HTHenk F. Tabak

Henk F. Tabak

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Henk F. Tabak has a total of 8 co-authors. Here are the top co-authors by number of shared publications:

  • Adri Mul

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication
  • Cristina Al-Khalili Szigyarto

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication
  • Guy P.M.A. Hardy

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication
  • Harmen J. Bussemaker

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication
  • Joost M. Teixeira de Mattos

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication
  • Kasia Piekarska

    Department of Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; †Department of Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 SM Amsterdam, The Netherlands; and §Department of Microbiology, University of Amsterdam, 1018 WV Amsterdam, The Netherlands

    1 shared publication

Latest Publications

  • Open Access

    Dissection of Transient Oxidative Stress Response inSaccharomyces cerevisiaeby Using DNA Microarrays

    by Marian Groot Koerkamp, Martijn Rep, Harmen J. Bussemaker, Guy P.M.A. Hardy, Adri Mul, Kasia Piekarska, Cristina Al-Khalili Szigyarto, Joost M. Teixeira de Mattos, Henk F. Tabak

    Yeast cells were grown in glucose-limited chemostat cultures and forced to switch to a new carbon source, the fatty acid oleate. Alterations in gene expression were monitored using DNA microarrays combined with bioinformatics tools, among which was included the recently developed algorithm REDUCE. Immediately after the switch to oleate, a transient and very specific stress response was observed, followed by the up-regulation of genes encoding peroxisomal enzymes required for fatty acid metabolism. The stress response included up-regulation of genes coding for enzymes to keep thioredoxin and glutathione reduced, as well as enzymes required for the detoxification of reactive oxygen species. Among the genes coding for various isoenzymes involved in these processes, only a specific subset was expressed. Not the general stress transcription factors Msn2 and Msn4, but rather the specific factor Yap1p seemed to be the main regulator of the stress response. We ascribe the initiation of the oxidative stress response to a combination of poor redox flux and fatty acid-induced uncoupling of the respiratory chain during the metabolic reprogramming phase.