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    The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair (Inhibition of BER by the HBV Protein X)

    van de Klundert, Maarten A. A, van Hemert, Formijn J, Zaaijer, Hans L, Kootstra, Neeltje A
    2012, Vol.7(11), p.e48940 [Peer Reviewed Journal]
    PLoS
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    Title: The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair (Inhibition of BER by the HBV Protein X)
    Author: van de Klundert, Maarten A. A; van Hemert, Formijn J; Zaaijer, Hans L; Kootstra, Neeltje A
    Contributor: Ahn, Sang-hoon (Editor)
    Subject: Research Article ; Biology ; Computer Science ; Medicine ; Infectious Diseases ; Molecular Biology ; Oncology ; Computer Science
    Description: The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other’s functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
    Is part of: 2012, Vol.7(11), p.e48940
    Identifier: 1932-6203 (E-ISSN); 10.1371/journal.pone.0048940 (DOI)

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    The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair

    Van De Klundert, Maarten A. A, Van Hemert, Formijn J, Zaaijer, Hans L, Kootstra, Neeltje A
    PLoS ONE, 2012, Vol.7(11) [Peer Reviewed Journal]
    U.S. National Library of Medicine (NIH/NLM)
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    Title: The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair
    Author: Van De Klundert, Maarten A. A; Van Hemert, Formijn J; Zaaijer, Hans L; Kootstra, Neeltje A
    Contributor: Ahn, Sang-Hoon (editor)
    Subject: Research Article ; Biology ; Computer Science ; Medicine
    Description: The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other’s functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
    Is part of: PLoS ONE, 2012, Vol.7(11)
    Identifier: 1932-6203 (E-ISSN); 10.1371/journal.pone.0048940 (DOI); 3493593 (PMCID); 23145031 (PMID)

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    The hepatitis B virus x protein inhibits thymine DNA glycosylase initiated base excision repair

    Van De Klundert, Maarten A A, Van Hemert, Formijn J, Zaaijer, Hans L, Kootstra, Neeltje A
    PloS one, 2012, Vol.7(11), pp.e48940 [Peer Reviewed Journal]
    MEDLINE/PubMed (U.S. National Library of Medicine)
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    More…
    Title: The hepatitis B virus x protein inhibits thymine DNA glycosylase initiated base excision repair
    Author: Van De Klundert, Maarten A A; Van Hemert, Formijn J; Zaaijer, Hans L; Kootstra, Neeltje A
    Subject: DNA Repair ; Thymine DNA Glycosylase -- Antagonists & Inhibitors ; Trans-Activators -- Genetics
    Description: The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other's functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
    Is part of: PloS one, 2012, Vol.7(11), pp.e48940
    Identifier: 1932-6203 (E-ISSN); 23145031 Version (PMID); 10.1371/journal.pone.0048940 (DOI)

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    The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair

    van Hemert, Formijn, Zaaijer, Hans, Kootstra, Neeltje
    PLoS One, Nov 2012, Vol.7(11), p.e48940 [Peer Reviewed Journal]
    © ProQuest LLC All rights reserved, Medical Database, Health & Medical Collection (Alumni edition), Medical Database (Alumni edition), Nursing & Allied Health Database (Alumni edition), ProQuest Pharma Collection, Health & Medical Collection, Nursing & Allied Health Database, ProQuest Agriculture Journals, Ecology Abstracts, Entomology Abstracts, Animal Behavior Abstracts, ProQuest Public Health, Materials Science Database, Advanced Technologies & Aerospace Database, Engineering Database, Biological Science Database, Publicly Available Content Database, Environmental Science Database (ProQuest), Engineering Research Database, Technology Research Database, ProQuest Nursing & Allied Health Source, ProQuest Agricultural Science Collection, ProQuest Atmospheric Science Collection, ProQuest Biological Science Collection, ProQuest Central, ProQuest Engineering Collection, ProQuest Environmental Science Collection, ProQuest Advanced Technologies & Aerospace Collection, ProQuest Hospital Collection, ProQuest Materials Science Collection, ProQuest Natural Science Collection, ProQuest Technology Collection, Hospital Premium Collection (Alumni edition), ProQuest SciTech Collection, ProQuest Health & Medical Complete, ProQuest Medical Library, Agricultural & Environmental Science Database, Earth, Atmospheric & Aquatic Science Database, Materials Science & Engineering Database, Natural Science Collection, ProQuest Central (new), ProQuest Central K-12, ProQuest Central Korea, SciTech Premium Collection, Technology Collection, Health Research Premium Collection, Health Research Premium Collection (Alumni edition), ProQuest Central Essentials, ProQuest One Academic, Environmental Science Index (ProQuest), Biological Science Index (ProQuest), Engineering Index (ProQuest), Environmental Science Collection (ProQuest), Materials Science Collection (ProQuest), Engineering Collection (ProQuest)
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    Title: The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair
    Author: van Hemert, Formijn; Zaaijer, Hans; Kootstra, Neeltje
    Subject: Netherlands ; Infections ; Laboratories ; Hepatitis B ; Replication ; Thymine ; Hepatitis ; Hbx Protein ; Genomes ; Mutation ; DNA Repair ; Immunology ; DNA Glycosylase ; Viruses ; Genomes ; Epigenetics ; Liver Cancer ; Penicillin ; Mutagenesis ; Rodents
    Description: The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other’s functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
    Is part of: PLoS One, Nov 2012, Vol.7(11), p.e48940
    Identifier: 19326203 (E-ISSN); 10.1371/journal.pone.0048940 (DOI)

    • Article
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    The hepatitis B virus x protein inhibits thymine DNA glycosylase initiated base excision repair

    Maarten A A van de Klundert, Formijn J van Hemert, Hans L Zaaijer, Neeltje A Kootstra
    PloS one, 01 January 2012, Vol.7(11), p.e48940 [Peer Reviewed Journal]
    Directory of Open Access Journals (DOAJ)
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    Title: The hepatitis B virus x protein inhibits thymine DNA glycosylase initiated base excision repair
    Author: Maarten A A van de Klundert; Formijn J van Hemert; Hans L Zaaijer; Neeltje A Kootstra
    Subject: Sciences (General)
    Description: The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other's functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
    Is part of: PloS one, 01 January 2012, Vol.7(11), p.e48940
    Identifier: 1932-6203 (E-ISSN); 10.1371/journal.pone.0048940 (DOI)