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Causes and consequences of micronuclei.

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TLDR
In this paper, the authors discuss how micronuclei are generated, what the consequences are, and what cellular mechanisms can be applied to protect against micronuclearation, with a focus on the effects of DNA degradation.
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This article is published in Current Opinion in Cell Biology.The article was published on 2021-06-01. It has received 60 citations till now. The article focuses on the topics: Chromothripsis & DNA repair.

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DNA damage and repair in age-related inflammation

TL;DR: In this article , the authors discuss the mechanisms by which DNA damage induces inflammation, such as through activation of the cGAS-STING axis and NF-κB activation by ATM.
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Current Methods and Pipelines for Image-Based Quantitation of Nuclear Shape and Nuclear Envelope Abnormalities

TL;DR: An overview of several nuclear abnormalities, including micronuclei, nuclear envelope invaginations, blebs and ruptures, and current methods used for image-based quantification of these abnormalities are reviewed, and several parameters that can be used to quantify nuclear shape are discussed.
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Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening

TL;DR: In this paper , the authors proposed that oxidative stress promotes rapid senescence by producing oxidative base lesions that drive replication-dependent telomere fragility and dysfunction in the absence of shortening and shelterin loss.
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Principles and functions of pericentromeric satellite DNA clustering into chromocenters.

TL;DR: In this article , a review of the literature on pericentromeric satellite DNA and its organization and functions across eukaryotic species is presented, focusing on chromocenters.
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Spontaneous activity of the mitochondrial apoptosis pathway drives chromosomal defects, the appearance of micronuclei and cancer metastasis through the Caspase-Activated DNAse

TL;DR: In this article , the authors tested whether spontaneously appearing micronuclei in cancer cells are linked to sub-lethal apoptotic signals and found that low-level activity in the mitochondrial apoptosis apparatus operates through CAD-dependent gene induction and STING-activation and has substantial impact on metastasis in cancer patients.
References
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Journal ArticleDOI

Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence

TL;DR: A role for innate DNA sensing in the regulation of senescence and the SASP is defined and it is found that cyclic GMP-AMP synthase (cGAS) recognizes cytosolic chromatin fragments in senescent cells.
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cGAS is essential for cellular senescence

TL;DR: It is shown that cGAS mediates cellular senescence and retards immortalization, a cytosolic DNA sensor that activates innate immunity, which is distinct from, and complementary to, the role ofcGAS in activating antitumor immunity.
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Catastrophic Nuclear Envelope Collapse in Cancer Cell Micronuclei

TL;DR: This study shows that NE collapse is a key event underlying MN dysfunction and establishes a link between aberrant NE organization and aneuploidy, suggesting that disrupted MN could be a useful objective biomarker for genomic instability in solid tumors.
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Chromothripsis and Kataegis Induced by Telomere Crisis.

TL;DR: It is proposed that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis through the generation of the ssDNA and the resolution of the chromatin bridges.
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Trex1 Exonuclease Degrades ssDNA to Prevent Chronic Checkpoint Activation and Autoimmune Disease

TL;DR: It is reported that Trex1, ordinarily associated with the endoplasmic reticulum (ER), relocalizes to the S phase nucleus after gamma irradiation or hydroxyurea treatment and acts on a single-stranded DNA polynucleotide species generated from processing of aberrant replication intermediates to attenuate DNA damage checkpoint signaling and prevent pathological immune activation.
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Trending Questions (1)
How to identify micronuclear dysfunction?

Micronuclear dysfunction can be identified by compromised integrity of the micronuclear envelope, delayed or disrupted DNA replication, inhibited DNA repair, and exposure of micronuclear DNA to the cytoplasm.