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  1. Article ; Online: Histone Displacement during Nucleotide Excision Repair

    Jiri Bartek / Simon Bekker-Jensen / Christoffel Dinant

    International Journal of Molecular Sciences, Vol 13, Iss 10, Pp 13322-

    2012  Volume 13337

    Abstract: Nucleotide excision repair (NER) is an important DNA repair mechanism required for cellular resistance against UV light and toxic chemicals such as those found in tobacco smoke. In living cells, NER efficiently detects and removes DNA lesions within the ... ...

    Abstract Nucleotide excision repair (NER) is an important DNA repair mechanism required for cellular resistance against UV light and toxic chemicals such as those found in tobacco smoke. In living cells, NER efficiently detects and removes DNA lesions within the large nuclear macromolecular complex called chromatin. The condensed nature of chromatin inhibits many DNA metabolizing activities, including NER. In order to promote efficient repair, detection of a lesion not only has to activate the NER pathway but also chromatin remodeling. In general, such remodeling is thought on the one hand to precede NER, thus allowing repair proteins to efficiently access DNA. On the other hand, after completion of the repair, the chromatin must be returned to its previous undamaged state. Chromatin remodeling can refer to three separate but interconnected processes, histone post-translational modifications, insertion of histone variants and histone displacement (including nucleosome sliding). Here we review current knowledge, and speculate about current unknowns, regarding those chromatin remodeling activities that physically displace histones before, during and after NER.
    Keywords nucleotide excision repair ; histone chaperone ; ATP-dependent chromatin remodeling ; histone variants ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 572 ; 500
    Language English
    Publishing date 2012-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells

    Elisabeth Anne Adanma Obara / Diana Aguilar-Morante / Rikke Darling Rasmussen / Alex Frias / Kristoffer Vitting-Serup / Yi Chieh Lim / Kirstine Juul Elbæk / Henriette Pedersen / Lina Vardouli / Kamilla Ellermann Jensen / Jane Skjoth-Rasmussen / Jannick Brennum / Lucie Tuckova / Robert Strauss / Christoffel Dinant / Jiri Bartek / Petra Hamerlik

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 14

    Abstract: Cancer stem cells can evade treatment. Here, the authors perform an in vitro screen to identify proteins that are involved in protecting glioma cancer stem cells from therapy and find that SPT6 increases BRCA1 expression and drives error-free DNA repair, ...

    Abstract Cancer stem cells can evade treatment. Here, the authors perform an in vitro screen to identify proteins that are involved in protecting glioma cancer stem cells from therapy and find that SPT6 increases BRCA1 expression and drives error-free DNA repair, thereby ensuring the survival of the cells.
    Keywords Science ; Q
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection

    Ana López-Saavedra / Daniel Gómez-Cabello / María Salud Domínguez-Sánchez / Fernando Mejías-Navarro / María Jesús Fernández-Ávila / Christoffel Dinant / María Isabel Martínez-Macías / Jiri Bartek / Pablo Huertas

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 14

    Abstract: A DNA double strand break can be repaired through either the non-homologous end-joining or the homologous recombination pathways. Here the authors conduct a genome-wide screen and identify a role for CCAR2 in pathway choice by regulating DNA end ... ...

    Abstract A DNA double strand break can be repaired through either the non-homologous end-joining or the homologous recombination pathways. Here the authors conduct a genome-wide screen and identify a role for CCAR2 in pathway choice by regulating DNA end resection by CtIP.
    Keywords Science ; Q
    Language English
    Publishing date 2016-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Dynamic interaction of TTDA with TFIIH is stabilized by nucleotide excision repair in living cells.

    Giuseppina Giglia-Mari / Catherine Miquel / Arjan F Theil / Pierre-Olivier Mari / Deborah Hoogstraten / Jessica M Y Ng / Christoffel Dinant / Jan H J Hoeijmakers / Wim Vermeulen

    PLoS Biology, Vol 4, Iss 6, p e

    2006  Volume 156

    Abstract: Transcription/repair factor IIH (TFIIH) is essential for RNA polymerase II transcription and nucleotide excision repair (NER). This multi-subunit complex consists of ten polypeptides, including the recently identified small 8-kDa trichothiodystrophy ... ...

    Abstract Transcription/repair factor IIH (TFIIH) is essential for RNA polymerase II transcription and nucleotide excision repair (NER). This multi-subunit complex consists of ten polypeptides, including the recently identified small 8-kDa trichothiodystrophy group A (TTDA)/ hTFB5 protein. Patients belonging to the rare neurodevelopmental repair syndrome TTD-A carry inactivating mutations in the TTDA/hTFB5 gene. One of these mutations completely inactivates the protein, whereas other TFIIH genes only tolerate point mutations that do not compromise the essential role in transcription. Nevertheless, the severe NER-deficiency in TTD-A suggests that the TTDA protein is critical for repair. Using a fluorescently tagged and biologically active version of TTDA, we have investigated the involvement of TTDA in repair and transcription in living cells. Under non-challenging conditions, TTDA is present in two distinct kinetic pools: one bound to TFIIH, and a free fraction that shuttles between the cytoplasm and nucleus. After induction of NER-specific DNA lesions, the equilibrium between these two pools dramatically shifts towards a more stable association of TTDA to TFIIH. Modulating transcriptional activity in cells did not induce a similar shift in this equilibrium. Surprisingly, DNA conformations that only provoke an abortive-type of NER reaction do not result into a more stable incorporation of TTDA into TFIIH. These findings identify TTDA as the first TFIIH subunit with a primarily NER-dedicated role in vivo and indicate that its interaction with TFIIH reflects productive NER.
    Keywords Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2006-06-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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