Genetic background modifies nuclear mutant huntingtin accumulation and HD CAG repeat instability in Huntington's disease knock-in mice.
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Rrs1 is involved in endoplasmic reticulum stress response in Huntington diseaseMouse models of polyglutamine diseases: review and data table. Part IMutant huntingtin gene-dose impacts on aggregate deposition, DARPP32 expression and neuroinflammation in HdhQ150 miceContinuous and periodic expansion of CAG repeats in Huntington's disease R6/1 miceEffects of deletion of mutant huntingtin in steroidogenic factor 1 neurons on the psychiatric and metabolic phenotype in the BACHD mouse model of Huntington diseaseHdhQ111 Mice Exhibit Tissue Specific Metabolite Profiles that Include Striatal Lipid AccumulationA broad phenotypic screen identifies novel phenotypes driven by a single mutant allele in Huntington's disease CAG knock-in mice.Force-plate quantification of progressive behavioral deficits in the R6/2 mouse model of Huntington's disease.Systematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models.Premature death and neurologic abnormalities in transgenic mice expressing a mutant huntingtin exon-2 fragment.Intergenerational and striatal CAG repeat instability in Huntington's disease knock-in mice involve different DNA repair genesA selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease miceQuantification of age-dependent somatic CAG repeat instability in Hdh CAG knock-in mice reveals different expansion dynamics in striatum and liverXpa deficiency reduces CAG trinucleotide repeat instability in neuronal tissues in a mouse model of SCA1.Msh2 acts in medium-spiny striatal neurons as an enhancer of CAG instability and mutant huntingtin phenotypes in Huntington's disease knock-in miceComprehensive behavioral and molecular characterization of a new knock-in mouse model of Huntington's disease: zQ175.MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease miceA cellular perspective on conformational disease: the role of genetic background and proteostasis networks.Natural genetic variation determines susceptibility to aggregation or toxicity in a C. elegans model for polyglutamine disease.Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approachesChromosome substitution strain assessment of a Huntington's disease modifier locusFinding the most appropriate mouse model of juvenile CLN3 (Batten) disease for therapeutic studies: the importance of genetic background and gender.Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesisMetabolic and behavioral effects of mutant huntingtin deletion in Sim1 neurons in the BACHD mouse model of Huntington's disease.DNA instability in postmitotic neurons.Effects of Pin1 Loss in Hdh(Q111) Knock-in Mice.Age-Dependent Resistance to Excitotoxicity in Htt CAG140 Mice and the Effect of Strain Background.Modifier genes as therapeutics: the nuclear hormone receptor Rev Erb alpha (Nr1d1) rescues Nr2e3 associated retinal diseaseSuppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models.Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice.Genetic modifiers of neurological diseaseAnimal models of Huntington's disease for translation to the clinic: best practices.Proteostasis in cardiac health and disease.Altered sensitivity to excitotoxic cell death and glutamate receptor expression between two commonly studied mouse strains.Huntington's disease: the case for genetic modifiers.High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgrounds.Long-term memory deficits in Huntington's disease are associated with reduced CBP histone acetylase activity.A Huntingtin Knockin Pig Model Recapitulates Features of Selective Neurodegeneration in Huntington's Disease.HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction.
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Genetic background modifies nuclear mutant huntingtin accumulation and HD CAG repeat instability in Huntington's disease knock-in mice.
description
2006 nî lūn-bûn
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2006年の論文
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2006年学术文章
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2006年学术文章
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2006年学术文章
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2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
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2006年學術文章
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name
Genetic background modifies nu ...... ngton's disease knock-in mice.
@en
Genetic background modifies nu ...... ngton's disease knock-in mice.
@nl
type
label
Genetic background modifies nu ...... ngton's disease knock-in mice.
@en
Genetic background modifies nu ...... ngton's disease knock-in mice.
@nl
prefLabel
Genetic background modifies nu ...... ngton's disease knock-in mice.
@en
Genetic background modifies nu ...... ngton's disease knock-in mice.
@nl
P2093
P50
P356
P1476
Genetic background modifies nu ...... ngton's disease knock-in mice.
@en
P2093
Alejandro Lloret
Allison Teed
Edith Lopez
Elisa Fossale
Ella Dragileva
Janice Espinola
Vanessa C Wheeler
P304
P356
10.1093/HMG/DDL125
P577
2006-05-10T00:00:00Z