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Do all of the neurologic diseases in patients with DNA repair gene mutations result from the accumulation of DNA damage?

Published in: DNA Repair

Date of publication: 2008-03-12

Language: English

Main subject: DNA damage

Bibliographic databases:

Cites articles 97

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DNA repair helicase: a component of BTF2 (TFIIH) basic transcription factor
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Microglia: a sensor for pathological events in the CNS
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Ataxia without telangiectasia masquerading as benign hereditary chorea
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Stimulation of RAR alpha activation function AF-1 through binding to the general transcription factor TFIIH and phosphorylation by CDK7
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A mouse model for the basal transcription/DNA repair syndrome trichothiodystrophy
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Glial cell-specific differences in response to alkylation damage
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Structural and functional neuropathology in transgenic mice with CNS expression of IFN-alpha
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Neurodegeneration in hereditary nucleotide repair disorders
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Defective neurogenesis resulting from DNA ligase IV deficiency requires Atm
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Manitoba aboriginal kindred with original cerebro-oculo- facio-skeletal syndrome has a mutation in the Cockayne syndrome group B (CSB) gene
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ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation
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Glial cell type-specific responses to menadione-induced oxidative stress
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Xeroderma pigmentosum/cockayne syndrome complex: first neuropathological study and review of eight other cases
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Ataxia telangiectasia mutated-dependent apoptosis after genotoxic stress in the developing nervous system is determined by cellular differentiation status
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The 14th Datta Lecture. TFIIH: from transcription to clinic
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Oxidative stress and disturbed glutamate transport in hereditary nucleotide repair disorders
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