Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?
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Pathways for repairing and tolerating the spectrum of oxidative DNA lesionsMsh2 deficiency leads to dysmyelination of the corpus callosum, impaired locomotion, and altered sensory function in miceThe cockayne syndrome B protein is essential for neuronal differentiation and neuritogenesisAuditory analysis of xeroderma pigmentosum 1971-2012: hearing function, sun sensitivity and DNA repair predict neurological degenerationNeurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection.An Xpb mouse model for combined xeroderma pigmentosum and cockayne syndrome reveals progeroid features upon further attenuation of DNA repair.A genome-wide siRNA screen reveals diverse cellular processes and pathways that mediate genome stability.Minimal peroxide exposure of neuronal cells induces multifaceted adaptive responsesPremature aging and cancer in nucleotide excision repair-disorders.Age-related neuronal degeneration: complementary roles of nucleotide excision repair and transcription-coupled repair in preventing neuropathologyOn the traces of XPD: cell cycle matters - untangling the genotype-phenotype relationship of XPD mutationsAicardi-Goutieres syndrome: from patients to genes and beyond.Tethering of the conserved piggyBac transposase fusion protein CSB-PGBD3 to chromosomal AP-1 proteins regulates expression of nearby genes in humans.Aicardi-Goutières syndrome and the type I interferonopathies.Oxidative DNA damage and nucleotide excision repair.Blinded by the UV light: how the focus on transcription-coupled NER has distracted from understanding the mechanisms of Cockayne syndrome neurologic diseaseAicardi-Goutieres syndrome.TFIIH subunit alterations causing xeroderma pigmentosum and trichothiodystrophy specifically disturb several steps during transcription.The sequence-specific transcription factor c-Jun targets Cockayne syndrome protein B to regulate transcription and chromatin structure.Identification of Novel Proteins Co-Purifying with Cockayne Syndrome Group B (CSB) Reveals Potential Roles for CSB in RNA Metabolism and Chromatin Dynamics.Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a murine model of Cockayne syndrome.The conserved Cockayne syndrome B-piggyBac fusion protein (CSB-PGBD3) affects DNA repair and induces both interferon-like and innate antiviral responses in CSB-null cells.Targets of immune regeneration in rheumatoid arthritis.Complete loss of function of the ubiquitin ligase HERC2 causes a severe neurodevelopmental phenotype.The role of the neuro-astro-vascular unit in the etiology of ataxia telangiectasia.Human Cockayne syndrome B protein reciprocally communicates with mitochondrial proteins and promotes transcriptional elongation.Alcohol-induced one-carbon metabolism impairment promotes dysfunction of DNA base excision repair in adult brain.TREX1 acts in degrading damaged DNA from drug-treated tumor cells.DNA damage and neurotoxicity of chronic alcohol abuseNucleic acid binding activity of human Cockayne syndrome B protein and identification of Ca(2+) as a novel metal cofactorDNA repair deficiency and neurological disease.What role (if any) does the highly conserved CSB-PGBD3 fusion protein play in Cockayne syndrome?Sources and consequences of oxidative damage from mitochondria and neurotransmitter signaling.Cockayne syndrome: Clinical features, model systems and pathways.Mutant Cockayne syndrome group B protein inhibits repair of DNA topoisomerase I-DNA covalent complex.Brain vascular changes in Cockayne syndrome.Age-related motor neuron degeneration in DNA repair-deficient Ercc1 mice.Cockayne syndrome: a diffusion tensor imaging and volumetric study.Neuroimaging in Cockayne syndrome.Absence of RNase H2 triggers generation of immunogenic micronuclei removed by autophagy.
P2860
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P2860
Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Do all of the neurologic disea ...... he accumulation of DNA damage?
@ast
Do all of the neurologic disea ...... he accumulation of DNA damage?
@en
type
label
Do all of the neurologic disea ...... he accumulation of DNA damage?
@ast
Do all of the neurologic disea ...... he accumulation of DNA damage?
@en
prefLabel
Do all of the neurologic disea ...... he accumulation of DNA damage?
@ast
Do all of the neurologic disea ...... he accumulation of DNA damage?
@en
P2093
P2860
P1433
P1476
Do all of the neurologic disea ...... he accumulation of DNA damage?
@en
P2093
Lori Cooper
P J Brooks
Tsu-Fan Cheng
P2860
P304
P356
10.1016/J.DNAREP.2008.01.017
P577
2008-03-12T00:00:00Z