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• W2091968052 abstract "The E3-ubiquitin ligase APC/C-Cdh1 is essential for endoreduplication but its relevance in the mammalian mitotic cell cycle is still unclear. Here we show that genetic ablation of Cdh1 in the developing nervous system results in hypoplastic brain and hydrocephalus. These defects correlate with enhanced levels of Cdh1 substrates and increased entry into the S phase in neural progenitors. However, cell division is prevented in the absence of Cdh1 due to hyperactivation of cyclin-dependent kinases, replicative stress, induction of p53, G2 arrest and apoptotic death of these progenitor cells. Concomitant ablation of p53 rescues apoptosis but not replicative stress, resulting in the presence of damaged neurons throughout the adult brain. These data indicate that the inactivation of Cdh1 in vivo results in replicative stress, cell cycle arrest and cell death, supporting recent therapeutic proposals aimed to inhibit the APC/C in tumours. The E3-ubiquitin ligase APC/C and its cofactor Cdh1 have been shown to play important roles in axonal growth and synaptic plasticity. In this study, Eguren et al.show that elimination of Cdh1 in the developing nervous system results in defects in the neural progenitor compartment, hydrocephalus and reduced lifespan." @default.
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• W2091968052 date "2013-12-04" @default.
• W2091968052 modified "2023-10-17" @default.
• W2091968052 title "The APC/C cofactor Cdh1 prevents replicative stress and p53-dependent cell death in neural progenitors" @default.
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• W2091968052 doi "https://doi.org/10.1038/ncomms3880" @default.
• W2091968052 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24301385" @default.
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