Phyllis I Hanson

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. ncbi request reprint AAA+ proteins: have engine, will work
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nat Rev Mol Cell Biol 6:519-29. 2005
  2. ncbi request reprint Structure/function analysis of four core ESCRT-III proteins reveals common regulatory role for extreme C-terminal domain
    Soomin Shim
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Traffic 8:1068-79. 2007
  3. pmc Ubiquitin depletion and dominant-negative VPS4 inhibit rhabdovirus budding without affecting alphavirus budding
    Gwen M Taylor
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Virol 81:13631-9. 2007
  4. ncbi request reprint Interaction of the mammalian endosomal sorting complex required for transport (ESCRT) III protein hSnf7-1 with itself, membranes, and the AAA+ ATPase SKD1
    Yuan Lin
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 280:12799-809. 2005
  5. ncbi request reprint Inclusion body myopathy-associated mutations in p97/VCP impair endoplasmic reticulum-associated degradation
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 15:189-99. 2006
  6. ncbi request reprint Luminal chloride-dependent activation of endosome calcium channels: patch clamp study of enlarged endosomes
    Mitsuyoshi Saito
    Department of Cell Biology and Physiology, Washington University, 660 S, Euclid Avenue, St Louis, MO 63110, USA
    J Biol Chem 282:27327-33. 2007
  7. pmc CHMP4B, a novel gene for autosomal dominant cataracts linked to chromosome 20q
    Alan Shiels
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St Louis, MO 63110, USA
    Am J Hum Genet 81:596-606. 2007
  8. pmc Plasma membrane deformation by circular arrays of ESCRT-III protein filaments
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Cell Biol 180:389-402. 2008
  9. ncbi request reprint Transgenic expression of inclusion body myopathy associated mutant p97/VCP causes weakness and ubiquitinated protein inclusions in mice
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Avenue, Saint Louis, MO 63110, USA
    Hum Mol Genet 16:919-28. 2007
  10. doi request reprint Cell biology of the ESCRT machinery
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Curr Opin Cell Biol 21:568-74. 2009

