BAIT
WEE1
WEE1A, WEE1hu
WEE1 G2 checkpoint kinase
GO Process (5)
GO Function (2)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- nucleoplasm [TAS]
- nucleus [TAS]
Homo sapiens
PREY
CDKN1B
CDKN4, KIP1, MEN1B, MEN4, P27KIP1
cyclin-dependent kinase inhibitor 1B (p27, Kip1)
GO Process (23)
GO Function (4)
GO Component (5)
Gene Ontology Biological Process
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [TAS]
- Fc-epsilon receptor signaling pathway [TAS]
- G1/S transition of mitotic cell cycle [IDA, TAS]
- activation of cysteine-type endopeptidase activity involved in apoptotic process [IDA]
- autophagic cell death [IDA]
- cell cycle arrest [IMP]
- cellular response to lithium ion [IDA]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- mitotic cell cycle [TAS]
- mitotic cell cycle arrest [IDA]
- negative regulation of cell growth [IDA]
- negative regulation of cell proliferation [IDA, IMP]
- negative regulation of kinase activity [IDA]
- negative regulation of mitotic cell cycle [IDA]
- negative regulation of phosphorylation [IDA]
- negative regulation of transcription, DNA-templated [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- phosphatidylinositol-mediated signaling [TAS]
- positive regulation of cell death [IDA]
- positive regulation of protein catabolic process [IDA]
- regulation of cyclin-dependent protein serine/threonine kinase activity [TAS]
Gene Ontology Molecular Function
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: MK-1775
- HeLa cervical cancer cell line
Curated By
- BioGRID