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 Posted: Sat Nov 01, 2008 12:12 am Post subject: Tissue-specific accelerated aging in nucleotide excision rep |
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I found an interesting connection though I>m not exactly sure what it
means. NER deficiency is the cause of several premayure aging
syndromes. RNA polymerase II regulates transcription generally of
microRNAs.
Mech Ageing Dev. 2008 Jul-Aug;129(7-8):408-15. Epub 2008 May 1. Links
..Niedernhofer LJ.
Department of Microbiology and Molecular Genetics, UP Cancer
Institute, University of Pittsburgh School of Medicine, 5117 Centre
Avenue, Pittsburgh, PA 15213, USA. niedernhoferl@upmc.edu
Nucleotide excision repair (NER) is a multi-step DNA repair mechanism
that removes helix-distorting modified nucleotides from the genome.
NER is divided into two subpathways depending on the location of DNA
damage in the genome and how it is first detected. Global genome NER
identifies and repairs DNA lesions throughout the genome. This
subpathway of NER primarily protects against the accumulation of
mutations in the genome. Transcription-coupled (TC)-NER rapidly
repairs lesions in the transcribed strand of DNA that block
transcription by RNA polymerase II. TC-NER prevents cell death in
response to stalled transcription. Defects in NER cause three distinct
human diseases: xeroderma pigmentosum, Cockayne syndrome and
trichothiodystrophy. Each of these syndromes is characterized by
premature onset of pathologies that overlap with those associated with
old age in humans. This reveals the contribution of DNA damage to
multiple age-related diseases. Tissues affected include the skin, eye,
bone marrow, nervous system and endocrine axis. This review emphasizes
accelerated aging associated with xeroderma pigmentosum and discusses
the cause of these pathologies, either mutation accumulation or cell
death as a consequence of failure to repair DNA damage.
PMID: 18538374 [PubMed - indexed for MEDLINE]
PMCID: PMC2518655 [Available on 07/01/09] |
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