DNA repair and aging: the impact of the p53 family

Nicolai, Sara; Rossi, Antonello; Daniele, Nicola Di; Melino, Gerry; Annicchiarico-Petruzzelli, Margherita; Raschellà, Giuseppe

doi:10.18632/aging.100858

Cited by 87 publications

(82 citation statements)

References 180 publications

(171 reference statements)

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“…16 p53 is a major regulator of the cellular response to DNA damage, including expression of DNA repair genes, and induction of senescence and apoptosis. 17 Such mechanisms are certainly relevant to response of neural and endothelial cells in the retina and optic disc to radiation damage.…”

Section: Genetic Risk Factors For Radiation Vasculopathymentioning

confidence: 99%

Genetic Risk Factors for Radiation Vasculopathy

Papakostas

Morrison

Lane

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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Section: Genetic Risk Factors For Radiation Vasculopathymentioning

confidence: 99%

Genetic Risk Factors for Radiation Vasculopathy

Papakostas

Morrison

Lane

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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“…Mice without p53 died of cancer 100-250 days after birth, unlike p53-positive mice that lived 500 days or more (7,8). P63 plays a pivotal role in the skin development, and p73 in the development of the nervous and immune system (9). In addition, P63 -/-mice die soon after the birth due to dehydration associated with poor skin and epithelial tissue development (10).…”

Section: Vavrova Et Al: Dose-rate As a Critical Aspect Of Cellular Rmentioning

confidence: 99%

Dose-Rate as a Critical Aspect of Cellular Response to Gamma-Radiation

Vávrová¹,

Řezáčová²,

Šinkorová³

et al. 2018

Mil. Med. Sci. Lett.

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SummaryIonizing radiation (IR) induces various types of damage in the cellular DNA, of which the most deleterious are double strand breaks. Double strand breaks lead to activation of signaling cascade aiming to repair the damage or to transiently or permanently arrest cell cycle, and/or induce cell death. In the case of high doses of ionizing radiation with a high dose-rate (0.5-1 Gy / min) where the cell repair capacity is insufficient, cell death often occurs in response to double-strand breaks. The response to the radiation exposure depends on many factors such as the cell type, its proliferation activity, and p53 status. In tumor cells, cell death is associated primarily with apoptosis or mitotic catastrophe. In normal fibroblasts, cells accumulate in the G1-phase of the cell cycle and so-called premature senescence occurs after irradiation.In cells with functional p53 protein an increase in the p21 protein (cell division inhibitor) and accumulation of the cells in the G1-phase occurs. In the case of very low-dose rate (LDR), this accumulation is transient; after DNA damage repair, the cells continue to divide. Upon irradiation with higher doses at a LDR, accumulation in the G1-phase is irreversible; p16 protein is upregulated and the status of premature senescence is induced. The same dose of radiation administered at LDRs results in more senescence than after an acute exposure.In the case of the use of IR for the eradication of tumor cells, the status of these cells is important in terms of p53 and proliferation. About fifty percent of tumor cells do not possess p53 protein or are mutant, and after irradiation they accumulate in the G2-phase and repair the IR-induced damage (e.g. HL-60 cells). In HL-60 cells (p53 -/-human promyelocytic leukemia), G2-phase accumulation occurs during irradiation with low dose rate, and their radioresistance increases if the cells are irradiated in the G2-phase. When the dose-rate is very low, the cells enter the mitotic cycle during irradiation, and because cels in mitosis are highly radiosensitive, apoptosis is induced and thus their radiosensitivity increases as well.

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“…These TFs are also capable of direct modulation of DNA repair genes and proteins [146]. Moreover, the p53 family could also be linked to ageing at the organism level [146,160].…”

Section: Transcriptional and Post-transcriptional Regulators As Sirtumentioning

confidence: 99%

“…These TFs are also capable of direct modulation of DNA repair genes and proteins [146]. Moreover, the p53 family could also be linked to ageing at the organism level [146,160]. Other emerging roles of p53 in glucose and lipid metabolism, ROS signalling and oxidative stress [64] suggest a significant functional overlap with SIRT pathways.…”

Section: Transcriptional and Post-transcriptional Regulators As Sirtumentioning

confidence: 99%

Sirtuins and their interactions with transcription factors and poly(ADP-ribose) polymerases

Jęśko

Strosznajder²

2016

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A b s t r a c tSirtuins vast number of targets in many cellular compartments, and some display additional enzymatic activities including mono(ADP-ribosyl)ation. SIRTs interact with multiple signalling proteins, transcription factors and enzymes including p53, FOXOs (forkhead box subgroup O), PPARs (peroxisome proliferator-activated receptors), NF-κB, and DNA-PK (DNA-dependent protein kinase). Sirtuins also interact extensively with the family of poly(ADPribose) polymerases (PARPs), a crucial and widespread class of NAD

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DNA repair and aging: the impact of the p53 family

Cited by 87 publications

References 180 publications

Genetic Risk Factors for Radiation Vasculopathy

Genetic Risk Factors for Radiation Vasculopathy

Dose-Rate as a Critical Aspect of Cellular Response to Gamma-Radiation

Sirtuins and their interactions with transcription factors and poly(ADP-ribose) polymerases

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