Linked Life Data

11523791

Source:http://linkedlifedata.com/resource/pubmed/id/11523791

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-8-28
pubmed:abstractText
Cells activate DNA repair pathways and cell cycle checkpoints when they suffer damage to their genome. They also activate tolerance pathways that facilitate survival. In Escherichia coli, a mechanism known as postreplication repair (PRR) is used to bypass lesions that would otherwise present a physical block to DNA polymerase. PRR has also been proposed to occur in eukaryotic cells, although the partitioning of DNA synthesis to a discrete S-phase would suggest that it is only operative within a defined period of the cell cycle. Eukaryotic PRR has been most extensively studied in the budding yeast Saccharomyces cerevisiae. Two important genes for components of this repair pathway are RAD6, which encodes an ubiquitin-conjugating enzyme, and RAD18, which encodes a RING-finger protein and forms a heterodimer with Rad6p. Rad18p can also bind to DNA. We report here the identification of the Schizosaccharomyces pombe homologue of RAD18, which we have denoted rhp18. rhp18 mutants are hypersensitive to DNA-damaging agents, but show this hypersensitivity throughout the cell cycle. rhp18 mutants are characterised by a longer than usual DNA damage checkpoint arrest that is required for their residual viability following irradiation. Genetic analyses show that rhp18 controls a unique DNA damage repair/tolerance pathway that extends beyond the requirement to tolerate damage during S-phase, suggesting a broader definition of the function of this eukaryotic PRR protein.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1617-4615
pubmed:author
pubmed:issnType
Print
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
993-1003
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11523791-Amino Acid Sequence, pubmed-meshheading:11523791-Cell Cycle, pubmed-meshheading:11523791-Cloning, Molecular, pubmed-meshheading:11523791-DNA Damage, pubmed-meshheading:11523791-DNA Repair, pubmed-meshheading:11523791-DNA Replication, pubmed-meshheading:11523791-DNA-Binding Proteins, pubmed-meshheading:11523791-Dose-Response Relationship, Radiation, pubmed-meshheading:11523791-Escherichia coli, pubmed-meshheading:11523791-Fungal Proteins, pubmed-meshheading:11523791-Kinetics, pubmed-meshheading:11523791-Molecular Sequence Data, pubmed-meshheading:11523791-Mutagenesis, pubmed-meshheading:11523791-Recombinant Proteins, pubmed-meshheading:11523791-Saccharomyces cerevisiae, pubmed-meshheading:11523791-Saccharomyces cerevisiae Proteins, pubmed-meshheading:11523791-Schizosaccharomyces, pubmed-meshheading:11523791-Schizosaccharomyces pombe Proteins, pubmed-meshheading:11523791-Sequence Alignment, pubmed-meshheading:11523791-Sequence Homology, Amino Acid, pubmed-meshheading:11523791-Time Factors, pubmed-meshheading:11523791-Ultraviolet Rays, pubmed-meshheading:11523791-Zinc Fingers
pubmed:year
2001
pubmed:articleTitle
A homologue of the Rad18 postreplication repair gene is required for DNA damage responses throughout the fission yeast cell cycle.
pubmed:affiliation
Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, Melbourne, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't