Ribonuclease activity of p53 in cytoplasm in response to various stress signals

Derech-Haim, Sanaz; Teiblum, Gabriel; Kadosh, Racheli; Rahav, Galia; Bonda, Elad; Sredni, Benjamin; Bakhanashvili, Mary

doi:10.4161/cc.19812

Cited by 5 publications

(3 citation statements)

References 53 publications

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“…Recombinant p53 has indeed been shown to promote a 1600-fold increase of RNA:RNA annealing [ 82 ]. Moreover, p53: RNA interaction has been shown to contribute in the 3′ to 5′ exonuclease activity of p53 in cytoplasm that favors degradation of AU-Rich Elements (ARE)-containing mRNAs, which are usually protected by the RBP HuR [ 84 ]. Furthermore, a fraction of the cytoplasmic p53 protein has been reported to be associated with polysomes [ 77 ].…”

Section: P53 As Direct Regulator Of Translationmentioning

confidence: 99%

40 Years of Research Put p53 in Translation

Marcel

Long

Diaz

2018

Cancers

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Since its discovery in 1979, p53 has shown multiple facets. Initially the tumor suppressor p53 protein was considered as a stress sensor able to maintain the genome integrity by regulating transcription of genes involved in cell cycle arrest, apoptosis and DNA repair. However, it rapidly came into light that p53 regulates gene expression to control a wider range of biological processes allowing rapid cell adaptation to environmental context. Among them, those related to cancer have been extensively documented. In addition to its role as transcription factor, scattered studies reported that p53 regulates miRNA processing, modulates protein activity by direct interaction or exhibits RNA-binding activity, thus suggesting a role of p53 in regulating several layers of gene expression not restricted to transcription. After 40 years of research, it appears more and more clearly that p53 is strongly implicated in translational regulation as well as in the control of the production and activity of the translational machinery. Translation control of specific mRNAs could provide yet unsuspected capabilities to this well-known guardian of the genome.

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Section: P53 As Direct Regulator Of Translationmentioning

confidence: 99%

40 Years of Research Put p53 in Translation

Marcel

Long

Diaz

2018

Cancers

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“…Recently, various important roles of p53 in the cytoplasm have been reported. These previous reports suggest that cytoplasmic p53 plays a role in autophagy suppression, adipose tissue aging, insulin resistance, mitochondrial apoptosis and RNA degradation . However, there is no report describing a relationship between cytoplasmic p53 and aging.…”

Section: Discussionmentioning

confidence: 96%

“…These previous reports suggest that cytoplasmic p53 plays a role in autophagy suppression, 21 adipose tissue aging, insulin resistance, 22 mitochondrial apoptosis 23 and RNA degradation. 24,25 However, there is no report describing a relationship between cytoplasmic p53 and aging. In addition to responding to the NER defect in the intranuclear compartment, p53 may also suppress autophagy and promote mitochondrial apoptosis in the cytoplasmic compartment, which may play a role in the acceleration of senescence.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of p53 but not Rb in the cytoplasm of neurons and small vessels in an autopsy of a patient with Cockayne syndrome

et al. 2014

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Cockayne syndrome presents senescence-like changes starting in early infancy; however, the mechanism of premature aging remains unclear. In an autopsy of a 23-year-old woman with Cockayne syndrome, we evaluated the correlation between Cockayne pathology and the expression patterns of the senescence-associated proteins p53 and Rb. Neuropathological findings in this case revealed basal ganglia calcification, tigroid leukodystrophy, bizarre reactive astrocytes, severe cerebellar atrophy with loss of Purkinje cells, and arteriolar/neuronal calcifications in the hypothalamus. Multiple arteriolar calcifications and sclerotic changes were seen in the central nervous system and kidney, but the endothelium of the aorta and coronary arteries remained intact appropriately for the individual's age without any finding of arteriosclerosis. Overexpression of p53 protein was confirmed in the cytoplasm of neurons in the basal ganglia, thalamus, hypothalamus, hippocampus and cerebellum, of arteriolar endothelial cells of the cerebrum and renal glomerular capillaries, and of cutaneous epithelial cells. The distribution of p53 overexpression was coincident with that of pathological alteration, such as neuronal loss, calcification and atrophy. High expression of p53 was localized in the cytoplasm, not in the nucleus. In contrast to p53, Rb was not expressed in any senescence lesion. In terms of senescence, distinct differences are found among organs in a patient with Cockayne syndrome. This segmental progeria differs from natural aging, and implicates p53 overexpression in the etiology of CS.

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