scholarly journals DNA damage responses in progeroid syndromes arise from defective maturation of prelamin A

2006 ◽  
Vol 119 (22) ◽  
pp. 4644-4649 ◽  
Author(s):  
Y. Liu ◽  
A. Rusinol ◽  
M. Sinensky ◽  
Y. Wang ◽  
Y. Zou
Open Biology ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 190168 ◽  
Author(s):  
Paulo F. L. da Silva ◽  
Björn Schumacher

Ageing appears to be a nearly universal feature of life, ranging from unicellular microorganisms to humans. Longevity depends on the maintenance of cellular functionality, and an organism's ability to respond to stress has been linked to functional maintenance and longevity. Stress response pathways might indeed become therapeutic targets of therapies aimed at extending the healthy lifespan. Various progeroid syndromes have been linked to genome instability, indicating an important causal role of DNA damage accumulation in the ageing process and the development of age-related pathologies. Recently, non-cell-autonomous mechanisms including the systemic consequences of cellular senescence have been implicated in regulating organismal ageing. We discuss here the role of cellular and systemic mechanisms of ageing and their role in ageing-associated diseases.


2020 ◽  
Author(s):  
Jared J. Luxton ◽  
Miles J. McKenna ◽  
Lynn E. Taylor ◽  
Kerry A. George ◽  
Sara Zwart ◽  
...  

2015 ◽  
Vol 15 (6) ◽  
pp. 533-541 ◽  
Author(s):  
Jinlu Ma ◽  
Dan Zhang ◽  
Xia Ying ◽  
Ying Zhao ◽  
Chenchen He ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Munetoshi Maeda ◽  
Masanori Tomita ◽  
Mika Maeda ◽  
Hideki Matsumoto ◽  
Noriko Usami ◽  
...  

AbstractWe recently showed that when a low X-ray dose is used, cell death is enhanced in nucleus-irradiated compared with whole-cell-irradiated cells; however, the role of the cytoplasm remains unclear. Here, we show changes in the DNA damage responses with or without X-ray microbeam irradiation of the cytoplasm. Phosphorylated histone H2AX foci, a surrogate marker for DNA double-strand breaks, in V79 and WI-38 cells are not observed in nucleus irradiations at ≤ 2 Gy, whereas they are observed in whole-cell irradiations. Addition of an ataxia telangiectasia mutated (ATM) kinase inhibitor to whole-cell irradiations suppresses foci formation at ≤ 2 Gy. ABL1 and p73 expression is upregulated following nucleus irradiation, suggesting the induction of p73-dependent cell death. Furthermore, CDKN1A (p21) is upregulated following whole-cell irradiation, indicating the induction of cell cycle arrest. These data reveal that cytoplasmic radioresponses modify ATM-mediated DNA damage responses and determine the fate of cells irradiated at low doses.


2010 ◽  
Vol 29 (18) ◽  
pp. 3130-3139 ◽  
Author(s):  
Sophie E Polo ◽  
Abderrahmane Kaidi ◽  
Linda Baskcomb ◽  
Yaron Galanty ◽  
Stephen P Jackson

2016 ◽  
Vol 136 (5) ◽  
pp. S101 ◽  
Author(s):  
S. Shaik ◽  
M. Pollet ◽  
J. Krutmann ◽  
T. Haarmann-Stemmann

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