Increased Alix (apoptosis-linked gene-2 interacting protein X) immunoreactivity in the degenerating striatum of rats chronically treated by 3-nitropropionic acid
暂无分享,去创建一个
S. Schiffmann | D. Blum | M. Galas | R. Sadoul | S. Torch | Fiona J. Hemming | F. Hemming | L. Cuvelier
[1] B. Blot,et al. Early increase of apoptosis-linked gene-2 interacting protein X in areas of kainate-induced neurodegeneration , 2004, Neuroscience.
[2] M. Hayden,et al. Inhibition of Calpain Cleavage of Huntingtin Reduces Toxicity , 2004, Journal of Biological Chemistry.
[3] S. Schiffmann,et al. Death of cortical and striatal neurons induced by mitochondrial defect involves differential molecular mechanisms , 2004, Neurobiology of Disease.
[4] B. Blot,et al. Alix, a Protein Regulating Endosomal Trafficking, Is Involved in Neuronal Death* , 2004, Journal of Biological Chemistry.
[5] S. Schiffmann,et al. Chronic intoxication with 3-nitropropionic acid in rats induces the loss of striatal dopamine terminals without affecting nigral cell viability , 2004, Neuroscience Letters.
[6] L. Thompson,et al. Autophagy regulates the processing of amino terminal huntingtin fragments. , 2003, Human molecular genetics.
[7] Philippe Hantraye,et al. In Vivo Calpain/Caspase Cross-talk during 3-Nitropropionic Acid-induced Striatal Degeneration , 2003, Journal of Biological Chemistry.
[8] M. Maki,et al. The ALG-2-interacting Protein Alix Associates with CHMP4b, a Human Homologue of Yeast Snf7 That Is Involved in Multivesicular Body Sorting* , 2003, Journal of Biological Chemistry.
[9] A. Calistri,et al. AIP1/ALIX Is a Binding Partner for HIV-1 p6 and EIAV p9 Functioning in Virus Budding , 2003, Cell.
[10] S. Krajewski,et al. Calpain Is a Major Cell Death Effector in Selective Striatal Degeneration Induced In Vivo by 3-Nitropropionate: Implications for Huntington's Disease , 2003, The Journal of Neuroscience.
[11] S. Schiffmann,et al. A Dual Role of Adenosine A2A Receptors in 3-Nitropropionic Acid-Induced Striatal Lesions: Implications for the Neuroprotective Potential of A2A Antagonists , 2003, The Journal of Neuroscience.
[12] David Blum,et al. Adenosine receptors and Huntington's disease: implications for pathogenesis and therapeutics , 2003, The Lancet Neurology.
[13] R. Sadoul,et al. Expression of Alix protein during early avian development. , 2003, Gene expression patterns : GEP.
[14] M. Maki,et al. Structures, functions and molecular evolution of the penta-EF-hand Ca2+-binding proteins. , 2002, Biochimica et biophysica acta.
[15] B. Blot,et al. Alix (ALG-2-interacting Protein X), a Protein Involved in Apoptosis, Binds to Endophilins and Induces Cytoplasmic Vacuolization* , 2002, The Journal of Biological Chemistry.
[16] S. Schiffmann,et al. Striatal and Cortical Neurochemical Changes Induced by Chronic Metabolic Compromise in the 3-Nitropropionic Model of Huntington's Disease , 2002, Neurobiology of Disease.
[17] James R. Burke,et al. Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines , 2002, Nature Neuroscience.
[18] L. Ellerby,et al. Calpain Activation in Huntington's Disease , 2002, The Journal of Neuroscience.
[19] S. Schiffmann,et al. Topological analysis of striatal lesions induced by 3-nitropropionic acid in the Lewis rat , 2001, Neuroreport.
[20] M. DiFiglia,et al. Huntingtin Expression Stimulates Endosomal–Lysosomal Activity, Endosome Tubulation, and Autophagy , 2000, The Journal of Neuroscience.
[21] O. Bogler,et al. The Glioma-associated Protein SETA Interacts with AIP1/Alix and ALG-2 and Modulates Apoptosis in Astrocytes* , 2000, The Journal of Biological Chemistry.
[22] F. Condé,et al. Major strain differences in response to chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid in rats: implications for neuroprotection studies , 2000, Neuroscience.
[23] Françoise Condé,et al. Replicating Huntington's disease phenotype in experimental animals , 1999, Progress in Neurobiology.
[24] K. W. Lo,et al. Apoptosis-linked gene product ALG-2 is a new member of the calpain small subunit subfamily of Ca2+-binding proteins. , 1999, Biochemistry.
[25] A. Nichols,et al. Alix, a novel mouse protein undergoing calcium-dependent interaction with the apoptosis-linked-gene 2 (ALG-2) protein , 1999, Cell Death and Differentiation.
[26] L. Pellegrini,et al. Cloning of AIP1, a Novel Protein That Associates with the Apoptosis-linked Gene ALG-2 in a Ca2+-dependent Reaction* , 1999, The Journal of Biological Chemistry.
[27] H. Lehrach,et al. SH3GL3 associates with the Huntingtin exon 1 protein and promotes the formation of polygln-containing protein aggregates. , 1998, Molecular cell.
[28] P. Vito,et al. Interfering with Apoptosis: Ca2+-Binding Protein ALG-2 and Alzheimer's Disease Gene ALG-3 , 1996, Science.
[29] B. Hyman,et al. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.