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  1. AU="Comai, Lucio"
  2. AU="Carey K. Anders, MD"
  3. AU="Miyamoto, Tomomi"
  4. AU="Vierling, John M"
  5. AU="Carlson, Elijah L"
  6. AU="El Kamouni, Soufiane"
  7. AU="Ishisaka, Takuya"
  8. AU="Gábor Bedics"
  9. AU=Nipp Ryan D.
  10. AU="Lucero, D E"
  11. AU="Isik, C"
  12. AU="Lange, Lana"
  13. AU="Morris, Ray"
  14. AU="Sun, Xiankai"
  15. AU=Jeggo Penny A.
  16. AU="Kanthamneni, Naveen"
  17. AU="Di Lorenzo, Raffaele"
  18. AU="Tiraboschi, Juan M"
  19. AU="Xiang, Jinzhu"
  20. AU="Diehl, Kyra"
  21. AU="Aparicio-Yuste, Raul"
  22. AU="Jiang, Gengbo"
  23. AU=Murrell Dedee F AU=Murrell Dedee F
  24. AU=Gupta Riya
  25. AU="Elmasry, Dalia M A" AU="Elmasry, Dalia M A"
  26. AU=Rosa Rafael Fabiano Machado
  27. AU="Bhatia, Vishwas"
  28. AU="Buchwitz, Michael"
  29. AU="Sadrozinski, H-F W."
  30. AU="Allan, Rachel"
  31. AU="Ma, Jiele"
  32. AU="Bizjak, Isabella"
  33. AU="Pelucchi, Paride"
  34. AU="Krug, Anne Barbara"
  35. AU="Pikridas, M"
  36. AU="Adams, Jonathan D"
  37. AU="Esquivel-Muelbert, A."
  38. AU="Khan, Meraj Alam"
  39. AU="Bullard, Stevan"
  40. AU="Wang, Peter H"
  41. AU="Preto, Jordane"
  42. AU="Pierce, Shaketha"
  43. AU="Sankar, Jishnu"
  44. AU="Yahagi, Naohisa"
  45. AU=Pinho Juliana
  46. AU="Brennan, Anna"
  47. AU="Lee, Theresa M"
  48. AU="Chunqing Ou"
  49. AU="Gwynn, Simon"
  50. AU="Holper, Sarah"
  51. AU="Haider, Farag Ibrahim"
  52. AU="Rice, Jordin L"
  53. AU="Gong, Xingguo"
  54. AU=Rother Magdalena B.
  55. AU="Petrov, Ksenia"
  56. AU="Rijneveld, R"
  57. AU=Lopez-Martinez Briceida
  58. AU=Astone Pia
  59. AU="Amaral, V"

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Treffer 1 - 10 von insgesamt 55

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  1. Buch: Proteomics

    Comai, Lucio / Katz, Jonathan / Mallick, Parag

    methods and protocols

    (Methods in molecular biology ; 1550 ; Springer protocols)

    2017  

    Serientitel Methods in molecular biology ; 1550
    Springer protocols
    Überordnung
    Schlagwörter biochemical techniques ; biological specimen ; mass spectrometers ; proteins ; proteomic analysis
    Sprache Englisch
    Umfang XII, 371 S. : Ill., graph. Darst., 25.4 cm x 17.8 cm, 0 g
    Verlag Humana Press
    Erscheinungsort New York, NY
    Erscheinungsland Vereinigte Staaten
    Dokumenttyp Buch
    HBZ-ID HT019203009
    ISBN 978-1-4939-6745-2 ; 1-4939-6745-2 ; 9781493967476 ; 1493967479
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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    Zs A 7042 -1550- verfügbar in Königswinter Königswinter

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  2. Artikel ; Online: Differential Outcomes of Infection by Wild-Type SARS-CoV-2 and the B.1.617.2 and B.1.1.529 Variants of Concern in K18-hACE2 Transgenic Mice.

    He, Yicheng / Henley, Jill / Sell, Philip / Comai, Lucio

    Viruses

    2023  Band 16, Heft 1

    Abstract: Background: SARS-CoV-2 is a respiratory virus with neurological complications including the loss of smell and taste, headache, and confusion that can persist for months or longer. Severe neuronal cell damage has also been reported in some cases. The ... ...

