Anka G Ehrhardt

Summary

Affiliation: University of Massachusetts Medical School
Country: USA

Publications

  1. ncbi request reprint Spindle pole fragmentation due to proteasome inhibition
    Anka G Ehrhardt
    Department of Cell Biology, University of Massachusetts Medical School, Worcester, 01605, USA
    J Cell Physiol 204:808-18. 2005
  2. pmc Requirement of JIP scaffold proteins for NMDA-mediated signal transduction
    Norman J Kennedy
    Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Genes Dev 21:2336-46. 2007
  3. pmc Supervillin modulation of focal adhesions involving TRIP6/ZRP-1
    Norio Takizawa
    Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Cell Biol 174:447-58. 2006

Collaborators

  • Gilles Martin
  • G Sluder
  • Chia Yi Kuan
  • Norman J Kennedy
  • Norio Takizawa
  • Roger J Davis
  • Richard A Flavell
  • Steven N Treistman
  • Pasko Rakic
  • Julie Cavanagh-Kyros
  • Jessica L Crowley
  • Thomas Nebl
  • Tara C Smith
  • Laura M Hoffman
  • Elizabeth J Luna
  • Mary C Beckerle
  • Lawrence M Lifshitz
  • Stephen J Palmieri

Detail Information

Publications3

  1. ncbi request reprint Spindle pole fragmentation due to proteasome inhibition
    Anka G Ehrhardt
    Department of Cell Biology, University of Massachusetts Medical School, Worcester, 01605, USA
    J Cell Physiol 204:808-18. 2005
    ..Together, this leads to the conclusion that the centrosome functions as proteolytic center during mitosis and proteolytic activity at the spindle poles is necessary for maintaining spindle pole integrity...
  2. pmc Requirement of JIP scaffold proteins for NMDA-mediated signal transduction
    Norman J Kennedy
    Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Genes Dev 21:2336-46. 2007
    ..JIP complexes interact with the SH2 domain of cFyn and may therefore promote tyrosine phosphorylation and activity of the NMDA receptor. We conclude that JIP scaffold proteins are critically required for normal NMDA receptor function...
  3. pmc Supervillin modulation of focal adhesions involving TRIP6/ZRP-1
    Norio Takizawa
    Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    J Cell Biol 174:447-58. 2006
    ..Thus, SV interactions with TRIP6 at FAs promote loss of FA structure and function. SV and TRIP6 binding partners suggest several specific mechanisms through which the SV-TRIP6 interaction may regulate FA maturation and/or disassembly...