BAIT
MAP2K1
CFC3, MAPKK1, MEK1, MKK1, PRKMK1
mitogen-activated protein kinase kinase 1
GO Process (36)
GO Function (6)
GO Component (11)
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- MAPK cascade [TAS]
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- Ras protein signal transduction [TAS]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- activation of MAPK activity [IDA, TAS]
- activation of MAPKK activity [TAS]
- axon guidance [TAS]
- cell cycle arrest [IMP]
- cellular component movement [TAS]
- cellular senescence [IMP]
- chemotaxis [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- negative regulation of cell proliferation [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- positive regulation of gene expression [IMP]
- positive regulation of protein serine/threonine kinase activity [IDA]
- regulation of Golgi inheritance [TAS]
- regulation of early endosome to late endosome transport [TAS]
- regulation of stress-activated MAPK cascade [TAS]
- signal transduction [TAS]
- small GTPase mediated signal transduction [TAS]
- stress-activated MAPK cascade [TAS]
- toll-like receptor 10 signaling pathway [TAS]
- toll-like receptor 2 signaling pathway [TAS]
- toll-like receptor 3 signaling pathway [TAS]
- toll-like receptor 4 signaling pathway [TAS]
- toll-like receptor 5 signaling pathway [TAS]
- toll-like receptor 9 signaling pathway [TAS]
- toll-like receptor TLR1:TLR2 signaling pathway [TAS]
- toll-like receptor TLR6:TLR2 signaling pathway [TAS]
- toll-like receptor signaling pathway [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
BLM
BS, RECQ2, RECQL2, RECQL3
Bloom syndrome, RecQ helicase-like
GO Process (20)
GO Function (12)
GO Component (8)
Gene Ontology Biological Process
- ATP catabolic process [IDA]
- DNA double-strand break processing [IDA]
- DNA duplex unwinding [IDA, IMP]
- DNA recombination [NAS]
- DNA repair [NAS]
- DNA strand renaturation [IDA]
- cellular response to DNA damage stimulus [IDA, IMP]
- cellular response to camptothecin [IDA]
- cellular response to hydroxyurea [IDA]
- cellular response to ionizing radiation [IDA]
- double-strand break repair via homologous recombination [NAS]
- mitotic G2 DNA damage checkpoint [IDA]
- negative regulation of DNA recombination [IMP]
- negative regulation of cell division [IMP]
- positive regulation of transcription, DNA-templated [IDA]
- protein oligomerization [IDA]
- regulation of cyclin-dependent protein serine/threonine kinase activity [IMP]
- replication fork processing [IDA]
- replication fork protection [NAS]
- response to X-ray [IDA]
Gene Ontology Molecular Function- ATP binding [IDA]
- ATP-dependent DNA helicase activity [IDA, IMP]
- ATP-dependent helicase activity [IDA]
- ATPase activity [IDA]
- G-quadruplex DNA binding [IDA]
- annealing helicase activity [IDA]
- bubble DNA binding [IDA]
- four-way junction helicase activity [IDA]
- helicase activity [IDA]
- p53 binding [IPI]
- protein binding [IPI]
- single-stranded DNA binding [IDA]
- ATP binding [IDA]
- ATP-dependent DNA helicase activity [IDA, IMP]
- ATP-dependent helicase activity [IDA]
- ATPase activity [IDA]
- G-quadruplex DNA binding [IDA]
- annealing helicase activity [IDA]
- bubble DNA binding [IDA]
- four-way junction helicase activity [IDA]
- helicase activity [IDA]
- p53 binding [IPI]
- protein binding [IPI]
- single-stranded DNA binding [IDA]
Gene Ontology Cellular Component
Homo sapiens
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
A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.
An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific drug targets. Here we use a multi-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy. First, we screen in yeast ∼169,000 potential interactions among orthologs of human tumor suppressor genes (TSG) and ... [more]
Mol. Cell Aug. 04, 2016; 63(3);514-25 [Pubmed: 27453043]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507) [hela cell (BTO:0000567)]
Additional Notes
- Chemo-genetic screen with siRNAs
- Drug: PD0325901
- HeLa cervical cancer cell line
Curated By
- BioGRID