Mechanism suppressing H3K9 trimethylation in pluripotent stem cells and its demise by polyQ-expanded huntingtin mutations

Author:

Irmak Dilber1,Fatima Azra1,Gutiérrez-Garcia Ricardo1,Rinschen Markus M1,Wagle Prerana1,Altmüller Janine23,Arrigoni Laura4,Hummel Barbara4,Klein Corinna1,Frese Christian K1,Sawarkar Ritwick4,Rada-Iglesias Alvaro12,Vilchez David1ORCID

Affiliation:

1. Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Strasse 26, Cologne, Germany

2. Center for Molecular Medicine Cologne (CMMC), University of Cologne, Robert-Koch-Strasse 21, Cologne, Germany

3. Cologne Center for Genomics (CCG), University of Cologne, Cologne, Germany

4. Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany

Funder

European Commission

Körber-Stiftung

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology,General Medicine

Reference123 articles.

1. Huntington's disease;Finkbeiner;Cold Spring Harb. Perspect. Biol.,2011

2. Proteostasis of huntingtin in health and disease;Koyuncu;Int. J. Mol. Sci.,2017

3. Normal huntingtin function: an alternative approach to Huntington's disease;Cattaneo;Nat. Rev. Neurosci.,2005

4. The biology of huntingtin;Saudou;Neuron,2016

5. Neuropathology of Huntington's disease;Vonsattel;Handb. Clin. Neurol.,2008

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