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Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS...

Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5299712

Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS-dependent but p53/p21-independent manner

About this item

Full title

Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS-dependent but p53/p21-independent manner

Publisher

London: Nature Publishing Group UK

Journal title

Cell death and differentiation, 2017-02, Vol.24 (2), p.288-299

Language

English

Formats

Publication information

Publisher

London: Nature Publishing Group UK

More information

Scope and Contents

Contents

We observed that the transient induction of mtDNA double strand breaks (DSBs) in cultured cells led to activation of cell cycle arrest proteins (p21/p53 pathway) and decreased cell growth, mediated through reactive oxygen species (ROS). To investigate this process
in vivo
we developed a mouse model where we could transiently induce mtDNA DSBs...

Alternative Titles

Full title

Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS-dependent but p53/p21-independent manner

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5299712

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5299712

Other Identifiers

ISSN

1350-9047

E-ISSN

1476-5403

DOI

10.1038/cdd.2016.123

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