Double-strand DNA break formation mediated by flap endonuclease-1.
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TLDR
It is reported that, instead of DNA polymerase δ/ϵ, flap endonuclease-1 (FEN-1), an enzyme involved in base excision repair, is responsible for the formation of double-strand DNA break in the assay.About:
This article is published in Journal of Biological Chemistry.The article was published on 2003-09-12 and is currently open access. It has received 18 citations till now. The article focuses on the topics: DNA damage & DNA clamp.read more
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Journal ArticleDOI
Flap Endonuclease 1: A Central Component of DNA Metabolism
TL;DR: FEN1 is a genome stabilization factor that prevents flaps from equilibrating into structures that lead to duplications and deletions and interacts with other nucleases and helicases that allow it to act efficiently on structured flaps.
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Multiple but dissectible functions of FEN-1 nucleases in nucleic acid processing, genome stability and diseases
TL;DR: This review summarizes the knowledge gained through efforts in the past decade to define its structural elements for specific activities and possible pathological consequences of altered functions of this multirole player.
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Flap endonuclease 1 is overexpressed in prostate cancer and is associated with a high Gleason score
John S. Lam,David Seligson,Hong Yu,Ai Li,Mervi Eeva,Allan J. Pantuck,Gang Zeng,Steve Horvath,Arie S. Belldegrun +8 more
TL;DR: To investigate the expression and potential clinical usefulness of structure‐specific flap endonuclease 1 (FEN‐1) in human primary prostate cancer using tissue microarray technology, as FEN-1 was recently identified to be overexpressed in CL1.1, the most aggressive clone generated from the hormone‐refractory prostate cancer cell line CL1.'
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Poly(ADP-ribosyl)ation as a DNA damage-induced post-translational modification regulating poly(ADP-ribose) polymerase-1-topoisomerase I interaction.
TL;DR: It is demonstrated that PARP-1 co-localizes with Topo I throughout the cell cycle and results suggest that a function for the automodification reaction is to regulate the interaction between PARp-1 and topoisomerase I, and consequently, the Topa I activity, in response to DNA damage.
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Hairpin Structure-forming Propensity of the (CCTG·CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2
TL;DR: The genetic instabilities of (CCTG·CAGG)n tetranucleotide repeats were investigated to evaluate the molecular mechanisms responsible for the massive expansions found in myotonic dystrophy type 2 (DM2) patients, and a marked propensity to adopt a defined base paired hairpin structure was found.
References
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Instability and decay of the primary structure of DNA
TL;DR: The spontaneous decay of DNA is likely to be a major factor in mutagenesis, carcinogenesis and ageing, and also sets limits for the recovery of DNA fragments from fossils.
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Genome maintenance mechanisms for preventing cancer
TL;DR: This review summarizes the main DNA caretaking systems and their impact on genome stability and carcinogenesis.
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The DNA damage response: putting checkpoints in perspective
TL;DR: The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development, and this work has shown that direct activation of DNA repair networks is needed to correct this problem.
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Resonant Formation of DNA Strand Breaks by Low-Energy (3 to 20 eV) Electrons
TL;DR: It is shown that reactions of such electrons, even at energies well below ionization thresholds, induce substantial yields of single- and double-strand breaks in DNA, which are caused by rapid decays of transient molecular resonances localized on the DNA's basic components.