http://www.cnr.it/ontology/cnr/individuo/prodotto/ID23568
Diethylsulphate and methylnitrosourea affect different targets in Chinese hamster fibroblasts: possible mechanisms of aneuploidy induction by these agents (Articolo in rivista)
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- Diethylsulphate and methylnitrosourea affect different targets in Chinese hamster fibroblasts: possible mechanisms of aneuploidy induction by these agents (Articolo in rivista) (literal)
- Anno
- 2003-01-01T00:00:00+01:00 (literal)
- Alternative label
Campagna M., Beffy P., Del Carratore R., Hauri L., Simi S., Bonatti S., Simili M. (2003)
Diethylsulphate and methylnitrosourea affect different targets in Chinese hamster fibroblasts: possible mechanisms of aneuploidy induction by these agents
in Mutagenesis
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- Campagna M., Beffy P., Del Carratore R., Hauri L., Simi S., Bonatti S., Simili M. (literal)
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- questo lavoro, nato dalla collaborazione con lIstituto Tumori di Genova, individua nella inibizione di proteine chinasi della trasduzione del segnale (S6K1) uno delle possibili cause della induzione di aneuploidia da parte di agenti alchilanti. (literal)
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- Institute of Clinical Physiology, CNR, Cellular Biology and Cytogenetics Unit, Pisa (Italy). (a) lIstituto Tumori di Genova (literal)
- Titolo
- Diethylsulphate and methylnitrosourea affect different targets in Chinese hamster fibroblasts: possible mechanisms of aneuploidy induction by these agents (literal)
- Abstract
- It has been shown that the ethylating agent diethylsulphate (DES) induces centromere-containing
micronuclei with kinetics suggesting that molecules other than DNA could be targets. In quiescent
Chinese hamster fibroblasts CHEF/18, O6-alkylated bases inhibit ribosomal protein S6 kinase
(S6K1), the terminal member of a kinase cascade responsible for an increased rate of protein
synthesis, but not extracellular signal-activated kinases (ERK1/2) or terminal kinases of a second
cascade which activates transcription. The inhibition correlates with the appearance of abnormal
metaphases at the following mitosis, suggesting that alkylation of the nucleotide pool and inhibition
of S6K1 could be one of the mechanisms leading to chromosome loss by alkylating agents. To
clarify the role of protein kinases in chromosome loss induced by alkylating agents, we have
studied the effects of DES and methylnitrosourea (MNU) on S6K1 and ERK1/2 activation by
growth factors. The alkylating agents were studied in a battery of Chinese hamster fibroblasts
(CHEF/18, CHO and ClB) with normal and mutated p53 to control for DNA damage-induced
activation of p53, which could indirectly inhibit protein kinases. The role of repair in induction of
micronuclei was studied in mismatch repair-proficient CHO and repair-deficient ClB cells. Our
results indicate that DES induced micronuclei in a mismatch repair-independent manner, within 8
h of treatment, in agreement with a role for S6K1 inhibition in micronucleus formation. MNU
induced centromere-containing micronuclei only in CHO cells, one cell cycle after treatment,
without any detectable influences on either kinase cascade, suggesting a role for mismatch repair
in chromosome loss.
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