naples Federico II, Dept Mat & Prod Engn, I-80139 Naples, Italy
CNR, Composite & Biomed Mat Inst, I-80125 Naples, Italy
Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA (literal)
- Titolo
- Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development (literal)
- Abstract
- The FEZ1/LZTS1 (LZTS1) protein is frequently downregulated in human cancers of different histotypes. LZTS1 is expressed in normal tissues, and its introduction in cancer cells inhibits cell growth and suppresses tumorigenicity, owing to an accumulation of cells in G2/M. Here we define its role in cell cycle regulation and tumor progression by generating Lzts1 knock-out mice. In Lzts1-/- mouse embryo fibroblasts (MEFs), Cdc25C degradation was increased during M phase resulting in decreased Cdk1 activity. As a consequence, -/- MEFs showed accelerated mitotic progression, resistance to taxol- and nocodazole-induced M phase arrest, and improper chromosome segregation. Accordingly, Lzts1 deficiency was associated with an increased incidence of both spontaneous and carcinogen-induced cancers in mice. (literal)
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