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| Open AccessBarrier-to-autointegration factor 1 (Banf1) regulates poly [ADP-ribose] polymerase 1 (PARP1) activity following oxidative DNA damage
Mutation of the nuclear envelope protein, barrier-to-autointegration factor 1 (Banf1), has previously been associated with the development of ageing associated diseases in a human progeria syndrome. Here, the authors reveal the functional link between Banf1-regulated, PARP1-directed repair of oxidative lesions.
- Emma Bolderson
- , Joshua T. Burgess
- & Derek J. Richard
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Article
| Open AccessDNA single-strand break-induced DNA damage response causes heart failure
DNA damage response (DDR) is activated in cardiomyocytes of the failing heart, but the type of DNA damage leading to DDR is unclear. Higoet al. show that in mice heart failure is caused in part by unrepaired DNA single-strand breaks in cardiomyocytes, which activate persistent DDR and trigger an NF-κB-dependent cardiac inflammation.
- Tomoaki Higo
- , Atsuhiko T. Naito
- & Issei Komuro
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Article
| Open AccessContracting CAG/CTG repeats using the CRISPR-Cas9 nickase
The expansion of trinucleotide repeats has been linked to several neurodegenerative disorders. Here, the authors show that the CRISPR-Cas9 nuclease induces both expansions and contractions of the repeat region, whereas the nickase leads predominantly to contractions.
- Cinzia Cinesi
- , Lorène Aeschbach
- & Vincent Dion
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Article
| Open AccessDefective DNA single-strand break repair is responsible for senescence and neoplastic escape of epithelial cells
It is recognized that cellular senescence is triggered by DNA damage as a protective mechanism against tumorigenesis. Here the authors show that DNA single-strand breaks of oxidative origin can induce a transient senescent state followed by the emergence of clonal transformed cells.
- Joe Nassour
- , Sébastien Martien
- & Corinne Abbadie
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Article
| Open AccessSUMO modification of the neuroprotective protein TDP1 facilitates chromosomal single-strand break repair
Tyrosyl DNA phosphodiesterase 1 (TDP1) repairs DNA breaks and is mutated in the disease Spinocerebellar Ataxia with Axonal Neuropathy. Here TDP1 is shown to be post-translationally modified by sumoylation of lysine 111, and cells carrying a mutation at this residue are inefficient at single-strand DNA break repair.
- Jessica J.R. Hudson
- , Shih-Chieh Chiang
- & Sherif F. El-Khamisy