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Instability and decay of the primary structure of DNA
TLDR
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. Expand
N6-Methyladenosine in Nuclear RNA is a Major Substrate of the Obesity-Associated FTO
  • G. Jia, Ye Fu, +8 authors C. He
  • Biology, Medicine
  • Nature chemical biology
  • 5 August 2011
TLDR
FTO exhibits efficient oxidative demethylation activity of abundant N6-methyladenosine (m6A) residues in RNA in vitro, and it is shown that FTO partially colocalizes with nuclear speckles, supporting m6A in nuclear RNA as a physiological substrate of FTO. Expand
Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice
TLDR
The results provide strong support for the DNA deamination model for antibody diversification with respect to class-switching as well as hypermutation and suggest that UNG is the major mouse DNA glycosylase responsible for processing the programmed dU/dG lesions within the immunoglobulin locus. Expand
Human DNA Repair Genes
TLDR
Modulation of DNA repair should lead to clinical applications including improvement of radiotherapy and treatment with anticancer drugs and an advanced understanding of the cellular aging process. Expand
The Obesity-Associated FTO Gene Encodes a 2-Oxoglutarate-Dependent Nucleic Acid Demethylase
TLDR
It is found that recombinant murine Fto catalyzes the Fe(II)- and 2OG-dependent demethylation of 3-methylthymine in single-stranded DNA, with concomitant production of succinate, formaldehyde, and carbon dioxide. Expand
Mutations in the gene encoding the 3′-5′ DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus
TLDR
TREX1, encoding the major mammalian 3′ → 5′ DNA exonuclease, is the AGS1 gene, and AGS-causing mutations result in abrogation of TREX1 enzyme activity, and failure of which results in the triggering of an abnormal innate immune response. Expand
Reconstitution of DNA base excision‐repair with purified human proteins: interaction between DNA polymerase beta and the XRCC1 protein.
TLDR
Data indicate that XRCC1, which has no known catalytic activity, might serve as a scaffold protein during base excision‐repair, allowing for more efficient ligation after filling of a single nucleotide patch. Expand
Second pathway for completion of human DNA base excision‐repair: reconstitution with purified proteins and requirement for DNase IV (FEN1)
TLDR
The structure‐specific nuclease DNase IV (FEN1) was essential for repair of a reduced AP site, which occurred through the long‐patch BER pathway, which was largely dependent on DNA polymerase β in cell extracts, but the reaction could be reconstituted with either DNA polymerases β or δ. Expand
Rate of depurination of native deoxyribonucleic acid.
Trex1 Exonuclease Degrades ssDNA to Prevent Chronic Checkpoint Activation and Autoimmune Disease
TLDR
It is reported that Trex1, ordinarily associated with the endoplasmic reticulum (ER), relocalizes to the S phase nucleus after gamma irradiation or hydroxyurea treatment and acts on a single-stranded DNA polynucleotide species generated from processing of aberrant replication intermediates to attenuate DNA damage checkpoint signaling and prevent pathological immune activation. Expand
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