BAIT
FEN1
FEN-1, MF1, RAD2
flap structure-specific endonuclease 1
GO Process (14)
GO Function (10)
GO Component (6)
Gene Ontology Biological Process
- DNA catabolic process, endonucleolytic [IDA, IMP]
- DNA catabolic process, exonucleolytic [TAS]
- DNA repair [TAS]
- DNA replication [TAS]
- DNA replication, removal of RNA primer [IDA]
- DNA strand elongation involved in DNA replication [TAS]
- RNA phosphodiester bond hydrolysis, endonucleolytic [IDA]
- UV protection [TAS]
- base-excision repair [TAS]
- double-strand break repair [TAS]
- mitotic cell cycle [TAS]
- telomere maintenance [TAS]
- telomere maintenance via recombination [TAS]
- telomere maintenance via semi-conservative replication [TAS]
Gene Ontology Molecular Function- 5'-3' exonuclease activity [IDA]
- 5'-flap endonuclease activity [IDA, IMP]
- DNA binding [IMP]
- RNA-DNA hybrid ribonuclease activity [IDA]
- damaged DNA binding [TAS]
- double-stranded DNA binding [TAS]
- double-stranded DNA exodeoxyribonuclease activity [TAS]
- endonuclease activity [TAS]
- exonuclease activity [TAS]
- protein binding [IPI]
- 5'-3' exonuclease activity [IDA]
- 5'-flap endonuclease activity [IDA, IMP]
- DNA binding [IMP]
- RNA-DNA hybrid ribonuclease activity [IDA]
- damaged DNA binding [TAS]
- double-stranded DNA binding [TAS]
- double-stranded DNA exodeoxyribonuclease activity [TAS]
- endonuclease activity [TAS]
- exonuclease activity [TAS]
- protein binding [IPI]
Gene Ontology Cellular Component
Homo sapiens
PREY
RAD57
putative DNA-dependent ATPase RAD57, L000001577, YDR004W
Protein that stimulates strand exchange; stimulates strand exchange by stabilizing the binding of Rad51p to single-stranded DNA; involved in the recombinational repair of double-strand breaks in DNA during vegetative growth and meiosis; forms heterodimer with Rad55p
GO Process (5)
GO Function (2)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
Synthetic Lethality
A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.
Publication
Modeling DNA trapping of anticancer therapeutic targets using missense mutations identifies dominant synthetic lethal interactions.
Genetic screens can identify synthetic lethal (SL) interactions and uncover potential anticancer therapeutic targets. However, most SL screens have utilized knockout or knockdown approaches that do not accurately mimic chemical inhibition of a target protein. Here, we test whether missense mutations can be utilized as a model for a type of protein inhibition that creates a dominant gain-of-function cytotoxicity. We ... [more]
Proc Natl Acad Sci U S A Dec. 06, 2020; 118(14); [Pubmed: 33782138]
Throughput
- Low Throughput
Ontology Terms
- phenotype: viability (APO:0000111)
Additional Notes
- Quantitative growth curve analysis validated 8 of the dominant SL interactions that resulted upon hFEN1-D181A expression
Curated By
- BioGRID