Collaborators

Detail Information

Publications25

  1. ncbi request reprint AAA+ proteins: have engine, will work
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nat Rev Mol Cell Biol 6:519-29. 2005
    ..Here, we review the structural organization of AAA+ proteins, the conformational changes they undergo, the range of different reactions they catalyse, and the diseases associated with their dysfunction...
  2. ncbi request reprint Structure/function analysis of four core ESCRT-III proteins reveals common regulatory role for extreme C-terminal domain
    Soomin Shim
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Traffic 8:1068-79. 2007
    ..Overall, our study supports a model in which ESCRT-III proteins cycle between a default 'closed' state and an activated 'open' state under control of sequences at their C-terminus and associated factors...
  3. pmc Ubiquitin depletion and dominant-negative VPS4 inhibit rhabdovirus budding without affecting alphavirus budding
    Gwen M Taylor
    Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Virol 81:13631-9. 2007
    ..In contrast, SFV budding was independent of both ubiquitin and the activity of VPS4, perhaps reflecting the important role of the highly organized envelope protein lattice during alphavirus budding...
  4. ncbi request reprint Interaction of the mammalian endosomal sorting complex required for transport (ESCRT) III protein hSnf7-1 with itself, membranes, and the AAA+ ATPase SKD1
    Yuan Lin
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 280:12799-809. 2005
    ..Together with earlier studies, our work suggests that a variety of ESCRT-III-containing polymers can assemble on membranes and recruit SKD1 during formation of the MVB...
  5. ncbi request reprint Inclusion body myopathy-associated mutations in p97/VCP impair endoplasmic reticulum-associated degradation
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 15:189-99. 2006
    ..Undegraded mutant DeltaF508-CFTR also accumulates in these aggregates. We conclude that IBMPFD mutations in p97/VCP disrupt ERAD and that this may contribute to the pathogenesis of IBMPFD...
  6. ncbi request reprint Luminal chloride-dependent activation of endosome calcium channels: patch clamp study of enlarged endosomes
    Mitsuyoshi Saito
    Department of Cell Biology and Physiology, Washington University, 660 S, Euclid Avenue, St Louis, MO 63110, USA
    J Biol Chem 282:27327-33. 2007
    ..The ECC shows a similar pharmacology to that of the TRPV2 channel. In addition, the ECC has a unique chloride-dependent regulation; it is inhibited by the endosome luminal chloride with a K(50) of 82 mm...
  7. pmc CHMP4B, a novel gene for autosomal dominant cataracts linked to chromosome 20q
    Alan Shiels
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St Louis, MO 63110, USA
    Am J Hum Genet 81:596-606. 2007
    ....
  8. pmc Plasma membrane deformation by circular arrays of ESCRT-III protein filaments
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Cell Biol 180:389-402. 2008
    ..We suggest that ESCRT-III polymers delineate and help generate the luminal vesicles of multivesicular bodies...
  9. ncbi request reprint Transgenic expression of inclusion body myopathy associated mutant p97/VCP causes weakness and ubiquitinated protein inclusions in mice
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Avenue, Saint Louis, MO 63110, USA
    Hum Mol Genet 16:919-28. 2007
    ..TgVCP-RH animals will be a valuable tool for understanding the pathogenesis of IBM and the role of the UPS in skeletal muscle...
  10. doi request reprint Cell biology of the ESCRT machinery
    Phyllis I Hanson
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Curr Opin Cell Biol 21:568-74. 2009
    ..Here we review recent studies suggesting that components of the ESCRT-III complex drive lumenal vesicle formation and consider possible mechanisms for this reaction...
  11. pmc Novel interactions of ESCRT-III with LIP5 and VPS4 and their implications for ESCRT-III disassembly
    Soomin Shim
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Mol Biol Cell 19:2661-72. 2008
    ..These studies point to a role for direct binding between LIP5 and ESCRT-III proteins that is likely to complement LIP5's previously described ability to regulate VPS4 activity...
  12. pmc LULL1 retargets TorsinA to the nuclear envelope revealing an activity that is impaired by the DYT1 dystonia mutation
    Abigail B Vander Heyden
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Mol Biol Cell 20:2661-72. 2009
    ..Together, our data suggest that LULL1 regulates the distribution and activity of TorA within the ER and NE lumen and reveal functional defects in the mutant protein responsible for DYT1 dystonia...
  13. pmc Impaired protein aggregate handling and clearance underlie the pathogenesis of p97/VCP-associated disease
    Jeong Sun Ju
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 283:30289-99. 2008
    ..Our study emphasizes the importance of protein aggregate trafficking to inclusion bodies in degenerative diseases and the therapeutic benefit of inclusion body formation...
  14. pmc Distinct roles for the AAA ATPases NSF and p97 in the secretory pathway
