Search

Your search keyword '"PRR, Postreplication repair"' showing total 2 results
Start Over Descriptor "PRR, Postreplication repair"
2 results on '"PRR, Postreplication repair"'

1. Roles of mouse UBC13 in DNA postreplication repair and Lys63-linked ubiquitination

Author

Ashley, Carolyn, Pastushok, Landon, McKenna, Sean, Ellison, Michael J., and Xiao, Wei

Subjects
*ANTISENSE DNA, *GLUTATHIONE transferase
Abstract

The E2 enzyme, Ubc13, and the E2 enzyme variants, Uevs, form stable, high affinity complexes for the assembly of Lys63-linked ubiquitin chains. This process is involved in error-free DNA postreplication repair, the activation of kinases in the NF-κB signaling pathway and possibly other cellular processes. To further investigate the roles played by Ubc13 in a whole animal model, we report here the molecular cloning of mouse UBC13 and show for the first time that a mammalian UBC13 gene is able to complement the yeast ubc13 null mutant. Furthermore, in vitro analyses and a yeast two-hybrid assay show that mUbc13 is able to form stable complexes with various Uevs. In the presence of E1 and ATP, mUbc13 forms thiolesters with ubiquitin; however, the formation of Lys63-linked di-ubiquitin and multi-ubiquitin chains is dependent on Uevs. These results suggest that the roles of UBC13 are conserved throughout eukaryotes and that the mouse is an appropriate model for the study of Ubc13-mediated Lys63-linked ubiquitin signaling pathways in humans. [Copyright &y& Elsevier]

Published
2002
Full Text
View/download PDF

2. DNA damage tolerance by recombination: Molecular pathways and DNA structures

Author

Dana Branzei and Barnabas Szakal

Subjects
0301 basic medicine, Genome instability, DNA End-Joining Repair, Base Pair Mismatch, NPS, Natural Pausing Sites, DNA-Directed DNA Polymerase, Biochemistry, DNA Mismatch Repair, Fork reversal, chemistry.chemical_compound, DNA Breaks, Double-Stranded, Polymerase, Genetics, Mammals, biology, Ubiquitin/SUMO modifications, SLDs, SUMO-like domains, CFS, Common Fragile Sites, DNA mismatch repair, DNA Replication, Saccharomyces cerevisiae Proteins, DNA damage, Mini Review, PCNA, proliferating cell nuclear antigen, HR, Homologous recombination, Computational biology, STR, Sgs1-Top3-Rmi1, Saccharomyces cerevisiae, DDR, DNA damage response, Genomic Instability, 03 medical and health sciences, DSBs, Double strand breaks, parasitic diseases, Chromosome replication, PCNA, Animals, Humans, Homologous recombination, Molecular Biology, DNA damage tolerance, PRR, Postreplication repair, DNA replication, HJ, Holliday Junction, DNA Helicases, Replication stress, Recombinational DNA Repair, Cell Biology, DNA, 030104 developmental biology, DDT, DNA damage tolerance, chemistry, TLS, Translesion Synthesis, biology.protein, ss, single stranded
Abstract

Replication perturbations activate DNA damage tolerance (DDT) pathways, which are crucial to promote replication completion and to prevent fork breakage, a leading cause of genome instability. One mode of DDT uses translesion synthesis polymerases, which however can also introduce mutations. The other DDT mode involves recombination-mediated mechanisms, which are generally accurate. DDT occurs prevalently postreplicatively, but in certain situations homologous recombination is needed to restart forks. Fork reversal can function to stabilize stalled forks, but may also promote error-prone outcome when used for fork restart. Recent years have witnessed important advances in our understanding of the mechanisms and DNA structures that mediate recombination-mediated damage-bypass and highlighted principles that regulate DDT pathway choice locally and temporally. In this review we summarize the current knowledge and paradoxes on recombination-mediated DDT pathways and their workings, discuss how the intermediate DNA structures may influence genome integrity, and outline key open questions for future research.

Published
2016

Catalog

Books, media, physical & digital resources
See catalog results