TOR2
Gene Ontology Biological Process
- TOR signaling [IC, IMP]
- actin filament reorganization involved in cell cycle [TAS]
- cytoskeleton organization [IMP]
- establishment or maintenance of actin cytoskeleton polarity [IMP]
- negative regulation of autophagy [IGI]
- positive regulation of Rho guanyl-nucleotide exchange factor activity [IGI, IMP]
- positive regulation of Rho protein signal transduction [IGI, IMP]
- positive regulation of endocytosis [IMP]
- regulation of cell cycle [TAS]
- regulation of cell growth [TAS]
- ribosome biogenesis [IMP]
- signal transduction [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
PKC1
Gene Ontology Biological Process
- actin filament organization [IGI]
- cytoplasmic mRNA processing body assembly [IMP]
- intracellular signal transduction [IMP]
- peroxisome degradation [IMP]
- protein phosphorylation [IDA]
- regulation of fungal-type cell wall organization [IMP]
- regulation of nuclear-transcribed mRNA poly(A) tail shortening [IMP]
- signal transduction [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Phosphorylation)
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.
Publication
Methylglyoxal activates the target of rapamycin complex 2-protein kinase C signaling pathway in Saccharomyces cerevisiae.
Methylglyoxal is a typical 2-oxoaldehyde derived from glycolysis. We show here that methylglyoxal activates the Pkc1-Mpk1 mitogen-activated protein (MAP) kinase cascade in a target of rapamycin complex 2 (TORC2)-dependent manner in the budding yeast Saccharomyces cerevisiae. We demonstrate that TORC2 phosphorylates Pkc1 at Thr(1125) and Ser(1143). Methylglyoxal enhanced the phosphorylation of Pkc1 at Ser(1143), which transmitted the signal to the ... [more]
Throughput
- Low Throughput
Additional Notes
- Figure 3
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| TOR2 PKC1 | 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 | 3537540 | |
| TOR2 PKC1 | Dosage Rescue Dosage Rescue A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene. | Low | - | BioGRID | 155017 | |
| TOR2 PKC1 | Dosage Rescue Dosage Rescue A genetic interaction is inferred when over expression or increased dosage of one gene rescues the lethality or growth defect of a strain that is mutated or deleted for another gene. | Low | - | BioGRID | 155018 | |
| PKC1 TOR2 | Negative Genetic Negative Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores. | High | -0.2738 | BioGRID | 1919828 | |
| TOR2 PKC1 | Negative Genetic Negative Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores. | High | -0.3756 | BioGRID | 1941914 |
Curated By
- BioGRID