    Abstract Background: SARS-CoV-2 is a respiratory virus with neurological complications including the loss of smell and taste, headache, and confusion that can persist for months or longer. Severe neuronal cell damage has also been reported in some cases. The objective of this study was to compare the infectivity of the wild-type virus, Delta (B.1.617.2) and Omicron (B.1.1.529) variants in transgenic mice that express the human angiotensin-converting enzyme 2 (hACE2) receptor under the control of the keratin 18 promoter (K18) and characterize the progression of infection and inflammatory response in the lungs, brain, medulla oblongata, and olfactory bulbs of these animals. We hypothesized that wild type, Delta and Omicron differentially infect K18-hACE2 mice, thereby inducing distinct cellular responses.
    Methods: K18-hACE2 female mice were intranasally infected with wild-type, Delta, or Omicron variants and euthanized either at 3 days post-infection (dpi) or at the humane endpoint. None of the animals infected with the Omicron variant reached the humane endpoint and were euthanized at day 8 dpi. Virological and immunological analyses were performed in the lungs, brains, medulla oblongata and olfactory bulbs isolated from infected mice.
    Results: At 3 dpi, mice infected with wild type and Delta displayed significantly higher levels of viral RNA in the lungs than mice infected with Omicron, while in the brain, Delta and Omicron resulted in higher levels of viral RNA than with the wild type. Viral RNA was also detected in the medulla oblongata of mice infected by all these virus strains. At this time point, the mice infected with wild type and Delta displayed a marked upregulation of many inflammatory markers in the lungs. On the other hand, the upregulation of inflammatory markers was observed only in the brains of mice infected with Delta and Omicron. At the humane endpoint, we observed a significant increase in the levels of viral RNA in the lungs and brains of mice infected with wild type and Delta, which was accompanied by the elevated expression of many inflammatory markers. In contrast, mice which survived infection with the Omicron variant showed high levels of viral RNA and the upregulation of cytokine and chemokine expression only in the lungs at 8 dpi, suggesting that infection and inflammatory response by this variant is attenuated in the brain. Reduced RNA levels and the downregulation of inflammatory markers was also observed in the medulla oblongata and olfactory bulbs of mice infected with Omicron at 8 dpi as compared with mice infected with wild-type and Delta at the humane end point. Collectively, these data demonstrate that wild-type, Delta, and Omicron SARS-CoV-2 induce distinct levels of infection and inflammatory responses in K18-hACE2 mice. Notably, sustained brain infection accompanied by the upregulation of inflammatory markers is a critical outcome in mice infected with wild type and Delta but not Omicron.
    Mesh-Begriff(e) Animals ; Female ; Humans ; Mice ; Angiotensin-Converting Enzyme 2/genetics ; COVID-19/pathology ; Keratin-18 ; Mice, Transgenic ; RNA, Viral/genetics ; SARS-CoV-2/genetics
    Chemische Substanzen Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Keratin-18 ; RNA, Viral
    Sprache Englisch
    Erscheinungsdatum 2023-12-29
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v16010060
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Brain infection by wild-type SARS-CoV-2 and the B.1.617.2 and B.1.1.529 variants of concern is a severe outcome in K18-hACE2 transgenic mice

    Yicheng He, Yicheng / Henley, Jill E / Sell, Philip / Comai, Lucio

    bioRxiv

    Abstract: Background: SARS-CoV-2 is a respiratory virus with neurological complications including loss of smell and taste, headache, and confusion that can persist for months or longer. Severe neuronal cell damage has also been reported in some cases. The ... ...

    Abstract Background: SARS-CoV-2 is a respiratory virus with neurological complications including loss of smell and taste, headache, and confusion that can persist for months or longer. Severe neuronal cell damage has also been reported in some cases. The objective of this study was to compare the infectivity of Wild-type, Delta, and Omicron variants in transgenic mice that express the human angiotensin-converting enzyme 2 (hACE2) receptor under the control of the keratin 18 promoter (K18) and characterize the progression of infection and inflammatory response in the lung and brain of these animals. Methods: K18-hACE2 female mice were intranasally infected with Wild-type, Delta, or Omicron variants and euthanized either at 3 days post-infection (dpi) or at the humane endpoint. None of the animals infected with the Omicron variant reached the humane endpoint and were euthanized at day 8 dpi. Virological and immunological analyses were performed in the lungs, olfactory bulbs, medulla oblongata, and brains. Results: We established that Wild-type, Delta, and Omicron infect the lung and brain of K18-hACE2 mice. At 3 dpi, mice infected with the Omicron variant show lower levels of viral RNA than those infected with Wild-type or Delta in the lung and brain. However, they still demonstrate upregulation of cytokines and chemokines, indicating that the Omicron variant can induce pulmonary and neuronal inflammation despite reduced viral proliferation after infection. At the humane endpoint/8dpi, there is a significant increase in viral RNA in mice infected with the Wild-type or Delta variant brains. However, viral RNA levels in Omicron-infected mice did not increase significantly as compared to 3dpi, and the expression of cytokines and chemokines in the brain, olfactory bulb, and medulla oblongata was downregulated, suggesting that infection by the Omicron variant results in attenuated neuroinflammation as compared with Wild-type and Delta.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2023-09-11
    Verlag Cold Spring Harbor Laboratory
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2023.09.08.556906
    Datenquelle COVID19

    Volltext online

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  4. Artikel ; Online: Measurements of Hydrogen Peroxide and Oxidative DNA Damage in a Cell Model of Premature Aging.

