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    Wyświetlanie 1-7 z 7
    Tytuł:
    Różne twarze naprawy DNA - Nobel 2015 w dziedzinie chemii
    Different faces of DNA repair - Nobel price 2015 in chemistry
    Autorzy:
    Tudek, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1034494.pdf
    Data publikacji:
    2016
    Wydawca:
    Polskie Towarzystwo Przyrodników im. Kopernika
    Tematy:
    Aziz Sancar
    naprawa DNA
    Nobel z chemii 2015
    Paul Modrich
    Thomas Lindahl
    Opis:
    W 2015 r. Nagroda Nobla w dziedzinie chemii została przyznana za badania mechanistyczne nad naprawą DNA Paulowi Modrichowi, Tomasowi Lindahlowi i Azizowi Sancarowi. Paul Modrich pracuje w Howard Hughes Medical Institute oraz Duke University School of Medicine, Durham, USA. Nagrodą zostały wyróżnione jego prace nad naprawą źle dopasowanych zasad, które powstają głównie podczas replikacji, zaś ten typ naprawy jest "pierwszą linią ochrony" stabilności genomu. Tomas Lindahl jest profesorem chemii medycznej i fizycznej, emerytowanym dyrektorem Cancer Research UK London Research Institute, Clare Hall Laboratories, South Mimms, Wielka Brytania. Nagrodę Nobla otrzymał za odkrycia w dziedzinie naprawy przez wycięcie zasady usuwającej z DNA niewielkie uszkodzenia, głównie oksydacyjne i alkilacyjne. Aziz Sancar jest profesorem biochemii i biofizyki na University of North Carolina School of Medicine, Chapel Hill, USA. Nagrodę Nobla otrzymał za osiągnięcia w dziedzinie naprawy przez wycięcie nukleotydu. System ten usuwa z DNA duże modyfikacje takie jak dimery pirymidynowe indukowane światłem ultrafioletowym. Badania uczonych stworzyły podwaliny pod zrozumienie mechanizmu ewolucji świata ożywionego, a także procesów nowotworowych i opracowanie nowoczesnych terapii.
    The Nobel Prize in chemistry for 2015 was awarded to Paul Modrich, Tomas Lindahl and Aziz Sancar for mechanistic studies on DNA repair. Paul Modrich works in Howard Hughes Medical Institute and Duke University School of Medicine, Durham, USA. The prize has been awarded for his work on Mismatch Repair, which removes mismatched nucleotides formed mainly during replication and is the "first line of defense" of genome stability. Tomas Lindahl is a professor of medical and physical chemistry, emeritus director of Cancer Research UK London Research Institute, Clare Hall Laboratories, South Mimms, United Kingdom. The Nobel Prize was awarded to him for discoveries on Base Excision Repair, which removes from the DNA small lesions, mainly alkylated and oxidatively formed damages. Aziz Sancar is a professor in biochemistry and biophysics at University of North Carolina School of Medicine, Chapel Hill, USA. He was awarded for the achievements on Nucleotide Excision Repair. The system removes from the DNA big lesions, such as pyrimidine dimers induced by ultraviolet light. Studies of these researchers made a basis for understanding of the evolution of living world as well as carcinogenic process and for elaboration of novel therapies.
    Źródło:
    Kosmos; 2016, 65, 3; 309-322
    0023-4249
    Pojawia się w:
    Kosmos
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells
    Autorzy:
    Maddukuri, Leena
    Dudzińska, Dominika
    Tudek, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1040922.pdf
    Data publikacji:
    2007
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    trichothiodystrophy
    Cockayne syndrome
    xeroderma pigmentosum
    DNA damage
    DNA repair
    nucleotide excision repair
    Opis:
    The eukaryotic cell encounters more than one million various kinds of DNA lesions per day. The nucleotide excision repair (NER) pathway is one of the most important repair mechanisms that removes a wide spectrum of different DNA lesions. NER operates through two sub pathways: global genome repair (GGR) and transcription-coupled repair (TCR). GGR repairs the DNA damage throughout the entire genome and is initiated by the HR23B/XPC complex, while the CSB protein-governed TCR process removes DNA lesions from the actively transcribed strand. The sequence of events and the role of particular NER proteins are currently being extensively discussed. NER proteins also participate in other cellular processes like replication, transcription, chromatin maintenance and protein turnover. Defects in NER underlay severe genetic disorders: xeroderma pigmentosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD).
