Results for 'damage repair'

983 found
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  1. Damaged identities, narrative repair.Hilde Lindemann - 2001 - Ithaca: Cornell University Press.
    Hilde Lindemann Nelson focuses on the stories of groups of people--including Gypsies, mothers, nurses, and transsexuals--whose identities have been defined by those with the power to speak for them and to constrain the scope of their actions. By placing their stories side by side with narratives about the groups in question, Nelson arrives at some important insights regarding the nature of identity. She regards personal identity as consisting not only of how people view themselves but also of how others view (...)
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  2.  21
    DNA damage tolerance, mismatch repair and genome instability.P. Karran & M. Bignami - 1994 - Bioessays 16 (11):833-839.
    DNA mismatch repair is an important pathway of mutation avoidance. It also contributes to the cytotoxic effects of some kinds of DNA damage, and cells defective in mismatch repair are resistant, or tolerant, to the presence of some normally cytotoxic base analogues in their DNA. The absence of a particular mismatch binding function from some mammalian cells confers resistance to the base analogues O6‐methylguanine and 6‐thioguanine in DNA. Cells also acquire a spontaneous mutator phenotype as a consequence (...)
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  3.  35
    Community Repair of Moral Damage from Domestic Violence.Alycia LaGuardia-LoBianco - 2022 - Social Philosophy Today 38:47-65.
    I argue that communities have a moral responsibility to repair and prevent moral damage that some survivors of domestic violence may experience. This responsibility is grounded in those communities’ complicity in domestic violence and the moral damage that may result. Drawing on Claudia Card’s work on domestic violence, I first explain two forms of moral damage that some survivors may experience. These are: 1) normative isolation, or abusive environments that are marked by distorted moral standards about (...)
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  4.  48
    Damage‐induced reactivation of cohesin in postreplicative DNA repair.Alexander R. Ball & Kyoko Yokomori - 2008 - Bioessays 30 (1):5-9.
    Cohesin establishes sister‐chromatid cohesion during S phase to ensure proper chromosome segregation in mitosis. It also facilitates postreplicative homologous recombination repair of DNA double‐strand breaks by promoting local pairing of damaged and intact sister chromatids. In G2 phase, cohesin that is not bound to chromatin is inactivated, but its reactivation can occur in response to DNA damage. Recent papers by Koshland's and Sjögren's groups describe the critical role of the known cohesin cofactor Eco1 (Ctf7) and ATR checkpoint kinase (...)
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  5.  11
    UV damage and repair mechanisms in mammalian cells.Silvia Tornaletti & Gerd P. Pfeifer - 1996 - Bioessays 18 (3):221-228.
    The formation of DNA photoproducts by ultraviolet (UV) light is responsible for induction of mutations and development of skin cancer. To understand UV mutagenesis, it is important to know the mechanisms of formation and repair of these lesions. Cyclobutane pyrimidine dimers and (6–4)photoproducts are the two major classes of UV‐induced DNA lesions. Their distribution along DNA sequences in vivo is strongly influenced by nucleosomes and other DNA binding proteins. Repair of UV photoproducts is dependent on the transcriptional status (...)
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  6.  61
    Bridging Diverging Perspectives and Repairing Damaged Relationships in the Aftermath of Workplace Transgressions.Tyler G. Okimoto & Michael Wenzel - 2014 - Business Ethics Quarterly 24 (3):443-473.
    ABSTRACT:Workplace transgressions elicit a variety of opinions about their meaning and what is required to address them. This diversity in views makes it difficult for managers to identify a mutually satisfactory response and to enable repair of the relationships between the affected parties. We develop a conceptual model for understanding how to bridge these diverging perspectives and foster relationship repair. Specifically, we argue that effective relationship repair is dependent on the parties’ reciprocal concern for others’ viewpoints and (...)
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  7.  22
    Repair and Reconstruction of Telomeric and Subtelomeric Regions and Genesis of New Telomeres: Implications for Chromosome Evolution.Chuna Kim, Sanghyun Sung, Jun Kim & Junho Lee - 2020 - Bioessays 42 (6):1900177.