    Iglesias-Pedraz, Juan Manuel / Comai, Lucio

    Methods in molecular biology (Clifton, N.J.)

    2020  Band 2144, Seite(n) 245–257

    Abstract: Reactive oxygen species (ROS) represent a number of highly reactive oxygen-derived by-products generated by the normal mitochondrial respiration and other cellular metabolic reactions. ROS can oxidize macromolecules including lipids, proteins, and ... ...

    Abstract Reactive oxygen species (ROS) represent a number of highly reactive oxygen-derived by-products generated by the normal mitochondrial respiration and other cellular metabolic reactions. ROS can oxidize macromolecules including lipids, proteins, and nucleic acids. Under physiological condition, the cellular levels of ROS are controlled by several antioxidant enzymes. However, an imbalance between ROS production and detoxification results in oxidative stress, which leads to the accumulation of macromolecular damage and progressive decline in normal physiological functions.Oxidative deterioration of DNA can result in lesion that are mutagenic and contribute to aging and age-related diseases. Therefore, methods for the detection of ROS and oxidative deterioration of macromolecules such as DNA in cells provide important tool in aging research. Here, we described protocols for the detection of cytoplasmic and mitochondria pools of hydrogen peroxide, and the DNA modification 8-oxoguanine, a biomarker of oxidative damage, that are applicable to cell-based studies on aging and other related areas.
    Mesh-Begriff(e) Aging/genetics ; Aging, Premature/genetics ; Aging, Premature/pathology ; Animals ; Antioxidants/metabolism ; DNA Damage/genetics ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Humans ; Hydrogen Peroxide/isolation & purification ; Hydrogen Peroxide/metabolism ; Mice ; Mitochondria ; Mutagenesis/genetics ; Mutation/genetics ; Oxidation-Reduction ; Oxidative Stress/genetics ; Reactive Oxygen Species/metabolism
    Chemische Substanzen Antioxidants ; DNA, Mitochondrial ; Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V)
    Sprache Englisch
    Erscheinungsdatum 2020-05-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-0592-9_22
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A GABA-receptor agonist reduces pneumonitis severity, viral load, and death rate in SARS-CoV-2-infected mice.

    Tian, Jide / Dillion, Barbara J / Henley, Jill / Comai, Lucio / Kaufman, Daniel L

    Frontiers in immunology

    2022  Band 13, Seite(n) 1007955

    Abstract: Gamma-aminobutyric acid (GABA) and GABA-receptors (GABA-Rs) form a major neurotransmitter system in the brain. GABA-Rs are also expressed by 1) cells of the innate and adaptive immune system and act to inhibit their inflammatory activities, and 2) lung ... ...

    Abstract Gamma-aminobutyric acid (GABA) and GABA-receptors (GABA-Rs) form a major neurotransmitter system in the brain. GABA-Rs are also expressed by 1) cells of the innate and adaptive immune system and act to inhibit their inflammatory activities, and 2) lung epithelial cells and GABA-R agonists/potentiators have been observed to limit acute lung injuries. These biological properties suggest that GABA-R agonists may have potential for treating COVID-19. We previously reported that GABA-R agonist treatments protected mice from severe disease induced by infection with a lethal mouse coronavirus (MHV-1). Because MHV-1 targets different cellular receptors and is biologically distinct from SARS-CoV-2, we sought to test GABA therapy in K18-hACE2 mice which develop severe pneumonitis with high lethality following SARS-CoV-2 infection. We observed that GABA treatment initiated immediately after SARS-CoV-2 infection, or 2 days later near the peak of lung viral load, reduced pneumonitis severity and death rates in K18-hACE2 mice. GABA-treated mice had reduced lung viral loads and displayed shifts in their serum cytokine/chemokine levels that are associated with better outcomes in COVID-19 patients. Thus, GABA-R activation had multiple effects that are also desirable for the treatment of COVID-19. The protective effects of GABA against two very different beta coronaviruses (SARS-CoV-2 and MHV-1) suggest that it may provide a generalizable off-the-shelf therapy to help treat diseases induced by new SARS-CoV-2 variants and novel coronaviruses that evade immune responses and antiviral medications. GABA is inexpensive, safe for human use, and stable at room temperature, making it an attractive candidate for testing in clinical trials. We also discuss the potential of GABA-R agonists for limiting COVID-19-associated neuroinflammation.
    Mesh-Begriff(e) Mice ; Humans ; Animals ; SARS-CoV-2 ; Viral Load ; COVID-19/drug therapy ; Pneumonia ; gamma-Aminobutyric Acid
    Chemische Substanzen K-18 conjugate ; gamma-Aminobutyric Acid (56-12-2)
    Sprache Englisch
    Erscheinungsdatum 2022-10-25
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1007955
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Impedimetric Sensing: An Emerging Tool for Combating the COVID-19 Pandemic.

