(Q43873037)

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Prolonged survival and decreased abnormal movements in transgenic model of Huntington disease, with administration of the transglutaminase inhibitor cystamine

scientific article published in February 2002

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1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Prolonged survival and decreased abnormal movements in transgenic model of Huntington disease, with administration of the transglutaminase inhibitor cystamine (English)

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Huntington's disease

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author name string

Marcela V Karpuj

1

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Mark W Becher

2

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Joe E Springer

3

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Dorothee Chabas

4

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Sawsan Youssef

5

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Rosetta Pedotti

6

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

Dennis Mitchell

7

1 reference

Europe PubMed Central

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27 November 2017

Lawrence Steinman

8

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

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publication date

1 February 2002

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Europe PubMed Central

PubMed publication ID

27 November 2017

Nature Medicine

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27 November 2017

8

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Europe PubMed Central

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27 November 2017

2

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Europe PubMed Central

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27 November 2017

143-149

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Europe PubMed Central

PubMed publication ID

27 November 2017

Human genetic diseases due to codon reiteration: relationship to an evolutionary mechanism

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Neurodegenerative diseases and transglutaminase

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DRPLA aggregation and transglutaminase, revisited

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Glutamine repeats and neurodegenerative diseases: molecular aspects

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A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes.

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Transglutaminase action imitates Huntington's disease: selective polymerization of Huntingtin containing expanded polyglutamine.

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Transglutaminase aggregates huntingtin into nonamyloidogenic polymers, and its enzymatic activity increases in Huntington's disease brain nuclei

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Suppression of aggregate formation and apoptosis by transglutaminase inhibitors in cells expressing truncated DRPLA protein with an expanded polyglutamine stretch.

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Transglutaminases

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Specificity of guinea pig liver transglutaminase for amine substrates

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Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

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Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease

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Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation

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Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain

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Intranuclear neuronal inclusions in Huntington's disease and dentatorubral and pallidoluysian atrophy: correlation between the density of inclusions and IT15 CAG triplet repeat length

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Amyloid formation by mutant huntingtin: threshold, progressivity and recruitment of normal polyglutamine proteins

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Ectopically expressed CAG repeats cause intranuclear inclusions and a progressive late onset neurological phenotype in the mouse

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Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions.

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Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease

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Reversing neurodegeneration: a promise unfolds

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Nuclear inclusions in glutamine repeat disorders: are they pernicious, coincidental, or beneficial?

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Transglutaminase: mechanistic features of the active site as determined by kinetic and inhibitor studies

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Fibrin-stabilizing factor (factor XIII)

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Transgenic mice in the study of polyglutamine repeat expansion diseases

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Formation of polyglutamine inclusions in non-CNS tissue

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NMDA receptor-mediated K+ efflux and neuronal apoptosis

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Substrate binding is required for assembly of the active conformation of the catalytic site in Ntn amidotransferases: evidence from the 1.8 A crystal structure of the glutaminase domain of glucosamine 6-phosphate synthase

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Tissue transglutaminase selectively modifies gliadin peptides that are recognized by gut-derived T cells in celiac disease

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Increased production of extracellular glutamate by the mitochondrial glutaminase following neuronal death.

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Decreased expression of striatal signaling genes in a mouse model of Huntington's disease

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Gene microarray identification of redox and mitochondrial elements that control resistance or sensitivity to apoptosis

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Genetic suppression of polyglutamine toxicity in Drosophila

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Structure of TPR domain-peptide complexes: critical elements in the assembly of the Hsp70-Hsp90 multichaperone machine

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Chaperones Hsp70 and Hsp40 suppress aggregate formation and apoptosis in cultured neuronal cells expressing truncated androgen receptor protein with expanded polyglutamine tract

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Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1.

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N(epsilon)-(gamma-L-glutamyl)-L-lysine (GGEL) is increased in cerebrospinal fluid of patients with Huntington's disease

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10.1038/NM0202-143

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

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PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

27 November 2017

ResearchGate publication ID

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