    DNA damage repair within telomeres are suppressed to maintain the integrity of linear chromosomes, but the accidental activation of repairs can lead to genome instability. This review develops the concept that mechanisms to repair DNA damage in telomeres contribute to genetic variability and karyotype evolution, rather than catastrophe. Spontaneous breaks in telomeres can be repaired by telomerase, but in some cases DNA repair pathways are activated, and can cause chromosomal rearrangements or fusions. The resultant changes (...)
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  8. Alternative repair pathways for UV‐induced DNA damage.Akira Yasui & Shirley J. McCready - 1998 - Bioessays 20 (4):291-297.
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  9.  16
    Chaperones for dancing on chromatin: Role of post‐translational modifications in dynamic damage detection hand‐offs during nucleotide excision repair.Bennett Van Houten, Brittani Schnable & Namrata Kumar - 2021 - Bioessays 43 (5):2100011.
    We highlight a recent study exploring the hand‐off of UV damage to several key nucleotide excision repair (NER) proteins in the cascade: UV‐DDB, XPC and TFIIH. The delicate dance of DNA repair proteins is choreographed by the dynamic hand‐off of DNA damage from one recognition complex to another damage verification protein or set of proteins. These DNA transactions on chromatin are strictly chaperoned by post‐translational modifications (PTM). This new study examines the role that ubiquitylation and (...)
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  10.  43
    Damaged Identities, Narrative Repair.Claudia Card - 2002 - International Philosophical Quarterly 42 (2):283-284.
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  11. Moral Repair: Reconstructing Moral Relations After Wrongdoing.Margaret Urban Walker - 2006 - Cambridge University Press.
    Moral Repair examines the ethics and moral psychology of responses to wrongdoing. Explaining the emotional bonds and normative expectations that keep human beings responsive to moral standards and responsible to each other, Margaret Urban Walker uses realistic examples of both personal betrayal and political violence to analyze how moral bonds are damaged by serious wrongs and what must be done to repair the damage. Focusing on victims of wrong, their right to validation, and their sense of justice, (...)
  12.  10
    Interplay between altered metabolism and DNA damage and repair in ovarian cancer.Apoorva Uboveja & Katherine M. Aird - 2024 - Bioessays 46 (8):2300166.
    Ovarian cancer is the most lethal gynecological malignancy and is often associated with both DNA repair deficiency and extensive metabolic reprogramming. While still emerging, the interplay between these pathways can affect ovarian cancer phenotypes, including therapeutic resistance to the DNA damaging agents that are standard‐of‐care for this tumor type. In this review, we will discuss what is currently known about cellular metabolic rewiring in ovarian cancer that may impact DNA damage and repair in addition to highlighting how (...)
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  13.  13
    Conserved mechanisms of repair: from damaged single cells to wounds in multicellular tissues.Katie Woolley & Paul Martin - 2000 - Bioessays 22 (10):911-919.
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  14.  26
    Between the Surface and the Inside Toward a Phenomenological Ontology of Skin Focused on the Damage and Repair.Hernán Alonso Jaramillo Fernández - 2022 - Ideas Y Valores 71 (179):35-58.
    RESUMEN Este artículo propone la piel como un concepto ontológico y fenomenológico indispensable para comprender el daño y repensar la dimensión sensible de la reparación. El trabajo tiene cuatro secciones. En primer lugar, introduce la relevancia de la fenomenologia para estudiar el dafio. En segundo lugar, formula una ontologia fenomenológica de la piel a la luz de dos componentes: la heteroafección y la autoafección. En tercer lugar, aplica la ontologia de la piel a la violencia. Finalmente, en cuarto lugar, concluye (...)
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  15.  42
    Mitosis, double strand break repair, and telomeres: A view from the end.Anthony J. Cesare - 2014 - Bioessays 36 (11):1054-1061.