    Ong, Victor / Soleimani, Ali / Amirghasemi, Farbod / Khazaee Nejad, Sina / Abdelmonem, Mona / Razaviyayn, Meisam / Hosseinzadeh, Parisa / Comai, Lucio / Mousavi, Maral P S

    Biosensors

    2023  Band 13, Heft 2

    Abstract: The COVID-19 pandemic revealed a pressing need for the development of sensitive and low-cost point-of-care sensors for disease diagnosis. The current standard of care for COVID-19 is quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). ...

    Abstract The COVID-19 pandemic revealed a pressing need for the development of sensitive and low-cost point-of-care sensors for disease diagnosis. The current standard of care for COVID-19 is quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). This method is sensitive, but takes time, effort, and requires specialized equipment and reagents to be performed correctly. This make it unsuitable for widespread, rapid testing and causes poor individual and policy decision-making. Rapid antigen tests (RATs) are a widely used alternative that provide results quickly but have low sensitivity and are prone to false negatives, particularly in cases with lower viral burden. Electrochemical sensors have shown much promise in filling this technology gap, and impedance spectroscopy specifically has exciting potential in rapid screening of COVID-19. Due to the data-rich nature of impedance measurements performed at different frequencies, this method lends itself to machine-leaning (ML) algorithms for further data processing. This review summarizes the current state of impedance spectroscopy-based point-of-care sensors for the detection of the SARS-CoV-2 virus. This article also suggests future directions to address the technology's current limitations to move forward in this current pandemic and prepare for future outbreaks.
    Mesh-Begriff(e) Humans ; COVID-19 ; SARS-CoV-2 ; Pandemics ; COVID-19 Testing ; Clinical Laboratory Techniques/methods ; Sensitivity and Specificity
    Sprache Englisch
    Erscheinungsdatum 2023-01-30
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2662125-3
    ISSN 2079-6374 ; 2079-6374
    ISSN (online) 2079-6374
    ISSN 2079-6374
    DOI 10.3390/bios13020204
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Mbnl2 loss alters novel context processing and impairs object recognition memory.

    Khandelwal, Abinash / Cushman, Jesse / Choi, Jongkyu / Zhuravka, Irina / Rajbhandari, Abha / Valiulahi, Parvin / Li, Xiandu / Zhou, Chenyu / Comai, Lucio / Reddy, Sita

    iScience

    2023  Band 26, Heft 5, Seite(n) 106732

    Abstract: Patients with myotonic dystrophy type I (DM1) demonstrate visuospatial dysfunction and impaired performance in tasks requiring recognition or memory of figures and objects. In DM1, CUG expansion RNAs inactivate the muscleblind-like (MBNL) proteins. We ... ...

    Abstract Patients with myotonic dystrophy type I (DM1) demonstrate visuospatial dysfunction and impaired performance in tasks requiring recognition or memory of figures and objects. In DM1, CUG expansion RNAs inactivate the muscleblind-like (MBNL) proteins. We show that constitutive Mbnl2 inactivation in
    Sprache Englisch
    Erscheinungsdatum 2023-04-25
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.106732
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  8. Artikel ; Online: GABA-receptors are a new druggable target for limiting disease severity, lung viral load, and death in SARS-CoV-2 infected mice

    Tian, Jide / Dillion, Barbara / Henley, Jill / Comai, Lucio / Kaufman, Daniel

    bioRxiv

    Abstract: GABA-receptors (GABA-Rs) are well-known neurotransmitter receptors in the central nervous system. GABA-Rs are also expressed by immune cells and lung epithelial cells and GABA-R agonists/potentiators reduce inflammatory immune cell activities and limit ... ...

