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WASHINGTON, April 23 — A mistake in the way the body's cells repair their DNA may lead to the onset of the incurable hereditary brain disorder Huntington's disease, researchers say.
ROS-induced damage to mitochondrial DNA may lead to reduced mitochondrial function in the cochlea and resultant hearing loss.
These results reveal that p21 is required for remodeling the oxygen-injured lung and suggest that failure to limit replication of damaged DNA may lead to cell death, inflammation, and abnormal remodeling.
Thus, the practice of identifying genetically distinct populations based on divergence in neutral DNA may lead to a taxonomy that ignores evolutionarily important, rapidly evolving, locally-adapted populations.
If unrepaired, these damaged DNA may lead to gene mutation and even tumor generation.
Oxidative damage of telomeric DNA may lead to dysfunction of telomeres thereby driving cells to undergo replicative senescence [ 18- 30].
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Nuclear oxidative stress damages genomic DNA and may lead to cell death, leading to aging and aging-related disorders.
Within less than a week after the publication of the scientific study, we already have "Scientists'hugelyly exciting' DNA research may lead to extending life", "DNA 'Clock' Could Predict How Long You'll Live" and "Is Your DNA Clock Running Fast?
These reports suggest that blood or urine mitochondrial DNA heteroplasmy levels, together with skeletal muscle mitochondrial DNA heteroplasmy, may lead to an improved prediction of disease prognosis.
Furthermore, the rapid evolution of repetitive DNA elements may lead to the origin of several unknown repetitive DNA elements.
But repetitive stress leading to continuous expression of heat-shock genes or DNA damage may lead to cancer [ 1, 11].
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