    Double strand break (DSB) repair is suppressed during mitosis because RNF8 and downstream DNA damage response (DDR) factors, including 53BP1, do not localize to mitotic chromatin. Discovery of the mitotic kinase‐dependent mechanism that inhibits DSB repair during cell division was recently reported. It was shown that restoring mitotic DSB repair was detrimental, resulting in repair dependent genome instability and covalent telomere fusions. The telomere DDR that occurs naturally during cellular aging and in cancer is known (...)
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  16.  39
    Recurrent Noncoding Mutations in Skin Cancers: UV Damage Susceptibility or Repair Inhibition as Primary Driver?Steven A. Roberts, Alexander J. Brown & John J. Wyrick - 2019 - Bioessays 41 (3):1800152.
    Somatic mutations arising in human skin cancers are heterogeneously distributed across the genome, meaning that certain genomic regions (e.g., heterochromatin or transcription factor binding sites) have much higher mutation densities than others. Regional variations in mutation rates are typically not a consequence of selection, as the vast majority of somatic mutations in skin cancers are passenger mutations that do not promote cell growth or transformation. Instead, variations in DNA repair activity, due to chromatin organization and transcription factor binding, have (...)
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  17.  32
    Nucleotide Excision Repair and Transcription‐Associated Genome Instability.Zivkos Apostolou, Georgia Chatzinikolaou, Kalliopi Stratigi & George A. Garinis - 2019 - Bioessays 41 (4):1800201.
    Transcription is a potential threat to genome integrity, and transcription‐associated DNA damage must be repaired for proper messenger RNA (mRNA) synthesis and for cells to transmit their genome intact into progeny. For a wide range of structurally diverse DNA lesions, cells employ the highly conserved nucleotide excision repair (NER) pathway to restore their genome back to its native form. Recent evidence suggests that NER factors function, in addition to the canonical DNA repair mechanism, in processes that facilitate (...)
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  18.  17
    Transcription‐independent functions of p53 in DNA repair pathway selection.Yu-Hsiu Wang & Michael P. Sheetz - 2023 - Bioessays 45 (1):2200122.
    Recently discovered transcription‐independent features of p53 involve the choice of DNA damage repair pathway after PARylation, and p53's complex formation with phosphoinositide lipids, PI(4,5)P2. PARylation‐mediated rapid accumulation of p53 at DNA damage sites is linked to the recruitment of downstream repair factors and tumor suppression. This links p53's capability to sense damaged DNA in vitro and its relevant functions in cells. Further, PI(4,5)P2 rapidly accumulates at damage sites like p53 and complexes with p53, while it (...)
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  19.  20
    Transcription‐blocking DNA damage in aging: a mechanism for hormesis.Björn Schumacher - 2009 - Bioessays 31 (12):1347-1356.
    Recent evidence from studies on DNA repair systems that are implicated in accelerated aging syndromes, have revealed a mechanism through which low levels of persistent damage might exert beneficial effects for both cancer prevention and longevity assurance. Beneficial effects of adaptive responses to low doses of insults that in higher concentrations show adverse effects are generally referred to as hormesis. There are numerous examples of hormetic effects ranging from mild stresses of irradiation to heat stress, hypergravity, pro‐oxidants, or (...)
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  20.  16
    DNA repair in man: Regulation by a multigene family and association with human disease.James E. Cleaver & Deneb Karentz - 1987 - Bioessays 6 (3):122-127.
    The major mechanism of repair of damage to DNA involves a conceptually simple process of enzymatic excision and resynthesis of small regions of DNA. In man and other mammals, this process is regulated by several gene loci; up to 15 mutually complementary genes or gene products may be involved. Repair deficiency results in an array of clinical symptoms in skin, central nervous system, and hematopoietic and immune systems, the major example being xeroderma pigmentosum (XP), a disease with (...)
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  21.  25
    Neural repair and glial proliferation: Parallels with gliogenesis in insects.Peter J. S. Smith, David Shepherd & John S. Edwards - 1991 - Bioessays 13 (2):65-72.