    Seema Dalal
    Washington University School of Medicine, Department of Cell Biology and Physiology, St Louis, Missouri 63110, USA
    Mol Biol Cell 15:637-48. 2004
    ..These findings demonstrate that ATP-hydrolysis-dependent activities of NSF and p97 in the cell are not equivalent and suggest that only NSF is directly involved in regulating membrane fusion...
  15. ncbi request reprint Defining the SNARE complex binding surface of alpha-SNAP: implications for SNARE complex disassembly
    Karla E Marz
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 278:27000-8. 2003
    ....
  16. pmc TorsinA in the nuclear envelope
    Teresa V Naismith
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 101:7612-7. 2004
    ..These results suggest that changes in interactions involving torsinA in the NE could be important for the pathogenesis of dystonia and point to torsinA and related proteins as a class of ATPases that may operate in the NE...
  17. pmc Interaction of torsinA with its major binding partners is impaired by the dystonia-associated DeltaGAG deletion
    Teresa V Naismith
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 284:27866-74. 2009
    ..Impaired interaction of torsinA with LULL1 and/or LAP1 may thus contribute to the development of dystonia...
  18. ncbi request reprint Sealed with a twist: complexin and the synaptic SNARE complex
    Karla E Marz
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8228, St Louis, MO 6311, USA
    Trends Neurosci 25:381-3. 2002
    ..This structure, together with NMR data, suggests that the role of complexin is to stabilize the SNARE complex as it forms from SNAREs in vesicle and target membranes...
  19. ncbi request reprint TorsinB--perinuclear location and association with torsinA
    Jeffrey W Hewett
    Departments of Neurology and Radiology, Molecular Neurogenetics Unit, Massachusetts General Hospital, 13th Street, Charlestown, MA 02129, USA
    J Neurochem 89:1186-94. 2004
    ..We conclude that torsinB and torsinA are localized in overlapping cell compartments within the same protein complex, and thus may carry out related functions in vivo...
  20. ncbi request reprint TorsinA in PC12 cells: localization in the endoplasmic reticulum and response to stress
    Jeffrey Hewett
    Molecular Neurogenetics Unit, Department of Neurology, Massachusetts General Hospital, and Neuroscience Program, Harvard Medical School, Boston, Massachusetts, USA
    J Neurosci Res 72:158-68. 2003
    ..Mutant torsinA may interfere with and/or compromise ER functions, especially in dopaminergic neurons, which have high levels of torsinA and are intrinsically vulnerable to oxidative stress...
  21. ncbi request reprint Effects of genetic variations in the dystonia protein torsinA: identification of polymorphism at residue 216 as protein modifier
    Norman Kock
    Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA
    Hum Mol Genet 15:1355-64. 2006
    ..They also suggest possible connections between the allelic polymorphism at residue 216 and the penetrance of DYT1 dystonia, as well as a possible role for this polymorphism in related disease states...
  22. ncbi request reprint The hyh mutation uncovers roles for alpha Snap in apical protein localization and control of neural cell fate
    Teresa H Chae
    Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center and Department of Neurology and Program in Neuroscience, Harvard Medical School, HIM 816, 4 Blackfan Circle, Boston, Massachusetts 02115, USA
    Nat Genet 36:264-70. 2004
    ..Apical localization of the SNARE Vamp7 is also disrupted. Thus, alpha Snap is essential for apical protein localization and cell fate determination in neuroepithelial cells...
  23. ncbi request reprint The early onset dystonia protein torsinA interacts with kinesin light chain 1
    Christoph Kamm
    Molecular Neurogenetics Unit, Departments of Neurology and Radiology, Massachusetts General Hospital and Neuroscience Program, Harvard Medical School, Boston, MA 02114, USA
    J Biol Chem 279:19882-92. 2004
    ..These studies suggest that wild-type torsinA undergoes anterograde transport along microtubules mediated by kinesin and may act as a molecular chaperone regulating kinesin activity and/or cargo binding...
  24. ncbi request reprint p97 Is in a complex with cholera toxin and influences the transport of cholera toxin and related toxins to the cytoplasm
    Ramzey J Abujarour
    Molecular and Cell Biology Department, The University of Texas at Dallas, Richardson, Texas 75083 0688, USA
    J Biol Chem 280:15865-71. 2005
    ..Altogether, these results provide functional and structural evidence that p97 participates in the transport of cholera toxin to the cytoplasm...
  25. ncbi request reprint NSF ATPase and alpha-/beta-SNAPs disassemble the AMPA receptor-PICK1 complex
    Jonathan G Hanley
    Howard Hughes Medical Institute, Department of Biochemistry, New York University School of Medicine, New York, NY 10016, USA
    Neuron 34:53-67. 2002
    ..This demonstrates that the previously reported synaptic stabilization of AMPARs by NSF involves disruption of GluR2-PICK1 interactions. Furthermore, we are reporting a non-SNARE substrate for NSF disassembly activity...