CDKN1B
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
SGK1
Gene Ontology Biological Process
- ion transmembrane transport [TAS]
- long-term memory [TAS]
- positive regulation of transporter activity [TAS]
- regulation of apoptotic process [TAS]
- regulation of blood pressure [TAS]
- regulation of catalytic activity [TAS]
- regulation of cell growth [TAS]
- regulation of cell migration [TAS]
- regulation of cell proliferation [TAS]
- regulation of gastric acid secretion [TAS]
- regulation of sequence-specific DNA binding transcription factor activity [TAS]
- renal sodium ion absorption [TAS]
- response to stress [TAS]
- sodium ion transport [TAS]
- transmembrane transport [TAS]
Gene Ontology Molecular Function
Positive Genetic
Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.
Publication
Exploring genetic interaction manifolds constructed from rich single-cell phenotypes.
How cellular and organismal complexity emerges from combinatorial expression of genes is a central question in biology. High-content phenotyping approaches such as Perturb-seq (single-cell RNA-sequencing pooled CRISPR screens) present an opportunity for exploring such genetic interactions (GIs) at scale. Here, we present an analytical framework for interpreting high-dimensional landscapes of cell states (manifolds) constructed from transcriptional phenotypes. We applied this ... [more]
Quantitative Score
- 2.954767369 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- cell proliferation (GO:0008283)
Additional Notes
- CRISPR GI Activation screen
- Cell Line:K-562 (BTO:0000664/CELLOSAURUS:CVCL_0004)
- Experimental Setup: In vitro proliferation
- GIST: A-phenotypic positive genetic interaction
- Library: CRISPRa GI library
- Significance Threshold: -2.77>GI score>2.83 (Figure 1F)
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| SGK1 CDKN1B | Biochemical Activity Biochemical Activity An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation. | Low | - | BioGRID | 1026565 |
Curated By
- BioGRID