Pathogenesis of Inclusion Bodies in (CAG)n/Qn-Expansion Diseases with Special Reference to the Role of Tissue Transglutaminase and to Selective Vulnerability
- 7 July 2008
- journal article
- review article
- Published by Wiley in Journal of Neurochemistry
- Vol. 72 (3) , 889-899
- https://doi.org/10.1046/j.1471-4159.1999.0720889.x
Abstract
No abstract availableKeywords
This publication has 91 references indexed in Scilit:
- Spinobulbar muscular atrophy: polyglutamine-expanded androgen receptor is proteolytically resistant in vitro and processed abnormally in transfected cellsHuman Molecular Genetics, 1998
- Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat LengthNeurobiology of Disease, 1998
- Transgenic models of Huntington's diseaseHuman Molecular Genetics, 1997
- Oxidative damage and metabolic dysfunction in Huntington's disease: Selective vulnerability of the basal gangliaAnnals of Neurology, 1997
- Use of the Transglutaminase Reaction To Study the Dissociation of Histone N-Terminal Tails from DNA in Nucleosome Core ParticlesBiochemistry, 1997
- The association of tissue transglutaminase with human recombinant tau results in the formation of insoluble filamentous structuresBrain Research, 1997
- Core Histones Are Glutaminyl Substrates for Tissue TransglutaminasePublished by Elsevier ,1996
- Trinucleotide repeat length and clinical progression in Huntington's diseaseNeurology, 1996
- Immunohistochemical detection of coagulation factor XIIIa in postmortem human brain tissueNeuroscience Letters, 1995
- Aging, energy, and oxidative stress in neurodegenerative diseasesAnnals of Neurology, 1995