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Derick G. Wansink

Researcher at Radboud University Nijmegen

Publications -  53
Citations -  6144

Derick G. Wansink is an academic researcher from Radboud University Nijmegen. The author has contributed to research in topics: Myotonic dystrophy & Trinucleotide repeat expansion. The author has an hindex of 20, co-authored 51 publications receiving 5079 citations. Previous affiliations of Derick G. Wansink include Radboud University Nijmegen Medical Centre.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Somatic expansion behaviour of the (CTG)n repeat in myotonic dystrophy knock-in mice is differentially affected by Msh3 and Msh6 mismatch–repair proteins

Walther J. A. A. van den Broek, +6 more
- 15 Jan 2002 - 
TL;DR: Competition of Msh3 and Msh6 for binding to Msh2 in functional complexes with different DNA mismatch-recognition specificity may explain why the somatic (CTG)n expansion rate is differentially affected by ablation of MSh3 andMsh6.
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Triplet-repeat oligonucleotide-mediated reversal of RNA toxicity in myotonic dystrophy.

Susan A. M. Mulders, +11 more
- 18 Aug 2009 - 
TL;DR: A fully 2′-O-methyl-phosphorothioate-modified (CAG)7 AON is identified that silences mutant DMPK RNA expression and reduces the number of ribonuclear aggregates in a selective and (CUG)n-length-dependent manner and demonstrates proof of principle for therapeutic use of simple sequence AONs in DM1 and potentially other unstable microsatellite diseases.
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Chromosome-wide nucleosome replacement and H3.3 incorporation during mammalian meiotic sex chromosome inactivation.

Godfried W. van der Heijden, +12 more
- 21 Jan 2007 - 
TL;DR: An extensive replacement of nucleosomes within unsynapsed chromatin is demonstrated, depending on and initiated shortly after induction of MSCI and MSUC, which provides a means for epigenetic reprogramming of sex chromatin presumably required for gene silencing in the male mammalian germ line.
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CRISPR/Cas9-Induced (CTG⋅CAG) n Repeat Instability in the Myotonic Dystrophy Type 1 Locus: Implications for Therapeutic Genome Editing

Ellen L. van Agtmaal, +12 more
- 04 Jan 2017 - 
TL;DR: It is demonstrated that single clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-cleavage in either its 5′ or 3′ unique flank promotes uncontrollable deletion of large segments from the expanded trinucleotide repeat, rather than formation of short indels usually seen after double-strand break repair.