Daniel Ungar

Summary

Affiliation: Princeton University
Country: USA

Publications

  1. ncbi request reprint SNARE protein structure and function
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    Annu Rev Cell Dev Biol 19:493-517. 2003
  2. ncbi request reprint Subunit architecture of the conserved oligomeric Golgi complex
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    J Biol Chem 280:32729-35. 2005
  3. pmc Structural basis for a human glycosylation disorder caused by mutation of the COG4 gene
    Brian C Richardson
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    Proc Natl Acad Sci U S A 106:13329-34. 2009
  4. ncbi request reprint Retrograde transport on the COG railway
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    Trends Cell Biol 16:113-20. 2006
  5. ncbi request reprint Structural analysis of conserved oligomeric Golgi complex subunit 2
    Lorraine F Cavanaugh
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    J Biol Chem 282:23418-26. 2007
  6. pmc Characterization of a mammalian Golgi-localized protein complex, COG, that is required for normal Golgi morphology and function
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    J Cell Biol 157:405-15. 2002
  7. pmc The COG and COPI complexes interact to control the abundance of GEARs, a subset of Golgi integral membrane proteins
    Toshihiko Oka
    Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
    Mol Biol Cell 15:2423-35. 2004
  8. ncbi request reprint Genetic analysis of the subunit organization and function of the conserved oligomeric golgi (COG) complex: studies of COG5- and COG7-deficient mammalian cells
    Toshihiko Oka
    Department of Biology and Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
    J Biol Chem 280:32736-45. 2005
  9. ncbi request reprint COG8 deficiency causes new congenital disorder of glycosylation type IIh
    Christian Kranz
    Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Hum Mol Genet 16:731-41. 2007

Collaborators

Detail Information

Publications9

  1. ncbi request reprint SNARE protein structure and function
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    Annu Rev Cell Dev Biol 19:493-517. 2003
    ....
  2. ncbi request reprint Subunit architecture of the conserved oligomeric Golgi complex
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    J Biol Chem 280:32729-35. 2005
    ..Vasile, E., Penman, M., Novina, C. D., Dykxhoorn, D. M., Ungar, D., Hughson, F. M., and Krieger, M. (2005) J. Biol. Chem. 280, 32736-32745)...
  3. pmc Structural basis for a human glycosylation disorder caused by mutation of the COG4 gene
    Brian C Richardson
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    Proc Natl Acad Sci U S A 106:13329-34. 2009
    ....
  4. ncbi request reprint Retrograde transport on the COG railway
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    Trends Cell Biol 16:113-20. 2006
    ..This hypothesis explains the impact of COG mutations by postulating that they impair the retrograde flow of resident Golgi proteins needed to maintain normal Golgi structure and function...
  5. ncbi request reprint Structural analysis of conserved oligomeric Golgi complex subunit 2
    Lorraine F Cavanaugh
    Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA
    J Biol Chem 282:23418-26. 2007
    ..These structures may represent platforms for interaction with other trafficking proteins including SNAREs (soluble N-ethylmaleimide factor attachment protein receptors) and Rabs...
  6. pmc Characterization of a mammalian Golgi-localized protein complex, COG, that is required for normal Golgi morphology and function
    Daniel Ungar
    Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA
    J Cell Biol 157:405-15. 2002
    ..Consideration of biochemical and genetic data for mammalian COG and its yeast homologue suggests a model for the subunit distribution within this complex, which plays critical roles in Golgi structure and function...
  7. pmc The COG and COPI complexes interact to control the abundance of GEARs, a subset of Golgi integral membrane proteins
    Toshihiko Oka
    Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
    Mol Biol Cell 15:2423-35. 2004
    ..COG and COPI may work in concert to ensure the proper retention or retrieval of a subset of proteins in the Golgi, and COG helps prevent the endoplasmic reticulum accumulation and degradation of some GEARs...
  8. ncbi request reprint Genetic analysis of the subunit organization and function of the conserved oligomeric golgi (COG) complex: studies of COG5- and COG7-deficient mammalian cells
    Toshihiko Oka
    Department of Biology and Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
    J Biol Chem 280:32736-45. 2005
    ..Only one or two of the seven Cog1- or Cog2-dependent Golgi membrane proteins called GEARs are also sensitive to Cog5 or Cog7 deficiency, indicating that the COG subunits play distinctive roles in controlling Golgi structure and function...
  9. ncbi request reprint COG8 deficiency causes new congenital disorder of glycosylation type IIh
    Christian Kranz
    Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Hum Mol Genet 16:731-41. 2007
    ..Lentiviral-mediated complementation with normal COG8 corrected mislocalization of other COG proteins, normalized sialylation and restored normal BFA-induced Golgi disruption. We propose to call this new disorder CDG-IIh or CDG-II/COG8...