Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins

Kumar, Namrata; Moreno, Natália Cestari; Feltes, Bruno César; Menck, Carlos Frederico Martins; Houten, Bennett Van

doi:10.1590/1678-4685-gmb-2019-0104

Cited by 54 publications

(40 citation statements)

References 120 publications

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“…NER-dependent DNA repair is carried out by six factors: replication protein A (RPA), Xeroderma Pigmentosum Complementation Group A, (XPA), Xeroderma Pigmentosum Complementation Group C (XPC) complexed with RAD23 Homolog B (HR23), Transcription factor II Human (TFIIH), Xeroderma Pigmentosum Complementation Group G (XPG), and Xeroderma Pigmentosum Complementation Group F (XPF). For a detailed view of this process the reader is referred to in-depth reviews [164][165][166]. In pioneering studies led by Aziz Sancar's group, NER mediated activity was shown to be rhythmic in brain [167] and liver, but not in testis [168] and skin [169].…”

Section: Cellular Processesmentioning

confidence: 99%

The circadian clock and metabolic homeostasis: entangled networks

Assis

Oster

2021

Cell. Mol. Life Sci.

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The circadian clock exerts an important role in systemic homeostasis as it acts a keeper of time for the organism. The synchrony between the daily challenges imposed by the environment needs to be aligned with biological processes and with the internal circadian clock. In this review, it is provided an in-depth view of the molecular functioning of the circadian molecular clock, how this system is organized, and how central and peripheral clocks communicate with each other. In this sense, we provide an overview of the neuro-hormonal factors controlled by the central clock and how they affect peripheral tissues. We also evaluate signals released by peripheral organs and their effects in the central clock and other brain areas. Additionally, we evaluate a possible communication between peripheral tissues as a novel layer of circadian organization by reviewing recent studies in the literature. In the last section, we analyze how the circadian clock can modulate intracellular and tissue-dependent processes of metabolic organs. Taken altogether, the goal of this review is to provide a systemic and integrative view of the molecular clock function and organization with an emphasis in metabolic tissues.

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Section: Cellular Processesmentioning

confidence: 99%

The circadian clock and metabolic homeostasis: entangled networks

Assis

Oster

2021

Cell. Mol. Life Sci.

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“…Nucleotide excision repair can be further subcategorized into two pathways: global genome NER (GG-NER) and transcription-coupled NER (TC-NER), which are distinguished based on how the lesions are initially recognized [ 52 ]. The crosstalk between NER protein and BER proteins in the removal of oxidative damage has been reviewed [ 53 , 54 , 55 ]. The role for a GG-NER recognition protein, XPC, in stimulation of SMUG1 activity was demonstrated by the Sugasawa group [ 56 ].…”

Section: Moonlighting Functions Of Smug1 Outside Bermentioning

confidence: 99%

The Multiple Cellular Roles of SMUG1 in Genome Maintenance and Cancer

Raja

Houten

2021

IJMS

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Single-strand selective monofunctional uracil DNA glycosylase 1 (SMUG1) works to remove uracil and certain oxidized bases from DNA during base excision repair (BER). This review provides a historical characterization of SMUG1 and 5-hydroxymethyl-2′-deoxyuridine (5-hmdU) one important substrate of this enzyme. Biochemical and structural analyses provide remarkable insight into the mechanism of this glycosylase: SMUG1 has a unique helical wedge that influences damage recognition during repair. Rodent studies suggest that, while SMUG1 shares substrate specificity with another uracil glycosylase UNG2, loss of SMUG1 can have unique cellular phenotypes. This review highlights the multiple roles SMUG1 may play in preserving genome stability, and how the loss of SMUG1 activity may promote cancer. Finally, we discuss recent studies indicating SMUG1 has moonlighting functions beyond BER, playing a critical role in RNA processing including the RNA component of telomerase.

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“…Finally, DNA-protein crosslinks are mainly repaired by HR. However, repair of DNA adducts can itself cause mutations, because intermediary steps generate abasic sites or strand breaks, which, if the repair process is not completed in a timely fashion, can lead to mutations [121][122][123]. Since DNA adducts cause genome instability, they result in loss of normal growth-control mechanisms and hence promote carcinogenesis.…”

Section: Pathways Producing the Metabolite Predicted Impacts On Genommentioning

confidence: 99%

Interplay between Cellular Metabolism and the DNA Damage Response in Cancer

Moretton

Loizou

2020

Cancers

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Metabolism is a fundamental cellular process that can become harmful for cells by leading to DNA damage, for instance by an increase in oxidative stress or through the generation of toxic byproducts. To deal with such insults, cells have evolved sophisticated DNA damage response (DDR) pathways that allow for the maintenance of genome integrity. Recent years have seen remarkable progress in our understanding of the diverse DDR mechanisms, and, through such work, it has emerged that cellular metabolic regulation not only generates DNA damage but also impacts on DNA repair. Cancer cells show an alteration of the DDR coupled with modifications in cellular metabolism, further emphasizing links between these two fundamental processes. Taken together, these compelling findings indicate that metabolic enzymes and metabolites represent a key group of factors within the DDR. Here, we will compile the current knowledge on the dynamic interplay between metabolic factors and the DDR, with a specific focus on cancer. We will also discuss how recently developed high-throughput technologies allow for the identification of novel crosstalk between the DDR and metabolism, which is of crucial importance to better design efficient cancer treatments.

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Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins

Cited by 54 publications

References 120 publications

The circadian clock and metabolic homeostasis: entangled networks

The circadian clock and metabolic homeostasis: entangled networks

The Multiple Cellular Roles of SMUG1 in Genome Maintenance and Cancer

Interplay between Cellular Metabolism and the DNA Damage Response in Cancer

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