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
MRE11
NGS1, RAD58, XRS4, MRX complex nuclease subunit, L000004732, L000001149, L000004275, YMR224C
Nuclease subunit of the MRX complex with Rad50p and Xrs2p; complex functions in repair of DNA double-strand breaks and in telomere stability; Mre11p associates with Ser/Thr-rich ORFs in premeiotic phase; nuclease activity required for MRX function; widely conserved; forms nuclear foci upon DNA replication stress
GO Process (11)
GO Function (9)
GO Component (3)
Gene Ontology Biological Process
- DNA double-strand break processing involved in repair via synthesis-dependent strand annealing [IMP]
- DNA repair [IMP]
- ascospore formation [IMP]
- base-excision repair [IMP]
- double-strand break repair via break-induced replication [IGI, IMP]
- double-strand break repair via nonhomologous end joining [IMP]
- meiotic DNA double-strand break formation [TAS]
- meiotic DNA double-strand break processing [TAS]
- mitochondrial double-strand break repair via homologous recombination [IMP]
- reciprocal meiotic recombination [IMP]
- regulation of transcription during meiosis [IMP]
Gene Ontology Molecular Function- 3'-5' exonuclease activity [IDA]
- G-quadruplex DNA binding [IDA]
- adenylate kinase activity [IDA]
- double-stranded telomeric DNA binding [IDA]
- endodeoxyribonuclease activity [IDA]
- endonuclease activity [IDA]
- protein complex scaffold [IGI, IMP]
- single-stranded telomeric DNA binding [IDA]
- telomeric DNA binding [IDA]
- 3'-5' exonuclease activity [IDA]
- G-quadruplex DNA binding [IDA]
- adenylate kinase activity [IDA]
- double-stranded telomeric DNA binding [IDA]
- endodeoxyribonuclease activity [IDA]
- endonuclease activity [IDA]
- protein complex scaffold [IGI, IMP]
- single-stranded telomeric DNA binding [IDA]
- telomeric DNA binding [IDA]
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