• Protein p56 encoded by the Bacillus subtilis phage phi29 inhibits host uracil-DNA glycosylase (UDG) activity. (nih.gov)
  • Correlated Mutation in the Evolution of Catalysis in Uracil DNA Glycosylase Superfamily. (musc.edu)
  • A structural determinant in the uracil DNA glycosylase superfamily for the removal of uracil from adenine/uracil base pairs. (musc.edu)
  • Specificity and catalytic mechanism in family 5 uracil DNA glycosylase. (musc.edu)
  • SMUG1 but not UNG DNA glycosylase contributes to the cellular response to recovery from 5-fluorouracil induced replication stress. (musc.edu)
  • New family of deamination repair enzymes in uracil-DNA glycosylase superfamily. (musc.edu)
  • Evaluation of the role of the vaccinia virus uracil DNA glycosylase and A20 proteins as intrinsic components of the DNA polymerase holoenzyme. (musc.edu)
  • Insights from xanthine and uracil DNA glycosylase activities of bacterial and human SMUG1: switching SMUG1 to UDG. (musc.edu)
  • Repair of deaminated base damage by Schizosaccharomyces pombe thymine DNA glycosylase. (musc.edu)
  • Vaccinia virus uracil DNA glycosylase interacts with the A20 protein to form a heterodimeric processivity factor for the viral DNA polymerase. (musc.edu)
  • In this work, we analyzed the ability of phi29 DNA polymerase to insert dUMP into DNA. (nih.gov)
  • Primer extension analysis showed that viral DNA polymerase incorporates dU opposite dA with a catalytic efficiency only 2-fold lower than that for dT. (nih.gov)
  • Using the phi29 DNA amplification system, we found that phi29 DNA polymerase is also able to carry out the extension of the dA:dUMP pair and replicate past uracil. (nih.gov)
  • Additionally, UDG and apurinic-apyrimidinic endonuclease treatment of viral DNA isolated from phi29-infected cells revealed that uracil residues arise in phi29 DNA during replication, probably as a result of misincorporation of dUMP by the phi29 DNA polymerase. (nih.gov)
  • The vaccinia virus DNA polymerase and its processivity factor. (musc.edu)
  • On the other hand, the action of UDG on uracil-containing phi29 DNA impaired in vitro viral DNA replication, which was prevented by the presence of protein p56. (nih.gov)
  • In previous studies, we suggested that this inhibition is likely a defense mechanism developed by phage phi29 to prevent the action of UDG if uracilation occurs in DNA either from deamination of cytosine or the incorporation of dUMP during viral DNA replication. (nih.gov)
  • Uracil incorporation into genomic DNA does not predict toxicity caused by chemotherapeutic inhibition of thymidylate synthase. (musc.edu)
  • Furthermore, transfection activity of uracil-containing phi29 DNA was significantly higher in cells that constitutively synthesized p56 than in cells lacking this protein. (nih.gov)
  • Thus, our data support a model in which protein p56 ensures an efficient viral DNA replication, preventing the deleterious effect caused by UDG when it eliminates uracil residues present in the phi29 genome. (nih.gov)
  • 1251 orc1%2Fcdc6 family replication initiation protein CP001857 CDS Arcpr_0002 1251. (go.jp)
  • The SAD1/RAD53 protein kinase controls multiple checkpoints and DNA damage-induced transcription in yeast. (academicinfluence.com)
  • 5-Hydroxymethylcytosine (5hmC) binding, ES-cell-specific (HMCES) crosslinks to apurinic or apyrimidinic (AP, abasic) sites in single-strand DNA (ssDNA). (nih.gov)
  • Thus, our study provides direct evidence that HMCES responds to ssDNA abasic sites in cells to prevent DNA cleavage and balance the engagement of TLS polymerases. (nih.gov)
  • Following oxidative DNA damage during mitosis, NEIL3 relocated to telomeres and recruited apurinic endonuclease 1 (APE1), indicating activation of base excision repair. (bvsalud.org)
  • This post-translational modification on lysine residues of proteins plays a crucial role in a number of cellular processes such as nuclear transport, DNA replication and repair, mitosis and signal transduction. (nih.gov)
  • HMCES Maintains Replication Fork Progression and Prevents Double-Strand Breaks in Response to APOBEC Deamination and Abasic Site Formation. (nih.gov)
  • Abasic sites induced by APOBEC3A slow both leading and lagging strand synthesis, and HMCES prevents further slowing of the replication fork by translesion synthesis (TLS) polymerases zeta (Polζ) and kappa (Polκ). (nih.gov)
  • In cells, TH10785 increases OGG1 recruitment to and repair of oxidative DNA damage. (bvsalud.org)
  • The increased repair of oxidative DNA lesions with a small molecule may have therapeutic applications in various diseases and aging. (bvsalud.org)
  • After amplification, these distinct clusters of DNA are then subject to repeated cycles of ligation or reversible single base chain terminated extension. (justia.com)
  • During these reactions, separate labeling with 4 florophores or haptens, one for each of the 4 DNA bases, allows for the identification of the incorporated base at any given position. (justia.com)