Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
about
FHX, a novel fork head factor with a dual DNA binding specificityA human HAP1 homologue. Cloning, expression, and interaction with huntingtinIron dysregulation in Huntington's diseaseOligomerization of Peptides LVEALYL and RGFFYT and Their Binding Affinity to InsulinDeficiency of huntingtin has pleiotropic effects in the social amoeba Dictyostelium discoideumA Crystal Structure of a Model of the Repeating r(CGG) Transcript Found in Fragile X SyndromeNuclear localization of a non-caspase truncation product of atrophin-1, with an expanded polyglutamine repeat, increases cellular toxicityHuntingtin is required for neurogenesis and is not impaired by the Huntington's disease CAG expansionAtomistic simulations of the effects of polyglutamine chain length and solvent quality on conformational equilibria and spontaneous homodimerizationWild-type huntingtin reduces the cellular toxicity of mutant huntingtin in vivoTransgenic mice expressing a Huntington's disease mutation are resistant to quinolinic acid-induced striatal excitotoxicityAn Analysis of Biomolecular Force Fields for Simulations of Polyglutamine in SolutionGlycolipid and ganglioside metabolism imbalances in Huntington's disease.A toxic RNA catalyzes the in cellulo synthesis of its own inhibitor.DFNA5: hearing impairment exon instead of hearing impairment gene?Modulating huntingtin half-life alters polyglutamine-dependent aggregate formation and cell toxicity.Antisense downregulation of mutant huntingtin in a cell model.Brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 prevent the death of striatal projection neurons in a rodent model of Huntington's disease.The neuropathology of CAG repeat diseases: review and update of genetic and molecular features.Molecular basis of genetic heterogeneity: role of the clinical neurologist.Activated JNK phosphorylates the c-terminal domain of MLK2 that is required for MLK2-induced apoptosis.Partial resistance to malonate-induced striatal cell death in transgenic mouse models of Huntington's disease is dependent on age and CAG repeat length.Neuronal grafts for Huntington's disease.Correction of hemophilia B in canine and murine models using recombinant adeno-associated viral vectors.Wild-type huntingtin protects neurons from excitotoxicity.Monozygotic twins suffering from Huntington's disease show different cognitive and behavioural symptoms.FOXOs modulate proteasome activity in human-induced pluripotent stem cells of Huntington's disease and their derived neural cells.Transformation between α-helix and β-sheet structures of one and two polyglutamine peptides in explicit water molecules by replica-exchange molecular dynamics simulations
P2860
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P2860
Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
1996年论文
@zh
1996年论文
@zh-cn
name
Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
@en
type
label
Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
@en
prefLabel
Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
@en
P1476
Huntington's disease: translating a CAG repeat into a pathogenic mechanism.
@en
P2093
M E MacDonald
P304
P356
10.1016/S0959-4388(96)80097-3
P577
1996-10-01T00:00:00Z