Characterization of valproic acid-initiated homologous recombination

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Valproic acid increases conservative homologous recombination frequency and reactive oxygen species formation: a potential mechanism for valproic acid-induced neural tube defects.

Valproic acid, a commonly used antiepileptic agent, is associated with a 1 to 2% incidence of neural tube defects when taken during pregnancy; however, the molecular mechanism by which this occurs has not been elucidated. Previous research suggests that valproic acid exposure leads to an increase in reactive oxygen species (ROS). DNA damage due to ROS can result in DNA double-strand breaks, whi...

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Homologous recombination

DNA damage, in the form of DNA double-strand breaks, poses a considerable threat to genomic integrity and cell survival. If left unrepaired, a single double-strand break is sufficient to cause cell death and, if repaired inappropriately, a double-strand break may give rise to a potentially oncogenic translocation. Double-strand breaks in genomic DNA may arise accidentally in a number of ways, i...

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Recombination: Homologous recombination branches out

Homologous recombination can be divided into three key steps: strand exchange, branch migration and resolution. The identification of a protein complex that catalyses branch migration and Holliday junction resolution argues that the mechanism of homologous recombination is conserved from bacteria to man.

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VALPROIC ACID- valproic acid solution Par Pharmaceutical ----------

WARNINGS: LIFE THREATENING ADVERSE REACTIONS See full prescribing information for complete boxed warning. Hepato toxicity, including fatalities, usually during first 6 months o f treatment. Children under the age of two years and patients with mitochondrial disorders are at higher risk. Monitor patients c losely, and perform serum liver testing prior to therapy and at frequent intervals thereaf...

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ژورنال

عنوان ژورنال: Birth Defects Research Part B: Developmental and Reproductive Toxicology

سال: 2010

ISSN: 1542-9733,1542-9741

DOI: 10.1002/bdrb.20236