Poly(ADP-ribose) catabolism in mammalian cells

Lagueux, Jean; Shah, Girish M.; M�nard, Luc; Thomassin, Hélène; Duchaine, Caroline; Hengartner, Christoph J.; Poirier, Guy G.

doi:10.1007/bf00928442

Cited by 9 publications

(2 citation statements)

References 40 publications

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“…At the same time, PARGs, the major enzymes that hydrolyze PAR, are highly active in cells [ 61 ]. The half-life of the major population of PAR may be close to one minute, but we cannot exclude that a small fraction of the polymer may have a cell half-life of several hours and be implicated in the cellular adaptation to stress conditions [ 21 , 62 ].…”

Section: Discussionmentioning

confidence: 99%

PARP1 Activation Controls Stress Granule Assembly after Oxidative Stress and DNA Damage

Singatulina

Sukhanova

Desforges

et al. 2022

Cells

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DNA damage causes PARP1 activation in the nucleus to set up the machinery responsible for the DNA damage response. Here, we report that, in contrast to cytoplasmic PARPs, the synthesis of poly(ADP-ribose) by PARP1 opposes the formation of cytoplasmic mRNA-rich granules after arsenite exposure by reducing polysome dissociation. However, when mRNA-rich granules are pre-formed, whether in the cytoplasm or nucleus, PARP1 activation positively regulates their assembly, though without additional recruitment of poly(ADP-ribose) in stress granules. In addition, PARP1 promotes the formation of TDP-43- and FUS-rich granules in the cytoplasm, two RNA-binding proteins which form neuronal cytoplasmic inclusions observed in certain neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal lobar degeneration. Together, the results therefore reveal a dual role of PARP1 activation which, on the one hand, prevents the early stage of stress granule assembly and, on the other hand, enables the persistence of cytoplasmic mRNA-rich granules in cells which may be detrimental in aging neurons.

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Section: Discussionmentioning

confidence: 99%

PARP1 Activation Controls Stress Granule Assembly after Oxidative Stress and DNA Damage

Singatulina

Sukhanova

Desforges

et al. 2022

Cells

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“…Following initial activation by a strand break, PARP1 modifies both itself and the localized histones, with a preference for automodification. In vitro turnover assays suggest that automodification soon reaches a steady state between PARylation and dissociation, at which point histone modification is favored, maintaining an open chromatin structure while repair occurs [130, 131]. Following completion of repair, PARP1 dissociates from the DNA and PARG activity hydrolyzes histone polymers to return the chromatin to its original state [107, 132].…”

Section: Parp1mentioning

confidence: 99%

Coordination of DNA single strand break repair

Abbotts

Wilson

2017

Free Radical Biology and Medicine

199

157

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The genetic material of all organisms is susceptible to modification. In some instances, these changes are programmed, such as the formation of DNA double strand breaks during meiotic recombination to generate gamete variety or class switch recombination to create antibody diversity. However, in most cases, genomic damage is potentially harmful to the health of the organism, contributing to disease and aging by promoting deleterious cellular outcomes. A proportion of DNA modifications are caused by exogenous agents, both physical (namely ultraviolet sunlight and ionizing radiation) and chemical (such as benzopyrene, alkylating agents, platinum compounds and psoralens), which can produce numerous forms of DNA damage, including a range of “simple” and helix-distorting base lesions, abasic sites, crosslinks and various types of phosphodiester strand breaks. More significant in terms of frequency are endogenous mechanisms of modification, which include hydrolytic disintegration of DNA chemical bonds, attack by reactive oxygen species and other byproducts of normal cellular metabolism, or incomplete or necessary enzymatic reactions (such as topoisomerases or repair nucleases). Both exogenous and endogenous mechanisms are associated with a high risk of single strand breakage, either produced directly or generated as intermediates of DNA repair. This review will focus upon the creation, consequences and resolution of single strand breaks, with a particular focus on two major coordinating repair proteins: poly(ADP-ribose) polymerase 1 (PARP1) and X-ray repair cross-complementing protein 1 (XRCC1).

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ADP-Ribosylation and the Cardiovascular System

Yau

Zahradka

2004

Pathophysiology of Cardiovascular Disease

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Poly(ADP-ribose) catabolism in mammalian cells

Cited by 9 publications

References 40 publications

PARP1 Activation Controls Stress Granule Assembly after Oxidative Stress and DNA Damage

PARP1 Activation Controls Stress Granule Assembly after Oxidative Stress and DNA Damage

Coordination of DNA single strand break repair

ADP-Ribosylation and the Cardiovascular System

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