HDAC8 mutations in Cornelia de Lange syndrome affect the cohesin acetylation cycle View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-08-12

AUTHORS

Matthew A. Deardorff, Masashige Bando, Ryuichiro Nakato, Erwan Watrin, Takehiko Itoh, Masashi Minamino, Katsuya Saitoh, Makiko Komata, Yuki Katou, Dinah Clark, Kathryn E. Cole, Elfride De Baere, Christophe Decroos, Nataliya Di Donato, Sarah Ernst, Lauren J. Francey, Yolanda Gyftodimou, Kyotaro Hirashima, Melanie Hullings, Yuuichi Ishikawa, Christian Jaulin, Maninder Kaur, Tohru Kiyono, Patrick M. Lombardi, Laura Magnaghi-Jaulin, Geert R. Mortier, Naohito Nozaki, Michael B. Petersen, Hiroyuki Seimiya, Victoria M. Siu, Yutaka Suzuki, Kentaro Takagaki, Jonathan J. Wilde, Patrick J. Willems, Claude Prigent, Gabriele Gillessen-Kaesbach, David W. Christianson, Frank J. Kaiser, Laird G. Jackson, Toru Hirota, Ian D. Krantz, Katsuhiko Shirahige

ABSTRACT

The deacetylase enzyme HDAC8 is identified as a crucial regulator of cohesin in humans, and loss-of-function mutations in the HDAC8 gene are found in patients with Cornelia de Lange syndrome.

PAGES

313-317

Journal

TITLE

Nature

ISSUE

7415

VOLUME

489

Author Affiliations

  • The Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, 19104, Philadelphia, Pennsylvania, USA
  • Research Center for Epigenetic Disease, Institute for Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan
  • Centre National de la Recherche Scientifique (CNRS), Research Institute of Genetics and Development (IGDR), Faculté de Médecine, Rennes 35043, France
  • School and Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama 226-8503, Japan
  • Division of Human Genetics and Molecular Biology, The Children’s Hospital of Philadelphia, 19104, Pennsylvania, USA
  • Department of Chemistry, University of Pennsylvania, 19104, Philadelphia, Pennsylvania, USA
  • Center for Medical Genetics, Ghent University Hospital, 9000 Ghent, Belgium
  • Institut für Klinische Genetik, Technische Universität Dresden, 01307 Dresden, Germany
  • Department of Genetics, Institute of Child Health, 11527 Athens, Greece
  • Division of Molecular Biotherapy, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan
  • Department of Pathology, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan
  • Virology Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan
  • Department of Medical Genetics, Antwerp University Hospital and University of Antwerp, B-2650 Antwerp, Belgium
  • Bio-Frontier Research Center, Tokyo Institute of Technology, Yokohama 226-8503, Japan
  • Department of Clinical Genetics, Aalborg Hospital, Aarhus University Hospital, 9100 Aalborg, Denmark
  • Medical Genetics, University of Western Ontario, London, Ontario N6A 5W9, Canada
  • Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 277-8561, Japan
  • Experimental Pathology, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan
  • GENDIA, 2020 Antwerp, Belgium
  • Institut für Humangenetik Lübeck, Universität zu Lübeck, 23538 Lübeck, Germany
  • Department of Obstetrics and Gynecology, Drexel University School of Medicine, 19102, Philadelphia, Pennsylvania, USA
  • CREST, JST, K’s Gobancho, 7, Gobancho, Chiyoda-ku, Tokyo 102-0076, Japan
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature11316

    DOI

    http://dx.doi.org/10.1038/nature11316

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1002930651

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/22885700


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