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Gerben J. Schaaf

Researcher at Erasmus University Rotterdam

Publications -  27
Citations -  955

Gerben J. Schaaf is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Skeletal muscle & Cell activation. The author has an hindex of 14, co-authored 25 publications receiving 827 citations. Previous affiliations of Gerben J. Schaaf include University of Amsterdam & University Medical Center Groningen.

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The role of oxidative stress in the ochratoxin A-mediated toxicity in proximal tubular cells.

TL;DR: Investigating the OTA-mediated oxidative stress response concluded that oxidative stress contributes to the tubular toxicity of OTA, and cellular GSH levels play a pivotal role in limiting the short-term toxicity of this mycotoxin in renal tubular cells.
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Genomic Imbalances in Rhabdomyosarcoma Cell Lines Affect Expression of Genes Frequently Altered in Primary Tumors: An Approach to Identify Candidate Genes Involved in Tumor Development

TL;DR: The ability to identify genes of potential significance in tumor development through combining genomic and transcriptomic profiles from representative cell lines with publicly available expression profiling data from primary tumors is illustrated.
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Management of Oxidative Stress by Heme Oxygenase-1 in Cisplatin-induced Toxicity in Renal Tubular Cells

TL;DR: It is concluded that heme oxygenase-1 is able to directly limit the CDDP-induced oxidative stress response and thus serves as safeguard of the cellular redox balance.
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Large-Scale Expansion of Human iPSC-Derived Skeletal Muscle Cells for Disease Modeling and Cell-Based Therapeutic Strategies

TL;DR: Fluorescence-activated cell sorting-purified myogenic progenitors generated from healthy controls and Pompe disease iPSCs can be robustly expanded as much as 5 × 1011-fold and is useful for modeling of skeletal muscle disorders and for using patient-derived, gene-corrected cells to develop cell-based strategies.
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Silencing of SPRY1 Triggers Complete Regression of Rhabdomyosarcoma Tumors Carrying a Mutated RAS Gene

TL;DR: It is argued that SPRY1 inhibition can offer a therapeutic strategy to treat childhood rhabdomyosarcoma and possibly other tumors carrying oncogenic RAS mutations.