FIGURE

Fig. 2.

ID

ZDB-FIG-190723-2377

Publication

Carneiro et al., 2016 - Telomeres in aging and disease: lessons from zebrafish

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Fig. 2.

Pathways modulated by the short-telomere–p53 axis. Telomere dysfunction, as well as exogenous genotoxic agents and deficiencies in DNA repair, activates p53 (Chin et al., 1999), causing PUMA-mediated apoptosis (Sperka et al., 2012) and p21 cell-cycle arrest, and, consequently, cell senescence (Choudhury et al., 2007). p53 upregulation also leads to impairments in energy homeostasis and potential suppression of IGF-1 signalling, which result in repression of master regulators (such as PGC1α/β) of mitochondrial biogenesis. This leads to mitochondrial dysfunction and, consequently, increased ROS levels, which promote further damage at telomeres. ROS, reactive oxygen species. For further information and references, see the main text.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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