    There is a growing recognition, stemming from work with both vertebrates and invertebrates, that the capacity for neuronal regeneration is critically dependent on the local microenvironment. That environment is largely created by the non‐neuronal elements of the nervous system, the neuroglia. Therefore an understanding of how glial cells respond to injury is crucial to understanding neuronal regeneration. Here we examine the process of repair in a relatively simple nervous system, that of the insect, in which it is possible to (...)
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  22.  20
    DNA damage and cell cycle regulation of ribonucleotide reductase.Stephen J. Elledge, Zheng Zhou, James B. Allen & Tony A. Navas - 1993 - Bioessays 15 (5):333-339.
    Ribonucleotide reductase (RNR) catalyzes the rate limiting step in the production of deoxyribonucleotides needed for DNA synthesis. In addition to the well documented allosteric regulation, the synthesis of the enzyme is also tightly regulated at the level of transcription. mRNAs for both subunits are cell cycle regulated and inducible by DNA damage in all organisms examined, including E. coli, S. cerevisiae and H. sapiens. This DNA damage regulation is thought to provide a metabolic state that facilitates DNA replicational (...)
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  23.  23
    The machine-like repair of aging. Disentangling the key assumptions of the SENS agenda.Pablo García-Barranquero & Marta Bertolaso - 2022 - Theoria: Revista de Teoría, Historia y Fundamentos de la Ciencia 37 (3):379-394.
    The possibility of curing aging is currently generating hopes and concerns among entrepreneurs, experts, and the general public. This article aims to clarify some of the key assumptions of the Strategies for Engineered Negligible Senescence agenda, one of the most prominent paradigms for rejuvenation. To do this, we present the three fundamental claims of this research program: (1) aging can be repaired; (2) rejuvenation is possible through the reversal of all molecular damage; (3) and the human organism is a (...)
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  24.  3
    Oxidative DNA damage, antioxidants, and cancer.John Sommerville - 1999 - Bioessays 21 (3):238-246.
    Oxidised bases, such as 8-oxo-guanine, occur in cellular DNA as a result of attack by oxygen free radicals. The cancer-protective effect of vegetables and fruit is attributed to the ability of antioxidants in them to scavenge free radicals, preventing DNA damage and subsequent mutation. Antioxidant supplements (e.g., β-carotene, vitamin C) increase the resistance of lymphocytes to oxidative damage, and a negative correlation is seen between antioxidant concentrations in tissues and oxidised bases in DNA. Large-scale intervention trials with β-carotene (...)
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  25.  95
    A model for repair of radiation‐induced DNA double‐strand breaks in the extreme radiophile Deinococcus radiodurans.Kenneth W. Minton & Michael J. Daly - 1995 - Bioessays 17 (5):457-464.
    The bacterium Deinococcus (formerly Micrococcus) radiodurans and other members of the eubacterial family Deinococaceae are extremely resistant to ionizing radiation and many other agents that damage DNA. Stationary phase D. radiodurans exposed to 1.0‐1.5 Mrad γ‐irradiation sustains >120 DNA double‐strand breaks (dsbs) per chromosome; these dsbs are mended over a period of hours with 100% survival and virtually no mutagenesis. This contrasts with nearly all other organisms in which just a few ionizing radiation induced‐dsbs per chromosome are lethal. In (...)
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  26.  17
    Cytoskeletal Exposure in the Regulation of Immunity and Initiation of Tissue Repair.Oliver Gordon & Caetano Reis E. Sousa - 2019 - Bioessays 41 (7):1900021.
    This article reviews and discusses emerging evidence suggesting an evolutionarily‐conserved connection between injury‐associated exposure of cytoskeletal proteins and the induction of tolerance to infection, repair of tissue damage and restoration of homeostasis. While differences exist between vertebrates and invertebrates with respect to the receptor(s), cell types, and effector mechanisms involved, the response to exposed cytoskeletal proteins appears to be protective and to rely on a conserved signaling cassette involving Src family kinases, the nonreceptor tyrosine kinase Syk, and tyrosine (...)
