Materials Map

Discover the materials research landscape. Find experts, partners, networks.

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The Materials Map is an open tool for improving networking and interdisciplinary exchange within materials research. It enables cross-database search for cooperation and network partners and discovering of the research landscape.

The dashboard provides detailed information about the selected scientist, e.g. publications. The dashboard can be filtered and shows the relationship to co-authors in different diagrams. In addition, a link is provided to find contact information.

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The Materials Map is still under development. In its current state, it is only based on one single data source and, thus, incomplete and contains duplicates. We are working on incorporating new open data sources like ORCID to improve the quality and the timeliness of our data. We will update Materials Map as soon as possible and kindly ask for your patience.

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in Cooperation with on an Cooperation-Score of 37%

Topics

Publications (1/1 displayed)

  • 2011Involvement of SLX4 in interstrand cross-link repair is regulated by the Fanconi anemia pathway180citations

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Hirota, Kouji
1 / 1 shared
Takeda, Shunichi
1 / 1 shared
Kobayashi, Shunsuke
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Kono, Koichi
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Takata, Minoru
1 / 1 shared
Kurumizaka, Hitoshi
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Yamamoto, Kimiyo N.
1 / 1 shared
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2011

Co-Authors (by relevance)

  • Hirota, Kouji
  • Takeda, Shunichi
  • Kobayashi, Shunsuke
  • Kono, Koichi
  • Takata, Minoru
  • Kurumizaka, Hitoshi
  • Yamamoto, Kimiyo N.
OrganizationsLocationPeople

article

Involvement of SLX4 in interstrand cross-link repair is regulated by the Fanconi anemia pathway

  • Hirota, Kouji
  • Takeda, Shunichi
  • Jiricny, Josef
  • Kobayashi, Shunsuke
  • Kono, Koichi
  • Takata, Minoru
  • Kurumizaka, Hitoshi
  • Yamamoto, Kimiyo N.
Abstract

<jats:p>Interstrand cross-links (ICLs) block replication and transcription and thus are highly cytotoxic. In higher eukaryotes, ICLs processing involves the Fanconi anemia (FA) pathway and homologous recombination. Stalled replication forks activate the eight-subunit FA core complex, which ubiquitylates FANCD2-FANCI. Once it is posttranslationally modified, this heterodimer recruits downstream members of the ICL repairosome, including the FAN1 nuclease. However, ICL processing has been shown to also involve MUS81-EME1 and XPF-ERCC1, nucleases known to interact with SLX4, a docking protein that also can bind another nuclease, SLX1. To investigate the role of SLX4 more closely, we disrupted the<jats:italic>SLX4</jats:italic>gene in avian DT40 cells. SLX4 deficiency caused cell death associated with extensive chromosomal aberrations, including a significant fraction of isochromatid-type breaks, with sister chromatids broken at the same site. SLX4 thus appears to play an essential role in cell proliferation, probably by promoting the resolution of interchromatid homologous recombination intermediates. Because ubiquitylation plays a key role in the FA pathway, and because the N-terminal region of SLX4 contains a ubiquitin-binding zinc finger (UBZ) domain, we asked whether this domain is required for ICL processing. We found that<jats:italic>SLX4</jats:italic><jats:sup>−/−</jats:sup>cells expressing UBZ-deficient SLX4 were selectively sensitive to ICL-inducing agents, and that the UBZ domain was required for interaction of SLX4 with ubiquitylated FANCD2 and for its recruitment to DNA-damage foci generated by ICL-inducing agents. Our findings thus suggest that ubiquitylated FANCD2 recruits SLX4 to DNA damage sites, where it mediates the resolution of recombination intermediates generated during the processing of ICLs.</jats:p>

Topics
  • impedance spectroscopy
  • zinc