    Abstract GABA-receptors (GABA-Rs) are well-known neurotransmitter receptors in the central nervous system. GABA-Rs are also expressed by immune cells and lung epithelial cells and GABA-R agonists/potentiators reduce inflammatory immune cell activities and limit acute lung injuries. Notably, plasma GABA levels are reduced in hospitalized COVID-19 patients. Hence, GABA-R agonists may have therapeutic potential for treating COVID-19. Here, we show that oral GABA treatment initiated just after SARS-CoV-2 infection, or 2 days later near the peak of lung viral load, reduced disease severity, lung coefficient index, and death rates in K18-hACE2 mice. GABA-treated mice had a reduced viral load in their lungs and displayed shifts in their serum cytokine and chemokine levels that are associated with better outcomes in COVID-19 patients. Thus, GABA-R activation had multiple beneficial effects in this mouse model which are also desirable for the treatment of COVID-19. A number of GABA-R agonists are safe for human use and can be readily tested in clinical trials with COVID-19 patients. We also discuss their potential for limiting COVID-19-associated neuroinflammation.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2022-06-07
    Verlag Cold Spring Harbor Laboratory
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2022.06.07.494579
    Datenquelle COVID19

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  9. Artikel: Recent advances in understanding the role of lamins in health and disease.

    Reddy, Sita / Comai, Lucio

    F1000Research

    2016  Band 5, Seite(n) 2536

    Abstract: Lamins are major components of the nuclear lamina, a network of proteins that supports the nuclear envelope in metazoan cells. Over the past decade, biochemical studies have provided support for the view that lamins are not passive bystanders providing ... ...

    Abstract Lamins are major components of the nuclear lamina, a network of proteins that supports the nuclear envelope in metazoan cells. Over the past decade, biochemical studies have provided support for the view that lamins are not passive bystanders providing mechanical stability to the nucleus but play an active role in the organization of the genome and the function of fundamental nuclear processes. It has also become apparent that lamins are critical for human health, as a large number of mutations identified in the gene that encodes for A-type lamins are associated with tissue-specific and systemic genetic diseases, including the accelerated aging disorder known as Hutchinson-Gilford progeria syndrome. Recent years have witnessed great advances in our understanding of the role of lamins in the nucleus and the functional consequences of disease-associated A-type lamin mutations. Many of these findings have been presented in comprehensive reviews. In this mini-review, we discuss recent breakthroughs in the role of lamins in health and disease and what lies ahead in lamin research.
    Sprache Englisch
    Erscheinungsdatum 2016
    Erscheinungsland England
    Dokumenttyp Review ; Journal Article
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.9260.1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: The Werner Syndrome Helicase Coordinates Sequential Strand Displacement and FEN1-Mediated Flap Cleavage during Polymerase δ Elongation

    Li, Baomin / Reddy, Sita / Comai, Lucio

    Molecular and Cellular Biology. 2017 Feb. 1, v. 37, no. 3 p.e00560-16-

    2017  

    Abstract: The Werner syndrome protein (WRN) suppresses the loss of telomeres replicated by lagging-strand synthesis by a yet to be defined mechanism. Here, we show that whereas either WRN or the Bloom syndrome helicase (BLM) stimulates DNA polymerase δ progression ...

    Abstract The Werner syndrome protein (WRN) suppresses the loss of telomeres replicated by lagging-strand synthesis by a yet to be defined mechanism. Here, we show that whereas either WRN or the Bloom syndrome helicase (BLM) stimulates DNA polymerase δ progression across telomeric G-rich repeats, only WRN promotes sequential strand displacement synthesis and FEN1 cleavage, a critical step in Okazaki fragment maturation, at these sequences. Helicase activity, as well as the conserved winged-helix (WH) motif and the helicase and RNase D C-terminal (HRDC) domain play important but distinct roles in this process. Remarkably, WRN also influences the formation of FEN1 cleavage products during strand displacement on a nontelomeric substrate, suggesting that WRN recruitment and cooperative interaction with FEN1 during lagging-strand synthesis may serve to regulate sequential strand displacement and flap cleavage at other genomic sites. These findings define a biochemical context for the physiological role of WRN in maintaining genetic stability.
    Schlagwörter DNA-directed DNA polymerase ; genetic stability ; genomics ; ribonucleases ; telomeres ; Werner syndrome ; DNA replication ; lagging-strand synthesis ; DNA helicase ; Okazaki fragment ; aging ; lagging strand
    Sprache Englisch
    Erscheinungsverlauf 2017-0201
    Erscheinungsort Taylor & Francis
    Dokumenttyp Artikel ; Online
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00560-16
    Datenquelle NAL Katalog (AGRICOLA)

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