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  27.  76
    Damaged Bodies, Damaged Identities.Hilde Lindemann Nelson - 2004 - Philosophy in the Contemporary World 11 (1):7-11.
    In this essay I examine Margaret Edson’s Pulitzer prizewinning play, Wit, to explore the numerous connections drawn there between damage to bodies and damage to identities. In the course of this exploration I aim to get clearer about the kinds of illness, injury, or medical interventions that damage patients’ identities; how the damage is inflicted; and what might be done to repair identities that have been damaged in these ways. I argue that just as bodily (...)
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  28.  30
    DNA excision repair in mammalian cell extracts.Richard D. Wood & Dawn Coverley - 1991 - Bioessays 13 (9):447-453.
    The many genetic complementation groups of DNA excision‐repair defective mammalian cells indicate the considerable complexity of the excision repair process. The cloning of several repair genes is taking the field a step closer to mechanistic studies of the actions and interactions of repair proteins. Early biochemical studies of mammalian DNA repair in vitro are now at hand. Repair synthesis in damaged DNA can be monitored by following the incorporation of radiolabelled nucleotides. Synthesis is carried (...)
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  29.  17
    Are there DNA damage checkpoints in E. coli?Bryn A. Bridges - 1995 - Bioessays 17 (1):63-70.
    The concept of regulatory ‘checkpoints’ in the eukaryotic cycle has proved to be a fruitful one. Here, its applicability to the bacterial cell cycle is examined. A primitive DNA damage checkpoint operates in E. coli such that, after exposure to ultraviolet light, while excision repair occurs, chromosome replication continues very slowly with the production of discontinuous daughter strands. The slower the rate of excision of photoproducts, the greater the delay before the normal rate of DNA replication is restored, (...)
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  30.  31
    Adaptive responses to genotoxic damage: Bacterial strategies to prevent ‐mutation and cell death.Bruce Demple - 1987 - Bioessays 6 (4):157-160.
    Bacteria are able to induce defense and DNA repair systems that specifically counteract the toxic effects of some important natural agents. «Adaptive responses» to alkylation and oxidation damage have revealed novel strategies for escape from certain kinds of genetic damage.
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  31.  20
    Eukaryotic DNA repair: Glimpses through the yeast Saccharomyces cerevisiae.Errol C. Friedberg - 1991 - Bioessays 13 (6):295-302.
    Eukaryotic cells are able to mount several genetically complex cellular responses to DNA damage. The yeast Saccharomyces cerevisiae is a genetically well characterized organism that is also amenable to molecular and biochemical studies. Hence, this organism has provided a useful and informative model for dissecting the biochemistry and molecular biology of DNA repair in eukaryotes.
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  32.  43
    How Acts of Infidelity Promote DNA Break Repair: Collision and Collusion Between DNA Repair and Transcription.Priya Sivaramakrishnan, Alasdair J. E. Gordon, Jennifer A. Halliday & Christophe Herman - 2018 - Bioessays 40 (10):1800045.
    Transcription is a fundamental cellular process and the first step in gene regulation. Although RNA polymerase (RNAP) is highly processive, in growing cells the progression of transcription can be hindered by obstacles on the DNA template, such as damaged DNA. The authors recent findings highlight a trade‐off between transcription fidelity and DNA break repair. While a lot of work has focused on the interaction between transcription and nucleotide excision repair, less is known about how transcription influences the (...) of DNA breaks. The authors suggest that when the cell experiences stress from DNA breaks, the control of RNAP processivity affects the balance between preserving transcription integrity and DNA repair. Here, how the conflict between transcription and DNA double‐strand break (DSB) repair threatens the integrity of both RNA and DNA are discussed. In reviewing this field, the authors speculate on cellular paradigms where this equilibrium is well sustained, and instances where the maintenance of transcription fidelity is favored over genome stability. (shrink)
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  33.  34
    Is there induced DNA repair in mammalian cells?David T. Denhardt & Jacek Kowalski - 1988 - Bioessays 9 (2‐3):70-72.
