Folate depletion in human lymphocytes up-regulates p53 expression despite marked induction of strand breaks in exons 5-8 of the gene [An article from: ... Toxicology and Environmental Mutagenesis]
Book Details
PublisherElsevier
ISBN / ASINB000PC6NJU
ISBN-13978B000PC6NJ4
AvailabilityAvailable for download now
MarketplaceUnited States 🇺🇸
Description
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2007. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Low dietary folate intake is associated with an elevated risk for carcinogenesis. One putative mechanism by which folate depletion promotes carcinogenesis is by inducing gene-specific strand breakage and impaired expression of affected genes. Primary human lymphocytes were cultured in media containing 15, 30 or 120nM folic acid. p53 strand breaks, gene and protein expression, and p21 transcript were determined. Cells grown in 15nM folate developed significant levels of p53 strand breaks, reflected by reductions in amplifiable DNA from p53 exons 5-8 (~40% loss, P
Description:
Low dietary folate intake is associated with an elevated risk for carcinogenesis. One putative mechanism by which folate depletion promotes carcinogenesis is by inducing gene-specific strand breakage and impaired expression of affected genes. Primary human lymphocytes were cultured in media containing 15, 30 or 120nM folic acid. p53 strand breaks, gene and protein expression, and p21 transcript were determined. Cells grown in 15nM folate developed significant levels of p53 strand breaks, reflected by reductions in amplifiable DNA from p53 exons 5-8 (~40% loss, P
