Stress Marks on the Genome: Use or Lose?

Bokhari, Bayan; Sharma, Sudha

doi:10.3390/ijms20020364

Cited by 24 publications

(19 citation statements)

References 97 publications

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“…Oxidative stress causes damage on the primary cellular components, including DNA, proteins, and lipids. In particular, ROS-induced DNA lesions include oxidized bases, abasic sites, single-strand breaks (SSBs), and DSBs, which during the replication process can lead to replication fork stalling, thus giving rise to mutations and genetic instability [84].…”

Section: Oxidative Stress Causes Dna Damage That Activates the Immunementioning

confidence: 99%

DNA Damage Response and Oxidative Stress in Systemic Autoimmunity

Souliotis

Vlachogiannis

Παππά

et al. 2019

IJMS

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The DNA damage response and repair (DDR/R) network, a sum of hierarchically structured signaling pathways that recognize and repair DNA damage, and the immune response to endogenous and/or exogenous threats, act synergistically to enhance cellular defense. On the other hand, a deregulated interplay between these systems underlines inflammatory diseases including malignancies and chronic systemic autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Patients with these diseases are characterized by aberrant immune response to self-antigens with widespread production of autoantibodies and multiple-tissue injury, as well as by the presence of increased oxidative stress. Recent data demonstrate accumulation of endogenous DNA damage in peripheral blood mononuclear cells from these patients, which is related to (a) augmented DNA damage formation, at least partly due to the induction of oxidative stress, and (b) epigenetically regulated functional abnormalities of fundamental DNA repair mechanisms. Because endogenous DNA damage accumulation has serious consequences for cellular health, including genomic instability and enhancement of an aberrant immune response, these results can be exploited for understanding pathogenesis and progression of systemic autoimmune diseases, as well as for the development of new treatments.

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Section: Oxidative Stress Causes Dna Damage That Activates the Immunementioning

confidence: 99%

DNA Damage Response and Oxidative Stress in Systemic Autoimmunity

Souliotis

Vlachogiannis

Παππά

et al. 2019

IJMS

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“…The guanine residues in GC-rich promoter sequences that adopt G4 structure are susceptible to oxidation. The 8-oxoG in the G4 motif in gene regulatory regions has been shown to couple DNA repair with transcriptional regulation [ 48 , 49 , 50 ]. A potential function of RECQ1 at G4 motifs could be to recognize and repair oxidative lesions, 8-oxoG, in the G4 motif.…”

Section: Non-canonical Roles Of Recq1mentioning

confidence: 99%

RECQ1 Helicase in Genomic Stability and Cancer

Debnath

Sharma

2020

Genes

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RECQ1 (also known as RECQL or RECQL1) belongs to the RecQ family of DNA helicases, members of which are linked with rare genetic diseases of cancer predisposition in humans. RECQ1 is implicated in several cellular processes, including DNA repair, cell cycle and growth, telomere maintenance, and transcription. Earlier studies have demonstrated a unique requirement of RECQ1 in ensuring chromosomal stability and suggested its potential involvement in tumorigenesis. Recent reports have suggested that RECQ1 is a potential breast cancer susceptibility gene, and missense mutations in this gene contribute to familial breast cancer development. Here, we provide a framework for understanding how the genetic or functional loss of RECQ1 might contribute to genomic instability and cancer.

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“…ROS may attack any of the four nucleotide bases but most frequently guanine owing to its low oxidation potential. Consequently, the structure of these bases gets disrupted and their pairing properties become altered [ 19 ]. These oxidative BDs can cause alterations in gene expression besides mutations that either induce the activation of oncogenes or the inactivation of tumor suppressor genes [ 20 ].…”

Section: Overview Of the Dna Damage Responsementioning

confidence: 99%

Modulation of DNA Damage Response by Sphingolipid Signaling: An Interplay that Shapes Cell Fate

Francis

Daher

Azzam

et al. 2020

IJMS

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Although once considered as structural components of eukaryotic biological membranes, research in the past few decades hints at a major role of bioactive sphingolipids in mediating an array of physiological processes including cell survival, proliferation, inflammation, senescence, and death. A large body of evidence points to a fundamental role for the sphingolipid metabolic pathway in modulating the DNA damage response (DDR). The interplay between these two elements of cell signaling determines cell fate when cells are exposed to metabolic stress or ionizing radiation among other genotoxic agents. In this review, we aim to dissect the mediators of the DDR and how these interact with the different sphingolipid metabolites to mount various cellular responses.

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Stress Marks on the Genome: Use or Lose?

Cited by 24 publications

References 97 publications

DNA Damage Response and Oxidative Stress in Systemic Autoimmunity

DNA Damage Response and Oxidative Stress in Systemic Autoimmunity

RECQ1 Helicase in Genomic Stability and Cancer

Modulation of DNA Damage Response by Sphingolipid Signaling: An Interplay that Shapes Cell Fate

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