    The problem we discuss is whether mammalian cells possess genes whose expression is specifically enhanced by DNA damage in order to cope with the damage. The paradigm is the SOS response in E. coli. We conclude that there is compelling evidence that DNA‐damaging agents do affect gene expression, and that mutation frequencies are increased, but proof that a repair process per se is induced remains elusive. We offer here the hypothesis that recognition of the presence of DNA (...)
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  34.  38
    Stopped for repairs.Yolanda Sanchez & Stephen J. Elledge - 1995 - Bioessays 17 (6):545-548.
    The tumor suppressor protein p53 is intimately involved in the cellular response to DNA damage, controlling cell cycle arrest, apoptosis and the transcriptional induction of DNA damage inducible genes. A transcriptional target of p53, Gadd45, was recently found to bind to PCNA, a component of DNA replication/repair complexes, thereby implicating Gadd45 in DNA metabolism(1). Using biochemical assays, a role for Gadd45 in excision repair in vitro has been demonstrated(1). Antisense experiments have also indicated an in vivo (...)
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  35.  30
    Recombinational DNA repair: the ignored repair systems.Kendric C. Smith - 2004 - Bioessays 26 (12):1322-1326.
    The recent finding of a role for the recA gene in DNA replication restart does not negate previous data showing the existence of recA‐dependent recombinational DNA repair, which occurs when there are two DNA duplexes present, as in the case for recA‐dependent excision repair, for postreplication repair (i.e., the repair of DNA daughter‐strand gaps), and for the repair of DNA double‐strand breaks. Recombinational DNA repair is critical for the survival of damaged cells. BioEssays 26:1322–1326, (...)
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  36.  18
    Post‐replication repair in DT40 cells: translesion polymerases versus recombinases.Helfrid Hochegger, Eichiro Sonoda & Shunichi Takeda - 2004 - Bioessays 26 (2):151-158.
    Replication forks inevitably stall at damaged DNA in every cell cycle. The ability to overcome DNA lesions is an essential feature of the replication machinery. A variety of specialized polymerases have recently been discovered, which enable cells to replicate past various forms of damage by a process termed translesion synthesis. Alternatively, homologous recombination can be used to restart DNA replication across the lesion. Genetic and biochemical studies have shed light on the impact of these two post‐replication repair pathways (...)
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  37.  18
    On‐site remodeling at chromatin: How multiprotein complexes are rebuilt during DNA repair and transcriptional activation.Thaleia Papadopoulou & Holger Richly - 2016 - Bioessays 38 (11):1130-1140.
    In this review, we discuss a novel on‐site remodeling function that is mediated by the H2A‐ubiquitin binding protein ZRF1. ZRF1 facilitates the remodeling of multiprotein complexes at chromatin and lies at the heart of signaling processes that occur at DNA damage sites and during transcriptional activation. In nucleotide excision repair ZRF1 remodels E3 ubiquitin ligase complexes at the damage site. During embryonic stem cell differentiation, it contributes to retinoic acid‐mediated gene activation by altering the subunit composition of (...)
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  38.  27
    Ecologies of Repair: A Post-human Approach to Other-Than-Human Natures.Gustavo Blanco-Wells - 2021 - Frontiers in Psychology 12.
    This conceptual paper explores the theoretical possibilities of posthumanism and presents ecologies of repair as a heuristic device to explore the association modes of different entities, which, when confronted with the effects of human-induced destructive events, seek to repair the damage and transform the conditions of coexistence of various life forms. The central idea is that severe socio-environmental crisis caused by an intensification of industrial activity are conducive to observing new sociomaterial configurations and affective dispositions that, through (...)
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  39.  24
    Genes controlling nucleotide excision repair in eukaryotic cells.Geert Weeda, Jan H. J. Hoeijmakers & Dirk Bootsma - 1993 - Bioessays 15 (4):249-258.
