Altered distributions of nucleocytoplasmic transport-related proteins in the spinal cord of a mouse model of amyotrophic lateral sclerosis

[1]  H. Rhim,et al.  Parkin Ubiquitinates and Promotes the Degradation of RanBP2* , 2006, Journal of Biological Chemistry.

[2]  S. Mirra,et al.  Nuclear Pore Complex Proteins in Alzheimer Disease , 2006, Journal of neuropathology and experimental neurology.

[3]  S. Nakano,et al.  Expression of an endoplasmic reticulum-resident chaperone, glucose-regulated stress protein 78, in the spinal cord of a mouse model of amyotrophic lateral sclerosis , 2005, Acta Neuropathologica.

[4]  Joseph Klafter,et al.  Nuclear localization signal peptides induce molecular delivery along microtubules. , 2005, Biophysical journal.

[5]  C. Montano,et al.  Activation of programmed cell death markers in ventral horn motor neurons during early presymptomatic stages of amyotrophic lateral sclerosis in a transgenic mouse model , 2004, Brain Research.

[6]  L. Pemberton,et al.  Karyopherins: from nuclear-transport mediators to nuclear-function regulators. , 2004, Trends in cell biology.

[7]  N. Imamoto,et al.  β-Catenin Shows an Overlapping Sequence Requirement but Distinct Molecular Interactions for Its Bidirectional Passage through Nuclear Pores* , 2004, Journal of Biological Chemistry.

[8]  J. Agar,et al.  Focal dysfunction of the proteasome: a pathogenic factor in a mouse model of amyotrophic lateral sclerosis , 2004, Journal of neurochemistry.

[9]  J. Cronshaw,et al.  The nuclear pore complex: disease associations and functional correlations , 2004, Trends in Endocrinology & Metabolism.

[10]  M. Koltzenburg,et al.  Axoplasmic Importins Enable Retrograde Injury Signaling in Lesioned Nerve , 2003, Neuron.

[11]  U. Kutay,et al.  Nucleocytoplasmic transport: taking an inventory , 2003, Cellular and Molecular Life Sciences CMLS.

[12]  S. R. Wente,et al.  Peering through the pore: nuclear pore complex structure, assembly, and function. , 2003, Developmental cell.

[13]  U. Kutay,et al.  Importin beta-depending nuclear import pathways: role of the adapter proteins in the docking and releasing steps. , 2003, Molecular Biology of the Cell.

[14]  S. Pelech,et al.  Protein kinase and protein phosphatase expression in the central nervous system of G93A mSOD over‐expressing mice , 2003, Journal of neurochemistry.

[15]  G. Rouleau,et al.  Familial amyotrophic lateral sclerosis , 2002, Muscle & nerve.

[16]  D. Price,et al.  Histological Evidence of Protein Aggregation in Mutant SOD1 Transgenic Mice and in Amyotrophic Lateral Sclerosis Neural Tissues , 2001, Neurobiology of Disease.

[17]  S. Kuersten,et al.  Nucleocytoplasmic transport: Ran, beta and beyond. , 2001, Trends in cell biology.

[18]  M. Rout,et al.  The Nuclear Pore Complex as a Transport Machine* , 2001, The Journal of Biological Chemistry.

[19]  René Hen,et al.  Decreased nuclear β‐catenin, tau hyperphosphorylation and neurodegeneration in GSK‐3β conditional transgenic mice , 2001 .

[20]  Y. Lazebnik,et al.  Caspases Disrupt the Nuclear-Cytoplasmic Barrier , 2000, The Journal of cell biology.

[21]  G. Punkosdy,et al.  CUL-2 is required for the G1-to-S-phase transition and mitotic chromosome condensation in Caenorhabditis elegans , 1999, Nature Cell Biology.

[22]  F. Bischoff,et al.  Evidence for Distinct Substrate Specificities of Importin α Family Members in Nuclear Protein Import , 1999, Molecular and Cellular Biology.

[23]  F. Bischoff,et al.  The importin β/importin 7 heterodimer is a functional nuclear import receptor for histone H1 , 1999, The EMBO journal.

[24]  G. Lipowsky,et al.  NTF2 mediates nuclear import of Ran , 1998, The EMBO journal.

[25]  L. Bruijn,et al.  Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. , 1998, Science.

[26]  D. Borchelt,et al.  ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions , 1997, Neuron.

[27]  G. Blobel,et al.  Mammalian karyopherin alpha 1 beta and alpha 2 beta heterodimers: alpha 1 or alpha 2 subunit binds nuclear localization signal and beta subunit interacts with peptide repeat-containing nucleoporins. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[28]  M. Gurney,et al.  Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS) , 1995, Brain Research.

[29]  M. Gurney,et al.  Development of central nervous system pathology in a murine transgenic model of human amyotrophic lateral sclerosis. , 1994, The American journal of pathology.

[30]  J. Haines,et al.  Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis , 1993, Nature.

[31]  L. Kurland,et al.  Familial amyotrophic lateral sclerosis. A subgroup characterized by posterior and spinocerebellar tract involvement and hyaline inclusions in the anterior horn cells. , 1967, Archives of neurology.

[32]  C. Miller,et al.  Phospho-β-catenin accumulation in alzheimer’s disease and in aggresomes attributable to proteasome dysfunction , 2007, Journal of Molecular Neuroscience.

[33]  K. Loveland,et al.  Expression of Nuclear Transport Importins beta 1 and beta 3 Is Regulated During Rodent Spermatogenesis1 , 2006, Biology of reproduction.

[34]  U. Kutay,et al.  Transport between the cell nucleus and the cytoplasm. , 1999, Annual review of cell and developmental biology.