Genomes and Genes

Species

Erik Meulmeester

Summary

Country: Germany

Publications

  1. ncbi request reprint Loss of HAUSP-mediated deubiquitination contributes to DNA damage-induced destabilization of Hdmx and Hdm2
    Erik Meulmeester
    Department of Molecular and Cell Biology, Leiden University Medical Center, P O Box 9503, 2300 RA Leiden, The Netherlands
    Mol Cell 18:565-76. 2005
  2. ncbi request reprint p53: a guide to apoptosis
    Erik Meulmeester
    Department of Biochemistry I, University of Goettingen, Humboldtallee 23, D 37073, Germany
    Curr Cancer Drug Targets 8:87-97. 2008
  3. ncbi request reprint Hdmx protein stability is regulated by the ubiquitin ligase activity of Mdm2
    Petra de Graaf
    Leiden University Medical Center, Department of Molecular and Cell Biology and Center for Biomedical Genetics, P O Box 9503, 2300 RA Leiden, The Netherlands
    J Biol Chem 278:38315-24. 2003
  4. pmc Amplification of Mdmx (or Mdm4) directly contributes to tumor formation by inhibiting p53 tumor suppressor activity
    Davide Danovi
    Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy
    Mol Cell Biol 24:5835-43. 2004
  5. ncbi request reprint ATM-mediated phosphorylations inhibit Mdmx/Mdm2 stabilization by HAUSP in favor of p53 activation
    Erik Meulmeester
    Department of Molecular and Cell Biology, Leiden University Medical Center, Leiden, The Netherlands
    Cell Cycle 4:1166-70. 2005

Collaborators

  • Petra de Graaf
  • Davide Danovi
  • Aart G Jochemsen
  • Jean Christophe Marine
  • Diego Pasini
  • Patrizia Gasparini
  • Ruth Frenk
  • Kristian Helin
  • Alberto Gobbi
  • Domenico Migliorini
  • Pier Giuseppe Pelicci
  • Maria Capra
  • Sarah Francoz
  • Stef J F Letteboer
  • Yolande F M Ramos
  • Natalie A Little

Detail Information

Publications5

  1. ncbi request reprint Loss of HAUSP-mediated deubiquitination contributes to DNA damage-induced destabilization of Hdmx and Hdm2
    Erik Meulmeester
    Department of Molecular and Cell Biology, Leiden University Medical Center, P O Box 9503, 2300 RA Leiden, The Netherlands
    Mol Cell 18:565-76. 2005
    ..Importantly, impaired deubiquitination of Hdmx/Hdm2 by HAUSP contributes to the DNA damage-induced degradation of Hdmx and transient instability of Hdm2...
  2. ncbi request reprint p53: a guide to apoptosis
    Erik Meulmeester
    Department of Biochemistry I, University of Goettingen, Humboldtallee 23, D 37073, Germany
    Curr Cancer Drug Targets 8:87-97. 2008
    ..The continually increasing understanding of the mechanisms of regulation of p53 may provide the basis for new drug designs that could eventually lead to therapeutics to reactivate p53 in cancers...
  3. ncbi request reprint Hdmx protein stability is regulated by the ubiquitin ligase activity of Mdm2
    Petra de Graaf
    Leiden University Medical Center, Department of Molecular and Cell Biology and Center for Biomedical Genetics, P O Box 9503, 2300 RA Leiden, The Netherlands
    J Biol Chem 278:38315-24. 2003
    ..Mdm2 appears only to require an intact RING domain to be able to ubiquitinate Hdmx and target it for proteasomal degradation. These findings highlight the intricate functional relationships between p53, Mdm2, and Hdmx...
  4. pmc Amplification of Mdmx (or Mdm4) directly contributes to tumor formation by inhibiting p53 tumor suppressor activity
    Davide Danovi
    Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy
    Mol Cell Biol 24:5835-43. 2004
    ..Together, these results make Hdmx a new putative drug target for cancer therapy...
  5. ncbi request reprint ATM-mediated phosphorylations inhibit Mdmx/Mdm2 stabilization by HAUSP in favor of p53 activation
    Erik Meulmeester
    Department of Molecular and Cell Biology, Leiden University Medical Center, Leiden, The Netherlands
    Cell Cycle 4:1166-70. 2005
    ..Further insight into the mechanism by which ATM switches the interactions between HAUSP, Mdmx, Mdm2 and p53, to favor p53 activation may offer new tools for therapeutic intervention in the p53 pathway for cancer treatment...