    The maintenance of genetic integrity is of vital importance to all living organisms. However, DNA – the carrier of genetic information – is continuously subject to damage induced by numerous agents from the environment and endogenous cellular metabolites. To prevent the deleterious consequences of DNA injury, an intricate network of repair systems has evolved. The biological impact of these repair mechanisms is illustrated by a number of genetic diseases that are characterized by a defect in one of (...)
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  40.  28
    Cell Fate Regulation upon DNA Damage: p53 Serine 46 Kinases Pave the Cell Death Road.Magdalena C. Liebl & Thomas G. Hofmann - 2019 - Bioessays 41 (12):1900127.
    Mild and massive DNA damage are differentially integrated into the cellular signaling networks and, in consequence, provoke different cell fate decisions. After mild damage, the tumor suppressor p53 directs the cellular response to cell cycle arrest, DNA repair, and cell survival, whereas upon severe damage, p53 drives the cell death response. One posttranslational modification of p53, phosphorylation at Serine 46, selectively occurs after severe DNA damage and is envisioned as a marker of the cell death (...)
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  41.  25
    Joining the PARty: PARP Regulation of KDM5A during DNA Repair (and Transcription?).Anthony Sanchez, Bethany A. Buck-Koehntop & Kyle M. Miller - 2022 - Bioessays 44 (7):2200015.
    The lysine demethylase KDM5A collaborates with PARP1 and the histone variant macroH2A1.2 to modulate chromatin to promote DNA repair. Indeed, KDM5A engages poly(ADP‐ribose) (PAR) chains at damage sites through a previously uncharacterized coiled‐coil domain, a novel binding mode for PAR interactions. While KDM5A is a well‐known transcriptional regulator, its function in DNA repair is only now emerging. Here we review the molecular mechanisms that regulate this PARP1‐macroH2A1.2‐KDM5A axis in DNA damage and consider the potential involvement of (...)
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  42.  66
    Meiotic versus mitotic recombination: Two different routes for double‐strand break repair.Sabrina L. Andersen & Jeff Sekelsky - 2010 - Bioessays 32 (12):1058-1066.
    Studies in the yeast Saccharomyces cerevisiae have validated the major features of the double‐strand break repair (DSBR) model as an accurate representation of the pathway through which meiotic crossovers (COs) are produced. This success has led to this model being invoked to explain double‐strand break (DSB) repair in other contexts. However, most non‐crossover (NCO) recombinants generated during S. cerevisiae meiosis do not arise via a DSBR pathway. Furthermore, it is becoming increasingly clear that DSBR is a minor pathway (...)
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  43.  8
    The DNA Damage Response in Telophase: Challenging Dogmas.Matthew K. Summers - 2020 - Bioessays 42 (7):2000085.
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  44.  21
    The evolution of meiosis: Recruitment and modification of somatic DNA-repair proteins.Edyta Marcon & Peter B. Moens - 2005 - Bioessays 27 (8):795-808.
    Several DNA-damage detection and repair mechanisms have evolved to repair double-strand breaks induced by mutagens. Later in evolutionary history, DNA single- and double-strand cuts made possible immune diversity by V(D)J recombination and recombination at meiosis. Such cuts are induced endogenously and are highly regulated and controlled. In meiosis, DNA cuts are essential for the initiation of homologous recombination, and for the formation of joint molecule and crossovers. Many proteins that function during somatic DNA-damage detection and (...) are also active during homologous recombination. However, their meiotic functions may be altered from their somatic roles through localization, posttranslational modifications and/or interactions with meiosis-specific proteins. Presumably, somatic repair functions and meiotic recombination diverged during evolution, resulting in adaptations specific to sexual reproduction. BioEssays 27:795–808, 2005. © 2005 Wiley Periodicals, Inc. (shrink)
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  45.  24
    The RAD6 DNA repair pathway in Saccharomyces cerevisiae: What does it do, and how does it do it?Christopher Lawrence - 1994 - Bioessays 16 (4):253-258.
