Sex-dependent mechanisms for expansions and contractions of the CAG repeat on affected Huntington disease chromosomes.
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Neural stem cells could serve as a therapeutic material for age-related neurodegenerative diseasesPredicting Disease Onset from Mutation Status Using Proband and Relative Data with Applications to Huntington's Disease.Measurement of mutational flow implies both a high new-mutation rate for Huntington disease and substantial underascertainment of late-onset cases.Therapeutic approaches to preventing cell death in Huntington diseaseMechanisms of trinucleotide repeat instability during human developmentThe likelihood of being affected with Huntington disease by a particular age, for a specific CAG sizeDifferent mechanisms underlie DNA instability in Huntington disease and colorectal cancerRisk reversals in predictive testing for Huntington disease.Phenotypic characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats.A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease.Trinucleotide repeat deletion via a unique hairpin bypass by DNA polymerase β and alternate flap cleavage by flap endonuclease 1.Further evidence of a maternal parent-of-origin effect on chromosome 10 in late-onset Alzheimer's disease.OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cellsPaternally transmitted FMR1 alleles are less stable than maternally transmitted alleles in the common and intermediate size range.Factors associated with HD CAG repeat instability in Huntington disease.Clinical and genetic investigation of a Brazilian family with Huntington's disease.Genetic Contributors to Intergenerational CAG Repeat Instability in Huntington's Disease Knock-In Mice.Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.Huntington disease--another chapter rewritten.HTT haplotypes contribute to differences in Huntington disease prevalence between Europe and East Asia.Population-specific genetic modification of Huntington's disease in Venezuela.Estimating the probability of de novo HD cases from transmissions of expanded penetrant CAG alleles in the Huntington disease gene from male carriers of high normal alleles (27-35 CAG).
P2860
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P2860
Sex-dependent mechanisms for expansions and contractions of the CAG repeat on affected Huntington disease chromosomes.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
1995年论文
@zh
1995年论文
@zh-cn
name
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@ast
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@en
type
label
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@ast
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@en
prefLabel
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@ast
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@en
P2093
P2860
P1476
Sex-dependent mechanisms for e ...... untington disease chromosomes.
@en
P2093
Almqvist E
Goldberg YP
Telenius H
Theilmann J
P2860
P304
P407
P577
1995-08-01T00:00:00Z