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Ronald J.A. Wanders

Researcher at University of Amsterdam

Publications -  687
Citations -  43190

Ronald J.A. Wanders is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Peroxisome & Peroxisomal disorder. The author has an hindex of 101, co-authored 674 publications receiving 38576 citations. Previous affiliations of Ronald J.A. Wanders include VU University Amsterdam & Boston Children's Hospital.

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Journal ArticleDOI

Biochemistry of mammalian peroxisomes revisited.

Ronald J.A. Wanders, +1 more
- 06 Jun 2006 - 
TL;DR: The identification and characterization of yeast mutants defective either in the biogenesis of peroxisomes or in one of its metabolic functions, notably fatty acid beta-oxidation, combined with the recognition of a group of genetic diseases in man, wherein these processes are also defective, have provided new insights in all aspects of perxisomes.
Journal ArticleDOI

Biochemistry of peroxisomes

H. van den Bosch, +3 more
- 01 Jan 1992 - 
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The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways.

Riekelt H. Houtkooper, +3 more
- 01 Apr 2010 - 
TL;DR: An integrated view on the pathways that control NAD(+) production and cycling, as well as its cellular compartmentalization, and novel data that show how modulation of NAD(+)-producing and -consuming pathways have a major physiological impact and hold promise for the prevention and treatment of metabolic disease are provided.
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A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation

Sander M. Houten, +1 more
- 02 Mar 2010 - 
TL;DR: In Inherited defects for most of the FAO enzymes have been identified and characterised and are currently included in neonatal screening programmes and will ultimately lead to better treatment.
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Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies

Gang Wang, +27 more
- 01 Jun 2014 - 
TL;DR: This study combined patient-derived and genetically engineered induced pluripotent stem cells (iPSCs) with tissue engineering to elucidate the pathophysiology underlying the cardiomyopathy of Barth syndrome, a mitochondrial disorder caused by mutation of the gene encoding tafazzin (TAZ).