    Źródło:
    Acta Biochimica Polonica; 2007, 54, 3; 469-482
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli
    Autorzy:
    Kowalczyk, Paweł
    Cieśla, Jarosław
    Saparbaev, Murat
    Laval, Jacques
    Tudek, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1041247.pdf
    Data publikacji:
    2006
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    chloroacetaldehyde
    p53
    replication
    exocyclic DNA adducts
    vinyl chloride
    LM-PCR
    DNA repair
    sequence-specific DNA damage
    Opis:
    Oxidative stress and certain environmental carcinogens, e.g. vinyl chloride and its metabolite chloroacetaldehyde (CAA), introduce promutagenic exocyclic adducts into DNA, among them 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC) and N2,3-ethenoguanine (εG). We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity. CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots. These perturbations inhibited DNA synthesis on undamaged template. We also studied the repair kinetics of CAA-induced DNA lesions in E. coli at nucleotide resolution level. A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5α strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent. Following transformation, plasmids were re-isolated from transformed cultures 35, 40, 50 min and 1-24 h after transformation, and further subjected to LM-PCR, using ANPG, MUG and Fpg glycosylases to identify the sites of DNA damage. In adaptive response-induced E. coli cells the majority of DNA lesions recognized by ANPG glycosylase were removed from plasmid DNA within 35 min, while MUG glycosylase excised base modifications only within 50 min, both in a sequence-dependent manner. In non-adapted cells resolution of plasmid topological forms was perturbed, suggesting inhibition of one or more bacterial topoisomerases by unrepaired ε-adducts. We also observed delayed consequences of DNA modification with CAA, manifesting as secondary DNA breaks, which appeared 3 h after transformation of damaged DNA into E. coli, and were repaired after 24 h.
    Źródło:
    Acta Biochimica Polonica; 2006, 53, 2; 337-347
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Mutagenic specificity of imidazole ring-opened 7-methylpurines in m13mp18 phage DNA
    Autorzy:
    Tudek, Barbara
    Grąziewicz, Marianna
    Kazanova, Olga
    Zastawny, Tomasz
    Obtułowicz, Tomasz
    Laval, Jacques
    Powiązania:
    https://bibliotekanauki.pl/articles/1044492.pdf
    Data publikacji:
    1999
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Źródło:
    Acta Biochimica Polonica; 1999, 46, 3; 785-799
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Inhibition of DNA repair glycosylases by base analogs and tryptophan pyrolysate, Trp-P-1.
    Autorzy:
    Speina, Elżbieta
    Cieśla, Jarosław
    Grąziewicz, Maria-Anna
    Laval, Jacques
    Kazimierczuk, Zygmunt
    Tudek, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1041475.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    base analogs
    Trp-P-1
    DNA repair enzymes
    inhibitors
    formamidopyrimidine DNA glycosylase
    Opis:
    DNA base analogs, 2,4,5,6-substituted pyrimidines and 2,6-substituted purines were tested as potential inhibitors of E. coli Fpg protein (formamidopyrimidine -DNA glycosylase). Three of the seventeen compounds tested revealed inhibitory properties. 2-Thioxanthine was the most efficient, inhibiting 50% of 2,6-diamino-4-hydroxy-5N-methyl-formamidopyrimidine (Fapy-7MeG) excision activity at 17.1 μM concentration. The measured Kgi was 4.44 ± 0.15 μM. Inhibition was observed only when the Fpg protein was first challenged to its substrate followed by the addition of the base analog, suggesting uncompetitive (catalytic) inhibition. For two other compounds, 2-thio- or 2-oxo-4,5,6-substituted pyrimidines, IC50 was only 343.3 ± 58.6 and 350 ± 24.4 μM, respectively. No change of the Fpg glycosylase activity was detected in the presence of Fapy-7MeG, up to 5 μM. We also investigated the effect of DNA structure modified by tryptophan pyrolysate (Trp-P-1) on the activity of base excision repair enzymes: Escherichia coli and human DNA glycosylases of oxidized (Fpg, Nth) and alkylated bases (TagA, AlkA, and ANPG), and for bacterial AP endonuclease (Xth protein). Trp-P-1, which changes the secondary DNA structure into non-B, non-Z most efficiently inhibited excision of alkylated bases by the AlkA glycosylase (IC50 = 1 μM). The ANPG, TagA, and Fpg proteins were also inhibited although to a lesser extent (IC50 = 76.5 μM, 96 μM, and 187.5 μM, respectively). Trp-P-1 also inhibited incision of DNA at abasic sites by the β-lyase activity of the Fpg and Nth proteins, and to a lesser extent by the Xth AP endonuclease. Thus, DNA conformation is critical for excision of damaged bases and incision of abasic sites by DNA repair enzymes.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 1; 167-178
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Oxidative damage to DNA and antioxidant status in aging and age-related diseases
    Autorzy:
    Olinski, Ryszard
    Siomek, Agnieszka
    Rozalski, Rafal
    Gackowski, Daniel
    Foksinski, Marek
    Guz, Jolanta
    Dziaman, Tomasz
    Szpila, Anna
    Tudek, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1041102.pdf
    Data publikacji:
    2007
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    ROS
    aging
    oxidative DNA damage
    age-related diseases
    BER
    GO system
    Opis:
    Aging is a complex process involving morphologic and biochemical changes in single cells and in the whole organism. One of the most popular explanations of how aging occurs at the molecular level is the oxidative stress hypothesis. Oxidative stress leads in many cases to an age-dependent increase in the cellular level of oxidatively modified macromolecules including DNA, and it is this increase which has been linked to various pathological conditions, such as aging, carcinogenesis, neurodegenerative and cardiovascular diseases. It is, however, possible that a number of short-comings associated with gaps in our knowledge may be responsible for the failure to produce definite results when applied to understanding the role of DNA damage in aging and age-related diseases.
    Źródło:
    Acta Biochimica Polonica; 2007, 54, 1; 11-26
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-7 z 7

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