    The RAD6 pathway of budding yeast, Saccharomyces cerevisiae, is responsible for a substantial fraction of this organism's resistance to DNA damage, and also for induced mutagenesis. The pathway appears to incorporate two different recovery processes, both regulated by RAD6. The error‐prone recovery prcess accounts for only a small amount of RAD6‐dependent resistance, but probably all induced mutagenesis. The underlying mechanism, for error‐prone recovery is very likely to be translesion synthesis. The error‐free recovery process accounts for most of RAD6‐dependent resistace, (...)
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  46.  5
    Oxidative DNA damage, antioxidants, and cancer.Andrew R. Collins - 1999 - Bioessays 21 (3):238-246.
    Oxidised bases, such as 8-oxo-guanine, occur in cellular DNA as a result of attack by oxygen free radicals. The cancer-protective effect of vegetables and fruit is attributed to the ability of antioxidants in them to scavenge free radicals, preventing DNA damage and subsequent mutation. Antioxidant supplements (e.g., β-carotene, vitamin C) increase the resistance of lymphocytes to oxidative damage, and a negative correlation is seen between antioxidant concentrations in tissues and oxidised bases in DNA. Large-scale intervention trials with β-carotene (...)
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  47.  4
    Accessing DNA damage in chromatin: Insights from transcription.Maria Meijer & Michael J. Smerdon - 1999 - Bioessays 21 (7):596-603.
    Recently, there has been a convergence of fields studying the processing of DNA, such as transcription, replication, and repair. This convergence has been centered around the packaging of DNA in chromatin. Chromatin structure affects all aspects of DNA processing because it modulates access of proteins to DNA. Therefore, a central theme has become the mechanism(s) for accessing DNA in chromatin. It seems likely that mechanisms involved in one of these processes may also be used in others. For example, the (...)
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  48.  36
    A cellular survival switch: poly(ADP‐ribosyl)ation stimulates DNA repair and silences transcription.Mathias Ziegler & Shiao Li Oei - 2001 - Bioessays 23 (6):543-548.
    Poly(ADP‐ribosyl)ation is a post‐translational modification occurring in the nucleus. The most abundant and best‐characterized enzyme catalyzing this reaction, poly(ADP‐ribose) polymerase 1 (PARP1), participates in fundamental nuclear events. The enzyme functions as molecular “nick sensor”. It binds with high affinity to DNA single‐strand breaks resulting in the initiation of its catalytic activity. Activated PARP1 promotes base excision repair. In addition, PARP1 modifies several transcription factors and thereby precludes their binding to DNA. We propose that a major function of PARP1 includes (...)
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  49.  31
    Menage á trois: Double strand break repair, V(D)J recombination and DNA‐PK.Penny A. Jeggo, Guillermo E. Taccioli & Stephen P. Jackson - 1995 - Bioessays 17 (11):949-957.
    All organisms possess mechanisms to repair double strand breaks (dsbs) generated in their DNA by damaging agents. Site‐specific dsbs are also introduced during V(D)J recombination. Four complementation groups of radiosensitive rodent mutants are defective in the repair of dsbs, and are unable to carry out V(D)J recombination effectively. The immune defect in Severe Combined Immunodeficient (scid) mice also results from an inability to undergo effective V(D)J recombination, and scid cell lines display a repair defect and belong to (...)
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  50.  26
    Factors contributing to the outcome of oxidative damage to nucleic acids.Mark D. Evans & Marcus S. Cooke - 2004 - Bioessays 26 (5):533-542.
    Oxidative damage to DNA appears to be a factor in cancer, yet explanations for why highly elevated levels of such lesions do not always result in cancer remain elusive. Much of the genome is non‐coding and lesions in these regions might be expected to have little biological effect, an inference supported by observations that there is preferential repair of coding sequences. RNA has an important coding function in protein synthesis, and yet the consequences of RNA oxidation are largely (...)
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